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9,700 | Clinical surveillance of a tined, bipolar, silicone-insulated ventricular pacing lead. | This study assesses short- and long-term performance of the S80TB ventricular lead manufactured by Sorin Biomedica, Italy.</AbstractText>Three hundred and thirty leads were implanted and had complete follow-up with us for a minimum of 60 months or up to failure, removal, and/or patient death (mean 40 months, range: 1 day to 81 months). Thirty-two patients (9.6%) had spontaneous lead-related complications: 7 (2.1%) occurred during the first week; 25 (7.6%) had chronic complications, of which 20 (6.1%) necessitated re-operations; 3 (0.9%) were lead material failures. Of the 110 re-operations (90 pacemaker replacements and 20 operations due to complications), 7 additional cases (6.4%) were complicated by unique connector damage that occurred during disconnection of the lead from the connector block. The Kaplan-Meier estimated 5-year lead survival free of lead material failure and free of any significant lead complication were 97.9 and 87%, respectively.</AbstractText>The S80TB lead demonstrates an acceptable rate of acute and chronic spontaneous complications and very few lead material failures over 5 years of follow-up. However, there seems to be a relatively high incidence of connector damage during disconnection from the connector block. Extra caution is required during those procedures in patients with this lead.</AbstractText> |
9,701 | Passive electrode effect reduces defibrillation threshold in bi-filament middle cardiac vein defibrillation. | To investigate whether a passive electrode effect decreases defibrillation threshold (DFT) in multi-filament middle cardiac vein (MCV) defibrillation.</AbstractText>Twelve pigs underwent active housing (AH) insertion, with defibrillation coils placed transvenously in right ventricular apex and superior vena cava. The MCV was cannulated, and 1.12F, 50 mm coil electrodes (Ela Medical SA, France) were deployed in its right and left branches. Lead placement was possible in 11 of 12 animals. DFT (J, mean +/- SD) was determined by three-reversal binary search and compared between the MCV monofilament (single filament deployed) and the AH (25.9 +/- 10.9) and the MCV mono + passive filaments (both filaments deployed, one connected) and the AH (19.9 +/- 11.4); 24% DFT reduction P = 0.008.</AbstractText>A bystander electrode adjacent to a monofilament electrode in the MCV reduces DFT by 24% when compared with monofilament MCV alone. Microfilament electrodes decrease DFT as auxiliary anode but not as sole anode.</AbstractText> |
9,702 | Abnormalities of pulmonary venous flow in patients with lone atrial fibrillation. | Mechanisms underlying lone atrial fibrillation (LAF) are poorly defined. We sought to investigate indices of left atrial (LA) function in patients with recurrent LAF, in comparison with that in healthy subjects.</AbstractText>Investigations were performed in 42 patients aged 51.8 +/- 8.7 at least 30 days after the last episode of LAF and in 38 healthy controls. Each subject underwent echocardiographic evaluation including left ventricular parameters and LA function indices. LA ejection fraction served as a measure of LA systolic performance, and acceleration (SAT) and deceleration time (SDT) of systolic phase of pulmonary venous flow (PVF) corresponded to LA relaxation and compliance, respectively. Patients with LAF showed significantly lower values of SAT (179.1 +/- 63.2 vs. 199.2 +/- 45.1 ms, P < 0.02) and higher values of SDT (250.8 +/- 81.6 vs. 211.7 +/- 57.3 ms, P < 0.01) when compared with controls. No significant differences were found with respect to other measured parameters. The combination of SAT < 185 ms and SDT > 239 ms showed a positive predictive value of 92% in the identification of patients prone to LAF.</AbstractText>This study suggests that (i) patients with LAF have abnormalities of the systolic phase of PVF and (ii) Doppler estimation of PVF seems to be very valuable in the evaluation of patients with LAF.</AbstractText> |
9,703 | The role of pacing mode in the development of atrial fibrillation. | Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients. |
9,704 | Predictors of chronotropic incompetence in the pacemaker patient population. | We prospectively evaluated results from cardiopulmonary exercise testing for chronotropic incompetence (CI) in a cohort of 292 pacemaker patients. In addition, we evaluated comorbidity and antiarrhythmic patient data as indicators of CI.</AbstractText>On the basis of exercise stress testing and application of the definition of CI by Wilkoff, 51% of our cohort was categorized as having CI. Indications for pacemaker implant for this patient group were 42% atrioventricular block, 56% sinus node disease, and 59% atrial fibrillation. Maximum oxygen uptake (VO(2) max) and exercise duration were significantly reduced among CI pacemaker patients, whereas oxygen uptake at the anaerobic threshold remained unchanged. The following clinical characteristics were significant predictors of CI: existence of coronary artery disease (P = 0.038), presence of an acquired valvular heart disease (P = 0.037), and former cardiac surgery (P = 0.041). Age, gender, arterial hypertension, cardiomyopathy, congenital heart disease, left ventricular ejection fraction, and time period between stress-exercise examination and pacemaker implantation were not significant predictors of CI. Chronic antiarrhythmic therapy with digitalis (P = 0.013), beta blockers (P = 0.036), and amiodarone (P = 0.045) were significant predictors of CI. In contrast, medication with class I and IV antiarrhythmics had no significant correlation with CI.</AbstractText>We found the following characteristics predictive of CI in this pacemaker patient population: VO(2) max, existence of coronary artery disease or acquired valvular heart disease, previous cardiac surgery, as well as medication with digitalis, beta blockers, and amiodarone.</AbstractText> |
9,705 | Upgrade to biventricular pacing in patients with conventional pacemakers and heart failure: a double-blind, randomized crossover study. | To investigate whether patients with previously implanted conventional pacemakers and severe heart failure benefit from an upgrade to a biventricular system.</AbstractText>Study inclusion criteria were New York Heart Association (NYHA) classes III and IV, dominant paced rhythm, and no left bundle branch block in the pre-pacing ECG. Ten patients with pacemakers (four VVIR due to slow atrial fibrillation and six DDDR, of which four were due to high-degree atrioventricular block and two to sinus node disease) were upgraded to a biventricular pacing (BVP) system. The median duration of pacing before the upgrade was 5.7 years. Assessments of 6-min walk test, symptom score, brain natriuretic peptide (pro-BNP), and echocardiography were made pre-operatively. After a run-in period of 1 month in BVP following the upgrade, the patients were randomized to a 2-month period in either BVP or right ventricular pacing (RVP), followed by 2 months in the other mode, in a double-blind crossover fashion. After each period, the pre-operative measurements were repeated. After study completion, patients were asked to select their preferred period. The median 6-min walking distance was significantly longer in BVP (400 m) vs. RVP (315 m), P = 0.02. The symptom score was also significantly better in BVP (P = 0.005). Median pro-BNP was significantly lower in BVP than in RVP, 3,030 vs. 5,064 ng/L (P = 0.005). Six patients demanded an early crossover in RVP but none in BVP (P = 0.015), and all patients except one expressed a preference for BVP. However, echo parameters did not show any significant differences between BVP and RVP.</AbstractText>Pacemaker patients with heart failure and dominant paced heart rhythm benefit substantially from an upgrade to BVP, in terms of physical performance and symptoms. The upgrade resulted in significantly improved cardiac function as reflected by reduced levels of pro-BNP.</AbstractText> |
9,706 | Rapid induction of cerebral hypothermia by aortic flush during normovolemic cardiac arrest in pigs. | Induction of deep cerebral hypothermia before reperfusion might improve neurologic outcome after cardiac arrest. We hypothesized that an aortic flush with cold saline during cardiac arrest is able to induce deep cerebral hypothermia and that the cooling efficiency can be enhanced by a) increasing the arteriovenous pressure gradient during the flush with vasopressin; b) improving the cerebral microcirculation during the flush with the thrombolytic agent alteplase; and c) increasing the arteriovenous pressure gradient further with venting the right heart by draining blood during the flush.</AbstractText>Prospective randomized experimental study.</AbstractText>University research laboratory.</AbstractText>Twenty-four pigs Large White breed (31-42 kg).</AbstractText>After 10 mins of ventricular fibrillation, pigs received an aortic flush (100 mL/kg, 4 degrees C, flow rate 35 mL/kg/min) into the descending aorta via a balloon catheter. The animals were subjected randomly to either an aortic flush with saline, saline plus vasopressin 1.2 IU/kg, saline plus alteplase 1 mg/kg, saline plus a combination of vasopressin 1.2 IU/kg and alteplase 1 mg/kg, or saline plus vasopressin 1.2 IU/kg and venting the right heart. Arterial and venous pressures and brain temperatures were recorded for an observation time of 10 mins after flush.</AbstractText>A sufficient arteriovenous pressure gradient and deep cerebral hypothermia were only achieved with a flush containing vasopressin (brain temperature 16.1+/-1.3 degrees C in the vasopressin group vs. 35.4+/-1.5 degrees C in the saline group, p<.001); combining vasopressin with alteplase, or venting the right heart, did not further enhance the cooling efficiency of the flush.</AbstractText>A cold saline aortic flush with vasopressin rapidly decreases brain temperature during prolonged normovolemic cardiac arrest in pigs. Whether deep cerebral hypothermia induced before reperfusion can improve neurologic outcome after cardiac arrest needs further investigation in large animal outcome studies.</AbstractText> |
9,707 | [Effect of oral cordarone in reversing persistent atrial fibrillation]. | To observe the efficacy and safety of oral cordarone dir reversing persistent atrial fibrillation (AF). METHODS; Eighty-two symptomatic chronic AF out-patients without history of acute diseases or severe hepatic/thyroid dysfunction were given oral cordarone at the loading dose of 200 mg thrice a day for 1-4 weeks followed by a twice-daily administration for another 1-4 weeks, with the maintenance dose of 200 or 100 mg once a day. The incidence of stroke and cardiac events and the mortality rate were compared between 43 patients with restored rhythm on cordarone and 39 patients on digoxin and/or betaloc for ventricular rhythm control.</AbstractText>Among the 82 patients, sinus rhythm restoration was achieved in 43, with a successful rate of 52%. In 18 patients, the ejection fraction increased from (32+/-8)% to (46+/-10)%, left atrium diameter decreased from (4.6+/-1.1) cm to (4.1+/-0.8) cm. Except for slight T4 increase, QT prolongation and bradycardia in 3 cases, severe side effects were not observed in this study. Only one patient with restored sinus rhythm required rehospitalization after half a year for worsened heart failure, but in patients with controlled ventricular rhythm, 1 developed stroke, 1 experienced heart attack and 1 died of heart failure with bleeding.</AbstractText>For patients with symptomatic reversible persistent AF, active treatment with cordarone can be convenient, effective and safe for sinus rhythm restoration.</AbstractText> |
9,708 | A role for CETP TaqIB polymorphism in determining susceptibility to atrial fibrillation: a nested case control study. | Studies investigating the genetic and environmental characteristics of atrial fibrillation (AF) may provide new insights in the complex development of AF. We aimed to investigate the association between several environmental factors and loci of candidate genes, which might be related to the presence of AF.</AbstractText>A nested case-control study within the PREVEND cohort was conducted. Standard 12 lead electrocardiograms were recorded and AF was defined according to Minnesota codes. For every case, an age and gender matched control was selected from the same population (n = 194). In addition to logistic regression analyses, the multifactor-dimensionality reduction (MDR) method and interaction entropy graphs were used for the evaluation of gene-gene and gene-environment interactions. Polymorphisms in genes from the Renin-angiotensin, Bradykinin and CETP systems were included.</AbstractText>Subjects with AF had a higher prevalence of electrocardiographic left ventricular hypertrophy, ischemic heart disease, hypertension, renal dysfunction, elevated levels of C-reactive protein (CRP) and increased urinary albumin excretion as compared to controls. The polymorphisms of the Renin-angiotensin system and Bradykinin gene did not show a significant association with AF (p > 0.05). The TaqIB polymorphism of the CETP gene was significantly associated with the presence of AF (p < 0.05). Using the MDR method, the best genotype-phenotype models included the combination of micro- or macroalbuminuria and CETP TaqIB polymorphism, CRP >3 mg/L and CETP TaqIB polymorphism, renal dysfunction and the CETP TaqIB polymorphism, and ischemic heart disease and CETP TaqIB polymorphism (1000 fold permutation testing, P < 0.05). Interaction entropy graph showed that the combination of albuminuria and CETP TaqIB polymorphism removed the most entropy.</AbstractText>CETP TaqIB polymorphism is significantly associated with the presence of AF in the context of micro- or macroalbuminuria, elevated C-reactive protein, renal dysfunction, and ischemic heart disease.</AbstractText> |
9,709 | Acutely decompensated heart failure: characteristics of hospitalized patients and opportunities to improve their care. | Heart failure (HF) remains a major public health problem in western countries, despite the enormous progress in its diagnosis and treatment. Acute and chronic decompensated HF are leading medical causes of hospitalization among people aged over 65 years in European countries, the USA, Australia and New Zealand. However, there have been few studies on acute and chronic decompensated HF and the European Society of Cardiology (ESC) guidelines on this subject have only just been published.</AbstractText>To evaluate the overall prevalence of hospitalization due to HF according to its subtypes, comorbidities, and decompensating factors, in the Medical Department of a central teaching hospital in an urban area.</AbstractText>We performed a retrospective observational study of patients admitted consecutively to the Medical Department via the emergency room between January and June 2001. Discharge casenotes on 1038 admissions were reviewed. Those with a diagnosis of HF or cardiovascular conditions associated with or precursors of HF were analyzed. Cases with a final diagnosis of HF according to the criteria of the ESC guidelines were included in the study. We evaluated the overall prevalence of HF and subtypes of cardiac dysfunction, etiological risk factors, patients' demographic characteristics, decompensating factors, comorbidity, mean length of hospital stay, and in-hospital mortality rate.</AbstractText>We identified 180 patients with HF (17.4%), mean age 74.6 +/- 14; 87 were male (48%), aged 73.7 +/- 14.2, and 93 female (52%), aged 75.6 +/- 14. Left ventricular systolic dysfunction (LVSD) was present in 42.2% of cases, preserved left ventricular systolic function in 32.6%, and valvular heart disease in 10.6%. Hypertension and coronary artery disease were the main etiological risk factors (62.2% and 42.8% respectively). Atrial fibrillation was recorded in 43.4% of the patients, diabetes was diagnosed in 21.6%, and anemia and chronic obstructive pulmonary disease in about one third. Infection, predominantly respiratory, was the main factor triggering decompensation, followed by uncontrolled hypertension and supraventricular tachyarrhythmia. At admission, 42.2% of the patients were in NYHA class III and 44.8% in NYHA class IV. HF patients had a mean hospital stay of 13.8 days, slightly shorter than the mean overall stay of patients admitted to the Medical Department in the same period (14.5 days). In-hospital mortality for HF patients was 7.7%, with HF being the first cause of admission to the Medical Department, followed by stroke (10.6%).</AbstractText>This study confirms the high prevalence of acute or chronic decompensated HF in patients hospitalized in the Medical Department of a central teaching hospital in an urban area. The patients were mainly elderly, of both genders, with a slightly higher proportion of HF due to LVSD. Most patients were in NYHA classes III and IV. Mean hospital stay was no longer than that of all patients admitted in the same period. The in-hospital mortality rate was low. The age-group affected and the high prevalence of multiple comorbidities emphasize the need to establish HF clinics with multidisciplinary teams to manage these patients, and health authorities must be made aware of the burden of this syndrome.</AbstractText> |
9,710 | [The role of transesophageal echocardiopgraphy in detection of cardiogenic and aortic sources of embolism in stroke and transient ischaemic attacks]. | To prospectively investigate the prevalence of definite and potential sources of cardiogenic embolism and embolism from ascending aorta and aortic arch in patients with a cryptogenic stroke or transient ischaemic attack (TIA).</AbstractText><AbstractText Label="MATERIAL/METHODS" NlmCategory="METHODS">The study group consisted of 218 consecutive patients (146 males, mean age 59.4 +/- 11.5, range 38-83 years) without significant stenoses of carotic and vertebral arteries. All patients underwent biplane/multiplane transesophageal echocardiography (TEE). 77.5% of patients suffered a stroke and 22.5% had a TIA. Sinus rhythm was in 74.8% of the patients, atrial fibrillation in 22.0% and pacemaker rhythm in 3.2%.</AbstractText>1. Definite source of embolism was identified in 21.6% of patients. The most frequent finding was a thrombus of the left atrial (LA) appendage - 12.4%. Less frequently found were mobile thrombus of aortic arch - 3.7%, thrombus of LA body - 2.3%, left ventricular thrombus - 2.3%, thrombus of valvular prosthesis - 1.4% and heart tumor - 0.5%. 2. The total prevalence of potential sources of embolism was 61.5%. Only potential source (without definite source) was demonstrated in 52.3% of patients. Very frequently were found patent foramen ovale - 58.3% and atherosclerosis of ascending aorta or aortic arch - 53.7%. Further sources were LA spontaneous echocontrast - 21.1%, reduced function of LA appendage - 18.3%, atrial septal aneurysm - 7.8%, atrial septal defect - 1.4%, cardiac foreign body - 0.5%. 3. TEE did not reveal any source of embolism in 26.1% of patients.</AbstractText>1. 21.6% of the patients suffering from stroke/TIA without hemodynamically significant stenoses of extracranial cerebral arteries had a definite cardiogenic or aortic source of embolism, 2. additional 52.3% of patients had only potential source of embolism (without definite source), 3. we consider TEE necessary in patients with stroke/TIA without a known etiology, despite complete neurological examination and transthoracic echocardography.</AbstractText> |
9,711 | The cardioprotective effect of uridine and uridine-5'-monophosphate: the role of the mitochondrial ATP-dependent potassium channel. | The activity of mitochondrial ATP-dependent potassium channel (mitoKATP) of rat heart and liver mitochondria was shown to decrease during aging. This partially explains the increase of risk of ischemia at a mature age since mitoKATP activation provides cardioprotection. We demonstrated that uridine-5'-diphosphate (UDP) possesses the property to activate mitoKATP. At a concentration of 30 microM, it reactivated mitoKATP in mitochondria, and 5-hydroxydecanoate (5-HD) eliminated this effect. In experimental animals, UDP precursors uridine and uridine-5'-monophosphate (UMP) (both 30 mg/kg, administered intravenously 5 min before coronary occlusion) decreased the myocardium ischemic alteration index (1.9 and 3.5 times, respectively) and the T-wave amplitude within 60 min after occlusion. Both effects were inhibited by Glibenclamide (Glib) and 5-HD. UMP and uridine decreased the number of premature ventricular beats 5.6 and 1.9 times and the duration of ventricular tachycardia 9.4 and 4.1 times, respectively. Glib and 5-HD inhibited the anti-arrhythmic parameters, 5-HD being less effective. Uridine and UMP decreased the duration of fibrillation 10.8 and 3.6 times, respectively, and this effect was not abolished by Glib and 5-HD. Thus, uridine and UMP, which are the precursors of UDP in the cell, possess cardioprotective properties. MitoKATP prevents mainly ischemic injuries and partially rhythm disorders. |
9,712 | [Effects of amiodarone versus sotalol in treatment of atrial fibrillation: a random controlled clinical study]. | To evaluate the effects and adverse reactions of amiodarone and sotalol in treatment of atrial fibrillation.</AbstractText>One hundred and two patients with atrial fibrillation, 56 males and 46 females, aged 56 +/- 11, were randomized into 2 equal groups: amiodarone group, taking amiodarone 600 mg/d for 7 days, 400 mg/d for 7 days, 200 mg/d for 7 days, and then 200 mg/d as maintenance dosage if conversion to sinus rhythm occurred; and sotalol group, taking sotalol 40-80 mg/d for one week, 160 mg/d for 2 weeks and then 40-80 mg/d as maintenance dosage if conversion to sinus rhythm occurred. If the cardiac rhythm failed to be converted to sinus rhythm after three week the medication was stopped. All the patients were followed up for 12-24 months and therapeutic effects were evaluated by echocardiography, electrocardiogram and Holter monitor.</AbstractText>(1) Conversion to sinus rhythm occurred in 40 patients in the amiodarone group with an effective rate of 78.4%, and in 36 patients in the sotalol group with an effective rate of 70.6%. (2) Conversion to sinus rhythm occurred in the first week in 34 patients of the amiodarone group and in 10 patients of the sotalol group. (3) 67.5% of the patients with conversion to sinus rhythm in the amiodarone group and 41.7% of the patients with conversion to sinus rhythm in the sotalol group maintained sinus rhythm in the following 12 months; and 44.4% patients with conversion to sinus rhythm in the amiodarone group and 26.7% of the patients with conversion to sinus rhythm in the following 24 months. (4) 10 patients in the sotalol group taking a maintenance dosage of 80 mg/d showed atrial ventricular block and severe bradycardia during the follow-up of 6-2 months, then the medication was stopped, but there was no severe arrhythmia in amiodarone group. (5) It was difficult to maintain sinus rhythm when atrial fibrillation lasting longer than 12 months was a predictive factor of failure to maintain sinus rhythm.</AbstractText>There is no significant difference between amiodarone and sotalol in converting atrial fibrillation to sinus rhythm. However, amiodarone is more effective in maintenance of sinus rhythm than sotalol. The adverse reaction of amiodarone on heart is less severe than that of sotalol.</AbstractText> |
9,713 | Incidence and causes of inappropriate detection and therapy by implantable defibrillators of cardioversion in patients with ventricular tachyarrhythmia. | Implantable cardioverter defibrillator (ICD) is the only effective therapy in patients with life threatening ventricular arrhythmias. Inappropriate detection and therapy by ICDs are the most common causes of side effects that affect the quality of life in ICD recipients. This study evaluated the incidence and causes of inappropriate detection and therapy by ICDs in patients in our hospital.</AbstractText>From January 2000 to December 2005, fifty patients who received ICD implantation for ventricular arrhythmias for prevention of sudden cardiac death were evaluated in this study. Each ICD was programmed using clinical arrhythmic and cardiac data of the patient before discharge. Patients were followed up by standard schedule after implantation and all data retrieved from each device were collected and saved for further analysis.</AbstractText>No arrhythmic event was detected in 12/50 (24%) patients during the period of follow-up. Among the remaining patients, 11 (22%) experienced inappropriate detections and therapies during follow-up in this study. ICD detected 383 ventricular tachyarrhythmia (VT) and 108 ventricular fibrillation (VF) episodes and delivered 678 therapies. In VT group, ICD delivered 413 antitachycardiac pacings (ATPs) and 118 shocks, among which 78 ATPs and 9 shocks were initiated by 55/383 (14.3%) inappropriate detections. In VF group ICD delivered 147 shocks, among which 56 shocks were initiated by 28/108 (26.9%) inappropriate detections. Overall, more than 50% of these episodes were caused by atrial fibrillation (AF) with rapid ventricular response, followed by electromagnetic or myopotential interference. In addition, most inappropriate therapies occurred within one year after ICD implantation.</AbstractText>About one fifth of patients experienced ICD inappropriate detection and therapy after implantation. The main cause was AF with rapid ventricular response, followed by electromagnetic or myopotential interference.</AbstractText> |
9,714 | Computed tomographic features of circulatory arrest. | Although computed tomography (CT) is used widely in evaluating injuries from various kinds of trauma, the CT features of circulatory events are rarely reported. Recognizing these features is crucial to proper emergency management of patients when circulatory events occur during CT examination. We report two trauma patients who developed circulatory arrest during CT. Both patients had similar CT features of contrast distribution over the dependent portion of the right-sided venous system, a finding that has been previously reported only in patients with cardiac arrest. The quick paddle look feature may be useful to identify the condition and initiate proper resuscitation of patients without electrocardiographic monitoring in CT rooms. |
9,715 | Delayed ventricular fibrillation following blunt chest trauma in a 4-year-old child. | A 4-year-old boy who was involved in a motor vehicle accident as a pedestrian and suffered blunt chest trauma was admitted to the emergency room. Unpredictable delayed ventricular fibrillation was diagnosed and treated successfully 2 h later. This case cannot be classified as commotio cordis as the ventricular fibrillation (VF) developed so long after the sustained chest injury. At the same time, other possible etiologies of VF such as cardiac pathology or electrolyte and metabolic disorders had been ruled out. Thus, an etiological link between the chest trauma and the subsequent VF could not be ruled out and is in fact plausible despite the late onset. |
9,716 | Acquired long QT syndrome and elective anesthesia in children. | We present the case of a child who had had a previous episode of torsades de pointes (TdP) and who was scheduled for elective surgery under general anesthesia. The pathophysiology of this condition and the anesthesia concerns are discussed. An 8-year-old male with a history of osteogenic sarcoma had undergone an uneventful limb salvage procedure 2 years earlier. During a subsequent admission to the hospital, he had had a cardiopulmonary arrest with complete recovery. Telemetry electrocardiogram (ECG) rhythm recordings obtained during the event showed TdP that degenerated into ventricular fibrillation, which then terminated spontaneously. On a subsequent ECG, the QTc interval was 694 ms. The prolonged QT interval was attributed to homeopathic use of cesium chloride supplements and the QT interval normalized after cesium was stopped. He presented for an elective procedure and, with an anesthetic plan that emphasized medications without known effect on the QT interval, had an uneventful perioperative course. The optimal anesthesia plan for patients with prolonged QT or those suspected to be at risk for prolongation of the QT interval has not been well described. Available evidence suggests that using total intravenous anesthesia with propofol may be the safest and was used uneventfully in this case. Additionally, this case emphasizes the need to inquire about the use of supplements and naturopathic medications, even in children, that may have life-threatening side effects or interactions with anesthetic agents. |
9,717 | Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts. | The effects of kernel extract obtained from sour cherry (Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% (P<0.05), and 25% (P<0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium. |
9,718 | A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation. | Brugada syndrome (BS) is an inherited electrical cardiac disorder characterized by right bundle branch block pattern and ST segment elevation in leads V1 to V3 on surface electrocardiogram that can potentially lead to malignant ventricular tachycardia and sudden cardiac death. About 20% of patients have mutations in the only so far identified gene, SCN5A, which encodes the alpha-subunit of the human cardiac voltage-dependent sodium channel (hNa(v)1.5). Fever has been shown to unmask or trigger the BS phenotype, but the associated molecular and the biophysical mechanisms are still poorly understood. We report on the identification and biophysical characterization of a novel heterozygous missense mutation in SCN5A, F1344S, in a 42-year-old male patient showing the BS phenotype leading to ventricular fibrillation during fever.</AbstractText>The mutation was reproduced in vitro using site-directed mutagenesis and characterized using the patch clamp technique in the whole-cell configuration.</AbstractText>The biophysical characterization of the channels carrying the F1344S mutation revealed a 10 mV mid-point shift of the G/V curve toward more positive voltages during activation. Raising the temperature to 40.5 degrees C further shifted the mid-point activation by 18 mV and significantly changed the slope factor in Na(v)1.5/F1344S mutant channels from -6.49 to -10.27 mV.</AbstractText>Our findings indicate for the first time that the shift in activation and change in the slope factor at a higher temperature mimicking fever could reduce sodium currents' amplitude and trigger the manifestation of the BS phenotype.</AbstractText> |
9,719 | Atrial and ventricular volume and function evaluated by magnetic resonance imaging in patients with persistent atrial fibrillation before and after cardioversion. | Atrial fibrillation (AF) is the most common cardiac arrhythmia and 25% of those >40 years old will experience AF. Left atrial size and left ventricular function are independently related to cardiovascular morbidity and mortality. Our aim was to evaluate cardiac volume and function using magnetic resonance imaging in patients with persistent AF and to describe the changes after cardioversion (CV). Sixty consecutive patients with persistent AF and 19 healthy volunteers had cardiac volumes evaluated by cinematographic breath-hold magnetic resonance imaging. Patients with AF were evaluated before CV and at 1, 30, and 180 days after CV, if still in sinus rhythm. All atrial and ventricular volumes and left ventricular mass decreased and ejection fractions increased significantly after CV (p <0.0001 for all variables). Atrial and ventricular diastolic volumes increased significantly the day after CV. The atrial diastolic volumes had decreased significantly at 30 days and ventricular volumes at 180 days. The atrial systolic volumes decreased significantly the day after CV, but the ventricular systolic volumes remained constant the day after CV and decreased thereafter. Only the right atrial volumes were normalized 180 days after CV. The same results were found in a subgroup of patients with lone AF. In conclusion, reversal of atrial dimensions and function happened earlier than ventricular reversal after CV in persistent AF. Atrial reversal began immediately and ventricular reversal was not seen before 30 days after CV. Our results suggest that the changes to the left atrium and both ventricles caused by AF could be permanent and that CV of AF may be preferable. |
9,720 | Recurrence rates of arrhythmias during pregnancy in women with previous tachyarrhythmia and impact on fetal and neonatal outcomes. | In women with heart disease, sustained arrhythmias can result in an increased risk to the mother and fetus. The purpose of this study was to determine the recurrence rates of arrhythmias during pregnancy in women with cardiac rhythm disorders and examine the impact on fetal and neonatal outcomes. Women with tachyarrhythmias before pregnancy who underwent obstetric care at the Toronto General and Mount Sinai Hospitals from 1990 to 2002 were included. The recurrence rates of arrhythmias were calculated. A multivariate logistic model was used to identify predictors of fetal complications. Seventy-three women had 87 pregnancies; 36 pregnancies were in women with a history of paroxysmal supraventricular tachycardia, 23 with paroxysmal atrial fibrillation or atrial flutter (AF/Afl), 6 with persistent AF/Afl, and 22 with ventricular tachycardia. In the women in sinus rhythm at baseline, 44% (36 of 81 pregnancies) developed recurrences of tachyarrhythmias during pregnancy or in the early postpartum period. The specific recurrence rates during pregnancy in women with a history of supraventricular tachycardia, paroxysmal AF/Afl, and ventricular tachycardia were 50%, 52%, and 27%, respectively. The 6 women in AF/Afl at baseline remained in this rhythm throughout their pregnancy. Adverse fetal events occurred in 17 of the 87 pregnancies (20%). Adverse fetal events occurred more commonly in women who developed antepartum arrhythmias (RR 3.4, 95% confidence interval 1.0 to 11.0, p = 0.045) compared with those who did not. In conclusion, in women with preexisting cardiac rhythm disorders, exacerbation of arrhythmia during pregnancy is common. Recurrence of arrhythmia during the antepartum period increases the risk of adverse fetal complications, independent of other maternal and fetal risk factors. |
9,721 | Drug therapy of paroxysmal atrial fibrillation in the elderly over 75 years old. | To investigate the effectiveness and safety of various agents on paroxysmal atrial fibrillation in the elderly over 75 years old.</AbstractText>Totally 264 in-patients (75-91 years old, 185 males and 79 females) with atrial fibrillation history of less than 7 days were enrolled in this study. A total of 611 atrial fibrillation episodes were recorded, but 130 episodes (22.3%) of atrial fibrillation were auto-converted to sinus rhythm. The rest 481 episodes of atrial fibrillation were divided into six groups based on the drug used.</AbstractText>The cardioversion ratio of atrial fibrillation were 9.5%, 46.9%, 71.7%, 55.9%, 32.7%, and 73.6% in control, cedilanid, amiodarone, propafenone, verapamil, and quinidine groups, respectively. Ventricular rate control were 5.4%, 83.6%, 84.9%, 77.9%, 78.8%, and 11.3% in those groups, respectively. The total effective rates of amiodarone and cedilanid groups were the highest. When the ventricular rate was controlled to below 90 bpm, the patients would almost complain of no discomfort. No severe side-effect was observed in each group.</AbstractText>Amiodarone and cedilanid may be the proper drugs for the treatment of paroxysmal atrial fibrillation in the elderly. The above antiarrhythmics in each therapeutic group were relatively safe and effective.</AbstractText> |
9,722 | [Antipsychotic drugs and cardiovascular safety: need for monitoring the QT interval]. | Torsades de pointes (TdP), a form of ventricular arrhythmia that can cause ventricular fibrillation and sudden death, may occur during prolongation of the QT interval. QT prolongation has recently been reported with antipsychotic drugs. Physicians should be able to obtain a corrected measurement of the QT interval. QT is measured from the beginning of the QRS complex to the end of the T wave (QTm). This value must then be corrected to take heartbeat into account. The most common formula in current use is Bazett's. In practice, a QTc interval value greater than 500 ms indicates an increased risk of TdP. Safe combinations of antipsychotic drugs have been recommended by the French drug agency (Agence française de sécurité sanitaire des produits de santé). Many other drugs, including psychotropic drugs such as tricyclic antidepressants, can prolong the QT interval. Combinations of these medications with one another, with antipsychotic medications, or with other concomitant factors, such as hypokalemia, also increase the risk. TdP is most often diagnosed only after observing QT prolongation. This underlines the need to monitor QT intervals attentively to prevent the risk of cardiac arrhythmia in patients treated with antipsychotic drugs. |
9,723 | Comparing intravenous amiodarone or lidocaine, or both, outcomes for inpatients with pulseless ventricular arrhythmias. | To compare survival rates of patients with in-hospital cardiac arrest due to pulseless ventricular tachycardia/ventricular fibrillation treated with lidocaine, amiodarone, or amiodarone plus lidocaine.</AbstractText>Multicenter retrospective medical record review.</AbstractText>Three academic medical centers in the United States.</AbstractText>Hospitalized adult patients who received amiodarone, lidocaine, or a combination for pulseless ventricular tachycardia/ventricular fibrillation between August 1, 2000, and July 31, 2002.</AbstractText>Data were collected according to the Utstein style. In-hospital proportion of patients living at 24 hrs and discharge were analyzed using chi-square analysis. Of the 605 patient medical records reviewed, 194 met criteria for inclusion (n=79 for lidocaine, n=74 for amiodarone, n=41 for combination). Available data showed no difference in proportion of patients alive 24 hrs post-cardiac arrest (p=.39). Cox regression analysis indicated a decreased likelihood of survival in patients with pulseless ventricular tachycardia/ventricular fibrillation as an initial rhythm as compared with those who presented with bradycardia followed by pulseless ventricular tachycardia/ventricular fibrillation and in those patients who received amiodarone as compared with lidocaine. However, only 14 patients (25%) in the amiodarone group received the recommended initial 300-mg intravenous bolus, and amiodarone was administered an average of 8 mins later in the code compared with lidocaine (p<.001).</AbstractText>These results generate the hypothesis that inpatients with cardiac arrest may have different benefits from lidocaine and amiodarone than previously demonstrated. Inadequate dosing and later administration of amiodarone in the code were two confounding factors in this study. Prospective studies evaluating these agents are warranted.</AbstractText> |
9,724 | Radiofrequency ablation of arrhythmias guided by non-fluoroscopic catheter location: a prospective randomized trial. | To compare the utility of non-fluoroscopic mapping systems (Carto and Ensite NavX) with that of conventional mapping in patients referred for catheter ablation of a wide variety of arrhythmias.</AbstractText>Patients referred for catheter ablation (excluding atrial fibrillation, atypical atrial flutter, ventricular tachycardia in structural heart disease, and complete AV nodal ablation) were randomized equally to a procedure guided by Carto, Ensite NavX, or conventional mapping. A total of 145 patients were recruited (82 men, aged 49+/-16, range 18-85). In 19 patients, no ablation was performed, and in the remaining, typical atrial flutter, atrioventricular nodal re-entrant tachycardia, and atrioventricular re-entrant tachycardias [including Wolff-Parkinson-White (WPW)] accounted for 93% of ablations. Overall procedure time, immediate and short-term success, complication rate, and freedom from symptoms at follow-up were identical for all groups. NavX led to the least X-ray exposure: Navx vs. conventional, median (range): 4 (0-50) vs. 13 (2-46) min (P<0.001); NavX vs. Carto, median (range): 4 (0-50) vs. 6 (1-55) min (P=0.008). Both Carto and NavX increased disposable costs by 50% when compared with conventional (P<0.001). For typical atrial flutter, Carto and NavX reduced screening times without increasing procedure cost. If ablation was not performed, NavX was twice as expensive as Carto or conventional.</AbstractText>Ensite NavX and Carto procedures have similar effectiveness and safety to a conventional approach; however, they both reduce X-ray exposure, with NavX producing a significantly greater effect than Carto. Although this benefit is achieved at a greater financial cost, there may be long-term benefits to catheter laboratory staff.</AbstractText> |
9,725 | [Strategy for cardiac arrhythmias in acute coronary syndrome]. | Acute coronary syndrome causes several types of arrhythmia because of its electrical instability and ischemia. The most important arrhythmia is ventricular tachycardia which degenerates to ventricular fibrillation. Prompt direct current cardioversion will be needed and prevention of ventricular tachyarrhythmia by potassium channel blocker became more popular in Japan. Nifekalant or amiodarone should be selected. Atrial fibrillation also occurred in the patients with acute coronary syndrome, and it may deteriorate hemodynamics condition. Therefore, termination and prevention of atrial fibrillation is another important issue in acute coronary syndrome. Aprindine, amiodarone, or bepridil will be the choice to prevent recurrent atrial fibrillation after direct current cardioversion. |
9,726 | [Patient-prosthesis mismatch after aortic valve replacement; tolerable lower limit of indexed effective orifice area]. | This study was aimed at determining the tolerable lower limit of the indexed effective orifice area (EOAI) to prevent patient-prosthesis mismatch (PPM). Echocardiography was performed in 87 consecutive patients who underwent aortic valve replacement (AVR). EOAI was estimated for each type and size of prosthesis and used to define PPM as moderate if >0.65 cm2/ m2 and < or = 0.85 cm2/m2, and severe if < or = 0.65 cm/m2. Aortic valve pressure gradients, left ventricular dimensions, and outcome (in-hospital and 1-year) were analyzed in the presence or absence of abnormal gradients (> or = 40 mmHg) to assess the influence of a small valve (19 mm or less labeled size). Severe PPM was found in 23% of all patients, and 50% of the severe PPM patients had an abnormal gradient. There was 1 death and 1 brain damage from ventricular fibrillation because of severe PPM in the abnormal gradient group with a small valve. In PPM patients with a small valve, EOAI (0.61 +/- 0.04 vs 0.69 +/- 0.07) and preoperative interventricular septal thickness (IVST : 16.4 +/- 2.6 mm vs 13.5 +/- 1.5 mm) were significantly different between abnormal and normal gradient groups. An EOAI > or = 0.69 appeared to be tolerable in patients with a lower level of hypertrophy (IVST < 16 mm). |
9,727 | Impact of sympathetic innervation on recurrent life-threatening arrhythmias in the follow-up of patients with idiopathic ventricular fibrillation. | Idiopathic ventricular fibrillation (IVF) is defined as VF in the absence of any identifiable structural or functional cardiac disease. The underlying pathophysiological mechanisms are unknown. This study was performed to investigate the potential impact of sympathetic dysfunction, assessed by (123)I-meta-iodo-benzylguanidine scintigraphy ((123)I-MIBG SPECT), on the long-term prognosis of patients with IVF.</AbstractText>(123)I-MIBG SPECT was performed in 20 patients (mean age 37+/-13 years) with IVF. Mean follow-up of patients after study entry was 7.2+/-1.5 years (range 4.9-10.5 years). Ten patients (five men, five women; mean age 43+/-12 years; p=NS versus study group) with medullary carcinoma of the thyroid gland served as an age-matched control group.</AbstractText>Abnormal (123)I-MIBG uptake was observed in 13 patients (65%). During follow-up, 18 episodes of VF/fast polymorphic ventricular tachycardias occurred in four IVF patients with abnormal (123)I-MIBG uptake whereas only two episodes of monomorphic ventricular tachycardia (and no VF) occurred in a single IVF patient with normal (123)I-MIBG uptake.</AbstractText>Impairment of sympathetic innervation may indicate a higher risk of future recurrent episodes of life-threatening ventricular tachyarrhythmias in patients with IVF. Studies in larger cohorts are required to validate the significance of (123)I-MIBG SPECT during the long-term follow-up of these patients.</AbstractText> |
9,728 | Clinical features and outcome of patients with apical hypertrophic cardiomyopathy in Taiwan. | The aim of this study was to analyze clinical characteristics and the outcome of patients with apical hypertrophic cardiomyopathy (ApHCM) followed in a Taiwan tertiary referral medical center.</AbstractText>ApHCM is regarded as a subgroup of nonobstructive HCM that occurs largely in Japanese patients. The clinical features, gender differences and prognosis of the disease in Taiwan are poorly understood.</AbstractText>A retrospective cohort study with 40 patients was performed. Diagnosis was based on the demonstration of left ventricular hypertrophy by echocardiography. Clinical features, cardiovascular morbidity and mortality were analyzed. Multiple logistic regression was used to adjust for potential confounding factors.</AbstractText>Among 40 patients, males predominated with a percentage of 75%. The female patients obviously had later onset of presentation (mean age +/- SD, 62.2 +/- 5.7 vs. 54.1 +/- 11.4 years; p = 0.038). During a mean follow-up of 72.2 +/- 60.1 months, there was no mortality. However, 13 patients (32.5%) had one or more major cardiovascular morbidities, the most frequent being syncope or near syncope (15%) and ischemic stroke-associated atrial fibrillation (10%). In a multivariate analysis, left atrial enlargement (odds ratio 5.85, 95% CI 1.15-29.40; p = 0.034) was the only predictor of cardiovascular morbidity.</AbstractText>Patients with ApHCM in Taiwan have a benign clinical course without association with sudden death and cardiovascular mortality. Left atrial enlargement was the only identified predictor of cardiovascular morbidity</AbstractText>Copyright 2006 S. Karger AG, Basel</CopyrightInformation> |
9,729 | The safety of digoxin as a pharmacological treatment of atrial fibrillation.<Pagination><StartPage>453</StartPage><EndPage>467</EndPage><MedlinePgn>453-67</MedlinePgn></Pagination><Abstract><AbstractText>Digoxin has traditionally been the drug of choice for ventricular rate control in patients with chronic atrial fibrillation (AF), with or without heart failure (HF) with systolic dysfunction. In patients with permanent AF, digoxin monotherapy is ineffective to control ventricular rate during exercise, but the combination of digoxin with a beta-blocker or a non-dihydropyridine calcium channel antagonist can control heart rate both at rest and during exercise. Only a few randomised, controlled studies have evaluated the adverse effects of digoxin in patients with AF in a systematic way and side effects requiring drug withdrawal have rarely been reported. When reported, the most frequent adverse effects were cardiac arrhythmias (ventricular arrhythmias, AV block of varying degrees and sinus pauses). This evidence suggested that, in contrast to other antiarrhythmic drugs, digoxin is a safe drug in patients with AF. However, this safety profile can be erroneous due to the short follow-up of the studies and patient selection. Because patients with HF have been excluded in most studies, the safety profile of digoxin in this population has not been directly addressed. Early recognition that an arrhythmia is related to digoxin intoxication as well as recognition of concomitant medications or medical conditions that may directly alter the pharmacokinetic profile of digoxin, or indirectly alter its cardiac effects by pharmacodynamic interactions remain essential for safe and effective use of digoxin in patients with AF.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tamargo</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, School of Medicine, Universidad Complutense, 28040 Madrid, Spain. jtamargo@med.ucm.es</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delpón</LastName><ForeName>Eva</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Caballero</LastName><ForeName>Ricardo</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Drug Saf</MedlineTA><NlmUniqueID>101163027</NlmUniqueID><ISSNLinking>1474-0338</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>73K4184T59</RegistryNumber><NameOfSubstance UI="D004077">Digoxin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001281" MajorTopicYN="N">Atrial Fibrillation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004077" MajorTopicYN="N">Digoxin</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004347" MajorTopicYN="N">Drug Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016903" MajorTopicYN="N">Drug Monitoring</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>113</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>10</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610972</ArticleId><ArticleId IdType="doi">10.1517/14740338.5.3.453</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610350</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2021</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal>Therapy for the Brugada syndrome.<Pagination><StartPage>305</StartPage><EndPage>330</EndPage><MedlinePgn>305-30</MedlinePgn></Pagination><Abstract><AbstractText>The Brugada syndrome is a congenital syndrome of sudden cardiac death first described as a new clinical entity in 1992. Electrocardiographically characterized by a distinct coved-type ST segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. The ECG manifestations of the Brugada syndrome are often dynamic or concealed and may be revealed or modulated by sodium channel blockers. The syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, and hypokalemia, as well as by alcohol and cocaine toxicity. An implantable cardioverter-defibrillator (ICD) is the most widely accepted approach to therapy. Pharmacological therapy aimed at rebalancing the currents active during phase 1 of the right ventricular action potential is used to abort electrical storms, as an adjunct to device therapy, and as an alternative to device therapy when use of an ICD is not possible. Isoproterenol and cilostazol boost calcium channel current, and drugs like quinidine inhibit the transient outward current, acting to diminish the action potential notch and thus suppress the substrate and trigger for ventricular tachycardia/fibrillation (VT/VF).</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Antzelevitch</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA. ca@mmrl.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fish</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL047678</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL47678</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Handb Exp Pharmacol</MedlineTA><NlmUniqueID>7902231</NlmUniqueID><ISSNLinking>0171-2004</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002037" MajorTopicYN="N">Bundle-Branch Block</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003645" MajorTopicYN="N">Death, Sudden</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017147" MajorTopicYN="N">Defibrillators, Implantable</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013577" MajorTopicYN="N">Syndrome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>4</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610350</ArticleId><ArticleId IdType="mid">NIHMS10275</ArticleId><ArticleId IdType="pmc">PMC1474239</ArticleId><ArticleId IdType="doi">10.1007/3-540-29715-4_12</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Aligs M, Wilde A. “Brugada” syndrome: clinical data and suggested pathophysiological mechanism. Circulation. 1999;99:666–673.</Citation><ArticleIdList><ArticleId IdType="pubmed">9950665</ArticleId></ArticleIdList></Reference><Reference><Citation>Alings M, Dekker L, Sadee A, Wilde A. Quinidine induced electrocardiographic normalization in two patients with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1420–1422.</Citation><ArticleIdList><ArticleId IdType="pubmed">11584468</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C. The Brugada syndrome: ionic basis and arrhythmia mechanisms. f Cardiovasc Electrophysiol. 2001a;12:268–272.</Citation><ArticleIdList><ArticleId IdType="pubmed">11232628</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C. The Brugada syndrome. Diagnostic criteria and cellular mechanisms. Eur Heart J. 2001b;22:356–363.</Citation><ArticleIdList><ArticleId IdType="pubmed">11207076</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada R. Fever and the Brugada syndrome. Pacing Clin Electrophysiol. 2002;25:1537–1539.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494608</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Shimizu W. Cellular mechanisms underlying the long QT syndrome. Curr Opin Cardiol. 2002;17:43–51.</Citation><ArticleIdList><ArticleId IdType="pubmed">11790933</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Sicouri S, Litovsky SH, Lukas A, Krishnan SC, Di Diego JM, Gintant GA, Liu DW. Heterogeneity within the ventricular wall: electrophysiology and pharmacology of epicardial, endocardial and M cells. Circ Res. 1991;69:1427–1449.</Citation><ArticleIdList><ArticleId IdType="pubmed">1659499</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Brugada J, Brugada R, Nademanee K, Towbin JA. The Brugada syndrome. In: Camm AJ, editor. Clinical approaches to tachyarrhythmias. Futura Publishing Company; Armonk: 1999a. pp. 1–99.</Citation></Reference><Reference><Citation>Antzelevitch C, Shimizu W, Yan GX, Sicouri S, Weissenburger J, Nesterenko V, Burashnikov A, Di Diego JM, Saffitz JE, Thomas GP. The M cell: Its contribution to the ECG and to normal and abnormal electrical function of the heart. J Cardiovasc Electrophysiol. 1999b;10:1124–1152.</Citation><ArticleIdList><ArticleId IdType="pubmed">10466495</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Brugada J, Brugada R, Shitmizu W, Gussak I, Perez Riera AR. Brugada syndrome: a decade of progress. Circ Res. 2002;91:1114–1118.</Citation><ArticleIdList><ArticleId IdType="pubmed">12480811</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Riera ARP, Tan H, Shimizu W, Schulze-Bahr E, Wilde A. Brugada syndrome. Report of the Second Consensus Conference. Circulation. 2005;111:659–670.</Citation><ArticleIdList><ArticleId IdType="pubmed">15655131</ArticleId></ArticleIdList></Reference><Reference><Citation>Araki T, Konno T, Itoh H, Ino H, Shimizu M. Brugada syndrome with ventricular tachycardia and fibrillation related to hypokalemia. Circ J. 2003;67:93–95.</Citation><ArticleIdList><ArticleId IdType="pubmed">12520160</ArticleId></ArticleIdList></Reference><Reference><Citation>Ayerza MR, de Zutter M, Goethals M, Wellens F, Geelen P, Brugada P. Heart transplantation as last resort against Brugada syndrome. J Cardiovasc Electrophysiol. 2002;13:943–944.</Citation><ArticleIdList><ArticleId IdType="pubmed">12380937</ArticleId></ArticleIdList></Reference><Reference><Citation>Babaliaros VC, Hurst JW. Tricyclic antidepressants and the Brugada syndrome: an example of Brugada waves appearing after the administration of desipramine. Clin Cardiol. 2002;25:395–398.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6654619</ArticleId><ArticleId IdType="pubmed">12173907</ArticleId></ArticleIdList></Reference><Reference><Citation>Balser JR. The cardiac sodium channel: gating function and molecular pharmacology. J Mol Cell Cardiol. 2001;33:599–613.</Citation><ArticleIdList><ArticleId IdType="pubmed">11273715</ArticleId></ArticleIdList></Reference><Reference><Citation>Belardinelli L, Antzelevitch C, Vos MA. Assessing predictors of drug-induced torsade de pointes. Trends Pharmacol Sci. 2003;24:619–625.</Citation><ArticleIdList><ArticleId IdType="pubmed">14654302</ArticleId></ArticleIdList></Reference><Reference><Citation>Belhassen B, Viskin S. Pharmacologic approach to therapy of Brugada syndrome: quinidine as an alternative to ICD therapy. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Blackwell Futura; Oxford: 2004. pp. 202–211.</Citation></Reference><Reference><Citation>Belhassen B, Viskin S, Fish R, Glick A, Setbon I, Eldar M. Effects of electrophysiologic-guided therapy with Class IA antiarrhythmic drugs on the long-term outcome of patients with idiopathic ventricular fibrillation with or without the Brugada syndrome [see comments] J Cardiovasc Electrophysiol. 1999;10:1301–1312.</Citation><ArticleIdList><ArticleId IdType="pubmed">10515552</ArticleId></ArticleIdList></Reference><Reference><Citation>Belhassen B, Viskin S, Antzelevitch C. The Brugada syndrome: is ICD the only therapeutic option. Pacing Clin Electrophysiol. 2002;25:1634–1640.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494624</ArticleId></ArticleIdList></Reference><Reference><Citation>Bezzina C, Veldkamp MW, van Den Berg MP, Postma AV, Rook MB, Viersma JW, Van Langen IM, Tan-Sindhunata G, Bink-Boelkens MT, Der Hout AH, Mannens MM, Wilde AA. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ Res. 1999;85:1206–1213.</Citation><ArticleIdList><ArticleId IdType="pubmed">10590249</ArticleId></ArticleIdList></Reference><Reference><Citation>Bolognesi R, Tsialtas D, Vasini P, Conti M, Manca C. Abnormal ventricular repolarization mimicking myocardial infarction after heterocyclic antidepressant overdose. Am J Cardiol. 1997;79:242–245.</Citation><ArticleIdList><ArticleId IdType="pubmed">9193039</ArticleId></ArticleIdList></Reference><Reference><Citation>Bordachar P, Reuter S, Garrigue S, Cai X, Hocini M, Jais P, Haissaguerre M, Clementy J. Incidence, clinical implications and prognosis of atrial arrhythmias in Brugada syndrome. Eur Heart J. 2004;25:879–884.</Citation><ArticleIdList><ArticleId IdType="pubmed">15140537</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3. A marker for sudden death in patients without demonstrable structural heart disease. Circulation. 1998;97:457–460.</Citation><ArticleIdList><ArticleId IdType="pubmed">9490240</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada J, Brugada R, Brugada P. Pharmacological and device approach to therapy of inherited cardiac diseases associated with cardiac arrhythmias and sudden death. J Electrocardiol. 2000a;33(Suppl):41–47.</Citation><ArticleIdList><ArticleId IdType="pubmed">11265735</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada R, Brugada J, Geelen P. Use of the prophylactic implantable cardioverter defibrillator for patients with normal hearts. Am J Cardiol. 1999;83:98D–1OOD.</Citation><ArticleIdList><ArticleId IdType="pubmed">10089849</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada J, Brugada R. Arrhythmia induction by antiarrhythmic drugs. Pacing Clin Electrophysiol. 2000b;23:291–292.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750126</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada R, Antzelevitch C, Nademanee K, Towbin f, Brugada J. The Brugada syndrome. In: Gussak I, Antzelevitch C, editors. Cardiac repolarization. bridging basic and clinical sciences. Humana Press; Totowa: 2003. pp. 427–446.</Citation></Reference><Reference><Citation>Brugada P, Bartholomay E, Mont L, Brugada R, Brugada J. Treatment of Brugada syndrome with an implantable cardioverter defibrillator. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Blackwell Futura; Oxford: 2004. pp. 194–201.</Citation></Reference><Reference><Citation>Brugada R, Brugada J, Antzelevitch C, Kirsch GE, Potenza D, Towbin JA, Brugada P. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation. 2000c;101:510–515.</Citation><ArticleIdList><ArticleId IdType="pubmed">10662748</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, Potenza D, Moya A, Borggrefe M, Breithardt G, Ortiz-Lopez R, Wang Z, Antzelevitch C, O‘Brien RE, Schultze-Bahr E, Keating MT, Towbin JA, Wang Q. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature. 1998;392:293–296.</Citation><ArticleIdList><ArticleId IdType="pubmed">9521325</ArticleId></ArticleIdList></Reference><Reference><Citation>Chinushi M, Aizawa Y, Ogawa Y, Shiba M, Takahashi K. Discrepant drug action of disopyramide on ECG abnormalities and induction of ventricular arrhythmias in a patient with Brugada syndrome. J Electrocardiol. 1997;30:133–136.</Citation><ArticleIdList><ArticleId IdType="pubmed">9141608</ArticleId></ArticleIdList></Reference><Reference><Citation>Di Diego JM, Cordeiro JM, Goodrow RJ, Fish JM, Zygmunt AC, Perez Gj, Scornik FS, Antzelevitch C. Ionic and cellular basis for the predominance of the Brugada syndrome phenotype in males. Circulation. 2002;106:2004–2011.</Citation><ArticleIdList><ArticleId IdType="pubmed">12370227</ArticleId></ArticleIdList></Reference><Reference><Citation>Dumaine R, Towbin JA, Brugada P, Vatta M, Nesterenko V, Nesterenko DV, Brugada J, Brugada R, Antzelevitch C. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 1999;85:803–809.</Citation><ArticleIdList><ArticleId IdType="pubmed">10532948</ArticleId></ArticleIdList></Reference><Reference><Citation>Dzielinska Z, Bilinska ZT, Szumowski L, Grzybowski J, Michalak E, Przybylski A, Lubiszewska B, Walczak P, Ruzyllo W. [Recurrent ventricular fibrillation during a febrile illness as the first manifestation of Brugada syndrome-a case report] Kardiol Pol. 2004;61:269–273.</Citation><ArticleIdList><ArticleId IdType="pubmed">15531939</ArticleId></ArticleIdList></Reference><Reference><Citation>Eckardt L, Kirchhof P, Johna R, Haverkamp W, Breithardt G, Borggrefe M. Wolff-Parkinson-White syndrome associated with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1423–1424.</Citation><ArticleIdList><ArticleId IdType="pubmed">11584469</ArticleId></ArticleIdList></Reference><Reference><Citation>Fish JM, Antzelevitch C. Role of sodium and calcium channel block in unmasking the Brugada syndrome. Heart Rhythm. 2004;1:210–217.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1524822</ArticleId><ArticleId IdType="pubmed">15851155</ArticleId></ArticleIdList></Reference><Reference><Citation>Fish JM, Extramiana F, Antzelevitch C. AVE0118, an Ito and IKur blocker, suppresses VT/VF in an experimental model of the Brugada syndrome. Circulation. 2004a;110:III–193.</Citation></Reference><Reference><Citation>Fish JM, Extramiana F, Antzelevitch C. Tedisamil abolishes the arrhythmogenic substrate responsible for VT/VF in an experimental model of the Brugada syndrome. Heart Rhythm. 2004b;1:S158. (abstr)</Citation></Reference><Reference><Citation>Fujiki A, Usui M, Nagasawa H, Mizumaki K, Hayashi H, Inoue H. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of Brugada syndrome [see comments] J Cardiovasc Electrophysiol. 1999;10:214–218.</Citation><ArticleIdList><ArticleId IdType="pubmed">10090224</ArticleId></ArticleIdList></Reference><Reference><Citation>Gasparini M, Priori SG, Mantica M, Napolitano C, Galimberti P, Ceriotti C, Simonini S. Flecainide test in Brugada syndrome: a reproducible but risky tool. Pacing Clin Electrophysiol. 2003;26:338–341.</Citation><ArticleIdList><ArticleId IdType="pubmed">12687841</ArticleId></ArticleIdList></Reference><Reference><Citation>Goldgran-Toledano D, Sideris G, Kevorkian JP. Overdose of cyclic antidepressants and the Brugada syndrome. N Engl J Med. 2002;346:1591–1592.</Citation><ArticleIdList><ArticleId IdType="pubmed">12015405</ArticleId></ArticleIdList></Reference><Reference><Citation>Gonzalez Rebollo G, Madrid H, Carcia A, Garcia de Casto A, Moro AM. Recurrent ventricular fibrillation during a febrile illness in a patient with the Brugada syndrome. Rev Esp Cardiol. 2000;53:755–757.</Citation><ArticleIdList><ArticleId IdType="pubmed">10816181</ArticleId></ArticleIdList></Reference><Reference><Citation>Gussak I, Antzelevitch C, Bjerregaard P, Towbin JA, Chaitman BR. The Brugada syndrome: clinical, electrophysiological and genetic aspects. J Am Coll Cardiol. 1999;33:5–15.</Citation><ArticleIdList><ArticleId IdType="pubmed">9935001</ArticleId></ArticleIdList></Reference><Reference><Citation>Haissaguerre M, Extramiana F, Hocini M, Cauchemez B, Jais P, Cabrera JA, Farre G, Leenhardt A, Sanders P, Scavee C, Hsu LF, Weerasooriya R, Shah DC, Frank R, Maury P, Delay M, Garrigue S, Clementy J. Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes. Circulation. 2003;108:925–928.</Citation><ArticleIdList><ArticleId IdType="pubmed">12925452</ArticleId></ArticleIdList></Reference><Reference><Citation>Hermida JS, Denjoy I, Clerc J, Extramiana F, Jarry G, Milliez P, Guicheney P, Di Fusco S, Rey JL, Cauchemez B, Leenhardt A. Hydroquinidine therapyin Brugada syndrome. J Am Coll Cardiol. 2004;43:1853–1860.</Citation><ArticleIdList><ArticleId IdType="pubmed">15145111</ArticleId></ArticleIdList></Reference><Reference><Citation>Hong K, Berruezo-Sanchez A, Poungvarin N, Oliva A, Vatta M, Brugada J, Brugada P, Towbin JA, Dumaine R, Pinero-Galvez C, Antzelevitch C, Brugada R. Phenotypic characterization of a large European family with Brugada syndrome displaying a sudden unexpected death syndrome mutation in SCN5A. J Cardiovasc Electrophysiol. 2004;15:64–69.</Citation><ArticleIdList><ArticleId IdType="pubmed">15028074</ArticleId></ArticleIdList></Reference><Reference><Citation>Horigome H, Shigeta 0, Kuga K, Isobe T, Sakakibara Y, Yamaguchi I, Matsui A. Ventricular fibrillation during anesthesia in association with J waves in the left precordial leads in a child with coarctation of the aorta. J Electrocardiol. 2003;36:339–343.</Citation><ArticleIdList><ArticleId IdType="pubmed">14661171</ArticleId></ArticleIdList></Reference><Reference><Citation>Kalla H, Yan GX, Marinchak R. Ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a Brugada syndrome variant. J Cardiovasc Electrophysiol. 2000;11:95–98.</Citation><ArticleIdList><ArticleId IdType="pubmed">10695469</ArticleId></ArticleIdList></Reference><Reference><Citation>Kasanuki H, Ohnishi S, Ohtuka M, Matsuda N, Nirei T, Isogai R, Shoda M, Toyoshimna Y, Hosoda S. Idiopathic ventricular fibrillation induced with vagal activity in patients with out obvious heart disease. Circulation. 1997;95:2277–2285.</Citation><ArticleIdList><ArticleId IdType="pubmed">9142005</ArticleId></ArticleIdList></Reference><Reference><Citation>Kies P, Wichter T, Schafers M, Paul M, Schafers KP, Eckardt L, Stegger L, Schulze-Bahr E, Rimoldi 0, Breithardt G, Schober 0, Camici PG. Abnormal myocardial presynaptic norepinephrine recycling in patients with Brugada syndromel. Circulation. 2004;110:3017–3022.</Citation><ArticleIdList><ArticleId IdType="pubmed">15520312</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Antzelevitch C. Sodium channel blockade produces opposite electrophysiologic effects in canine ventricular epicardium and endocardium. Circ Res. 1991;69:277–291.</Citation><ArticleIdList><ArticleId IdType="pubmed">1650294</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Antzelevitch C. Flecainide-induced arrhythmia in canine ventricular epicardium: phase 2 reentry. Circulation. 1993;87:562–572.</Citation><ArticleIdList><ArticleId IdType="pubmed">8425300</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Josephson ME. ST segment elevation induced by class IC antiarrhythmic agents: underlying electrophysiologic mechanisms and insights into drug-induced proarrhythmia. J Cardiovasc Electrophysiol. 1998;9:1167–1172.</Citation><ArticleIdList><ArticleId IdType="pubmed">9835260</ArticleId></ArticleIdList></Reference><Reference><Citation>Kum L, Fung JWH, Chan WWL, Chan GK, Chan YS, Sanderson JE. Brugada syndrome unmasked by febrile illness. Pacing Clin Electrophysiol. 2002;25:1660–1661.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494630</ArticleId></ArticleIdList></Reference><Reference><Citation>Kurita T, Shimizu W, Inagaki M, Suyama K, Taguchi A, Satomi K, Aihara N, Kamakura S, Kobayashi J, Kosakai Y. The electrophysiologic mechanism of ST-segment elevation in Brugada syndrome. J Am Coil Cardiol. 2002;40:330–334.</Citation><ArticleIdList><ArticleId IdType="pubmed">12106940</ArticleId></ArticleIdList></Reference><Reference><Citation>Litovsky SH, Antzelevitch C. Differences in the electrophysiological response of canine ventricular subendocardium and subepicardium to acetylcholine and isoproterenol. A direct effect of acetylcholine in ventricular myocardium. Circ Res. 1990;67:615–627.</Citation><ArticleIdList><ArticleId IdType="pubmed">2397572</ArticleId></ArticleIdList></Reference><Reference><Citation>Littmann L, Monroe MH, Svenson RH. Brugada-type electrocardiographic pattern induced by cocaine. Mayo Clin Proc. 2000;75:845–849.</Citation><ArticleIdList><ArticleId IdType="pubmed">10943241</ArticleId></ArticleIdList></Reference><Reference><Citation>Lukas A, Antzelevitch C. Phase 2 reentry as a mechanism of initiation of circus movement reentry in canine epicardium exposed to simulated ischemia. The antiarrhythmic effects of 4-aminopyridine. Cardiovasc Res. 1996;32:593–603.</Citation><ArticleIdList><ArticleId IdType="pubmed">8881520</ArticleId></ArticleIdList></Reference><Reference><Citation>Madle A, Kratochvil Z, Polivkova A. [The Brugada syndrome] Vnitr Lek. 2002;48:255–258.</Citation><ArticleIdList><ArticleId IdType="pubmed">11968588</ArticleId></ArticleIdList></Reference><Reference><Citation>Matana A, Goldner V, Stanic K, Mavric Z, Zaputovic L, Matana Z. Unmasking effect of propafenone on the concealed form of the Brugada phenomenon. Pacing Clin Electrophysiol. 2000;23:416–418.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750149</ArticleId></ArticleIdList></Reference><Reference><Citation>Matsuo K, Shimizu W, Kurita T, Inagaki M, Aihara N, Kamakura S. Dynamic changes of 12-lead electrocardiograms in a patient with Brugada syndrome. J Cardiovasc Electrophysiol. 1998;9:508–512.</Citation><ArticleIdList><ArticleId IdType="pubmed">9607459</ArticleId></ArticleIdList></Reference><Reference><Citation>Miyasaka Y, Tsuji H, Yamada K, Tokunaga S, Saito D, Imuro Y, Matsumoto N, Iwasaka T. Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan. J Am Coll Cardiol. 2001;38:771–774.</Citation><ArticleIdList><ArticleId IdType="pubmed">11527631</ArticleId></ArticleIdList></Reference><Reference><Citation>Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa Y, Ogawa S. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome. J Am Coll Cardiol. 1996;27:1061–1070.</Citation><ArticleIdList><ArticleId IdType="pubmed">8609322</ArticleId></ArticleIdList></Reference><Reference><Citation>Mizumaki K, Fujiki A, Tsuneda T, Sakabe M, Nishida K, Sugao M, Inoue H. Vagal activity modulates spontaneous augmentation of ST elevation in daily life of patients with Brugada syndrome. J Cardiovasc Electrophysiol. 2004;15:667–673.</Citation><ArticleIdList><ArticleId IdType="pubmed">15175062</ArticleId></ArticleIdList></Reference><Reference><Citation>Mok NS, Chan NY, Chi-Suen CA. Successful use of quinidine in treatment of electrical storm in Brugada syndrome. Pacing Clin Electrophysiol. 2004;27:821–823.</Citation><ArticleIdList><ArticleId IdType="pubmed">15189543</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita H, Kusano-Fukushima K, Nagase S, Fujimoto Y, Hisamatsu K, Fujio H, Haraoka K, Kobayashi M, Morita ST, Nakamura K, Emori T, Matsubara H, Hina K, Kita T, Fukatani M, Ohe T. Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome. J Am Coll Cardiol. 2002;40:1437.</Citation><ArticleIdList><ArticleId IdType="pubmed">12392834</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita H, Fukushima-Kusano K, Nagase S, Miyaji K, Hiramatsu S, Banba K, Nishii N, Watanabe A, Kakishita M, Takenaka-Morita S, Nakamura K, Saito H, Emori T, Ohe T. Sinus node function in patients with Brugada-type ECG. Circ J. 2004;68:473–476.</Citation><ArticleIdList><ArticleId IdType="pubmed">15118291</ArticleId></ArticleIdList></Reference><Reference><Citation>Nademanee K, Veerakul G, Nimmannit S, Chaowakul V, Bhuripanyo K, Likittanasombat K, Tunsanga K, Kuasirikul S, Malasit P, Tansupasawadikul S, Tatsanavivat P. Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation. 1997;96:2595–2600.</Citation><ArticleIdList><ArticleId IdType="pubmed">9355899</ArticleId></ArticleIdList></Reference><Reference><Citation>Nimmannit S, Malasit P, Chaovakul V, Susaengrat W, Vasuvattakul S, Nilwarangkur S. Pathogenesis of sudden unexplained nocturnal death (lai tai) and endemic distal renal tubular acidosis. Lancet. 1991;338:930–932.</Citation><ArticleIdList><ArticleId IdType="pubmed">1681278</ArticleId></ArticleIdList></Reference><Reference><Citation>Noda T, Shimizu W, Taguchi A, Satomi K, Suyama K, Kurita T, Aihara N, Kamakura S. ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome. J Am Coll Cardiol. 2002;40:1841–1847.</Citation><ArticleIdList><ArticleId IdType="pubmed">12446069</ArticleId></ArticleIdList></Reference><Reference><Citation>Nogami A, Nakao M, Kubota S, Sugiyasu A, Doi H, Yokoyama K, Yumoto K, Tamaki T, Kato K, Hosokawa N, Sagai H, Nakamura H, Nitta J, Yamauchi Y, Aonuma K. Enhancement of J-ST-segment elevation by the glucose and insulin test in Brugada syndrome. Pacing Clin Electrophysiol. 2003;26:332–337.</Citation><ArticleIdList><ArticleId IdType="pubmed">12687840</ArticleId></ArticleIdList></Reference><Reference><Citation>Ortega-Carnicer J, Bertos-Polo J, Gutierrez-Tirado C. Aborted sudden death, transient Brugada pattern, and wide QRS dysrhythmias after massive cocaine ingestion. J Electrocardiol. 2001;34:345–349.</Citation><ArticleIdList><ArticleId IdType="pubmed">11590577</ArticleId></ArticleIdList></Reference><Reference><Citation>Ortega-Carnicer J, Benezet J, Ceres F. Fever-induced ST-segment elevation and T-wave alternans in a patient with Brugada syndrome. Resuscitation. 2003;57:315–317.</Citation><ArticleIdList><ArticleId IdType="pubmed">12804811</ArticleId></ArticleIdList></Reference><Reference><Citation>Pastor A, Nunez A, Cantale C, Cosio FG. Asymptomatic Brugada syndrome case unmasked during dimenhydrinate infusion. J Cardiovasc Electrophysiol. 2001;12:1192–1194.</Citation><ArticleIdList><ArticleId IdType="pubmed">11699532</ArticleId></ArticleIdList></Reference><Reference><Citation>Pitzalis MV, Anaclerio M, Iacoviello M, Forleo C, Guida P, Troccoli R, Massari F, Mastropasqua F, Sorrentino S, Manghisi A, Rizzon P. QT-interval prolongation in right precordial leads: an additional electrocardiographic hallmark of Brugada syndrome. J Am Coil Cardiol. 2003;42:1632–1637.</Citation><ArticleIdList><ArticleId IdType="pubmed">14607451</ArticleId></ArticleIdList></Reference><Reference><Citation>Porres JM, Brugada J, Urbistondo V, Garcia F, Reviejo K, Marco P. Fever unmasking the Brugada syndrome. Pacing Clin Electrophysiol. 2002;25:1646–1648.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494626</ArticleId></ArticleIdList></Reference><Reference><Citation>Potet F, Mabo P, Le Coq G, Probst V, Schott Jf, Airaud F, Guihard G, Daubert JC, Escande D, Le Marec H. Novel Brugada SCNSA mutation leading to ST segment elevation in the inferior or the right precordial leads. J Cardiovasc Electrophysiol. 2003;14:200–203.</Citation><ArticleIdList><ArticleId IdType="pubmed">12693506</ArticleId></ArticleIdList></Reference><Reference><Citation>Priori SG, Napolitano C, Gasparini M, Pappone C, Della BP, Brignole M, Giordano U, Giovannini T, Menozzi C, Bloise R, Crotti L, Terreni L, Schwartz PJ. Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome: a prospective evaluation of 52 families. Cfrculation. 2000;102:2509–2515.</Citation><ArticleIdList><ArticleId IdType="pubmed">11076825</ArticleId></ArticleIdList></Reference><Reference><Citation>Priori SG, Napolitano C, Gasparini M, Pappone C, Della BP, Giordano U, Bloise R, Giustetto C, De Nardis R, Grillo M, Ronchetti E, Faggiano G, Nastoli J. Natural history of Brugada syndrome: insights for risk stratification and management. Circulation. 2002;105:1342–1347.</Citation><ArticleIdList><ArticleId IdType="pubmed">11901046</ArticleId></ArticleIdList></Reference><Reference><Citation>Proclemer A, Facchin D, Feruglio GA, Nucifora R. Recurrent ventricular fibrillation, right bundle-branch block and persistent ST segment elevation in V1-V3: a new arrhythmia syndrome? A clinical case report [see comments] G Ital Cardiol. 1993;23:1211–1218.</Citation><ArticleIdList><ArticleId IdType="pubmed">8174872</ArticleId></ArticleIdList></Reference><Reference><Citation>Rolf S, Bruns HJ, Wichter T, Kirchhof P, Ribbing M, Wasmer K, Paul M, Breithardt G, Haverkamp W, Eckardt L. The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. Eur Heart J. 2003;24:1104–1112.</Citation><ArticleIdList><ArticleId IdType="pubmed">12804924</ArticleId></ArticleIdList></Reference><Reference><Citation>Rouleau F, Asfar P, Boulet S, Dube L, Dupuis JM, Alquier P, Victor J. Transient ST segment elevation in right precordial leads induced by psychotropic drugs: relationship to the Brugada syndrome. J Cardiovasc Electrophysiol. 2001;12:61–65.</Citation><ArticleIdList><ArticleId IdType="pubmed">11204086</ArticleId></ArticleIdList></Reference><Reference><Citation>Sangwatanaroj S, Prechawat S, Sunsaneewitayakul B, Sitthisook S, Tosukhowong P, Tungsanga K. New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives. Eur Heart J. 2001;22:2290–2296.</Citation><ArticleIdList><ArticleId IdType="pubmed">11728150</ArticleId></ArticleIdList></Reference><Reference><Citation>Saura D, Garcia-Alberola A, Carrillo P, Pascual D, Martinez-Sanchez J, Valdes M. Brugada-like electrocardiographic pattern induced by fever. Pacing Clin Electrophysiol. 2002;25:856–859.</Citation><ArticleIdList><ArticleId IdType="pubmed">12049381</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W. Acquired forms of Brugada syndrome. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Black-well Futura; Oxford: 2004. pp. 166–177.</Citation></Reference><Reference><Citation>Shimizu W, Antzelevitch C, Suyama K, Kurita T, Taguchi A, Aihara N, Takaki H, Sunagawa K, Kamakura S. Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome. J Cardiovasc Electrophysiol. 2000a;11:1320–1329.</Citation><ArticleIdList><ArticleId IdType="pubmed">11196553</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W, Matsuo K, Takagi M, Tanabe Y, Aiba T, Taguchi A, Suyama K, Kurita T, Aihara N, Kamakura S. Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms. J Cardiovasc Electrophysiol. 2000b;11:396–404.</Citation><ArticleIdList><ArticleId IdType="pubmed">10809492</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W, Aiba T, Kurita T, Kamakura S. Paradoxic abbreviation of repolarization in epicardium of the right ventricular outflow tract during augmentation of Brugada-type ST segment elevation. J Cardiovasc Electrophysiol. 2001;12:1418–1421.</Citation><ArticleIdList><ArticleId IdType="pubmed">11798001</ArticleId></ArticleIdList></Reference><Reference><Citation>Smits JP, Eckardt L, Probst V, Bezzina CR, Schott JJ, Remme CA, Haverkamp W, Breithardt G, Escande D, Schulze-Bahr E, LeMarec H, Wilde AA. Genotype-phenotype relationship in Brugada syndrome: electrocardiographic features differentiate SCN5A-related patients from non-SCN5A-related patients. J Am Coll Cardiol. 2002;40:350–356.</Citation><ArticleIdList><ArticleId IdType="pubmed">12106943</ArticleId></ArticleIdList></Reference><Reference><Citation>Suzuki H, Torigoe K, Numata 0, Yazaki S. Infant case with a malignant form of Brugada syndrome. J Cardiovasc Electrophysiol. 2000;11:1277–1280.</Citation><ArticleIdList><ArticleId IdType="pubmed">11083249</ArticleId></ArticleIdList></Reference><Reference><Citation>Tada H, Nogami A, Shimizu W, Naito S, Nakatsugawa M, Oshima S, Taniguchi K. ST segment and T wave alternans in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2000;23:413–415.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750148</ArticleId></ArticleIdList></Reference><Reference><Citation>Tada H, Sticherling C, Oral H, Morady F. Brugada syndrome mimicked by tricyclic antidepressant overdose. J Cardiovasc Electrophysiol. 2001;12:275.</Citation><ArticleIdList><ArticleId IdType="pubmed">11232630</ArticleId></ArticleIdList></Reference><Reference><Citation>Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, Kikuchi K. A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill. J Intern Med. 2004;255:137–142.</Citation><ArticleIdList><ArticleId IdType="pubmed">14687250</ArticleId></ArticleIdList></Reference><Reference><Citation>Takenaka S, Emori T, Koyama S, Morita H, Fukushima K, Ohe T. Asymptomatic form of Brugada syndrome. Pacing Clin Electrophysiol. 1999;22:1261–1263.</Citation><ArticleIdList><ArticleId IdType="pubmed">10461307</ArticleId></ArticleIdList></Reference><Reference><Citation>Tan HL, Bezzina CR, Smits JP, Verkerk AO, Wilde AA. Genetic control of sodium channel function. Cardiovasc Res. 2003;57:961–973.</Citation><ArticleIdList><ArticleId IdType="pubmed">12650874</ArticleId></ArticleIdList></Reference><Reference><Citation>Tanaka H, Kinoshita 0, Uchikawa S, Kasai H, Nakamura M, Izawa A, Yokoseki 0, Kitabayashi H, Takahashi W, Yazaki Y, Watanabe N, Imamura H, Kubo K. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1293–1294.</Citation><ArticleIdList><ArticleId IdType="pubmed">11523620</ArticleId></ArticleIdList></Reference><Reference><Citation>Tsuchiya T, Ashikaga K, Honda T, Arita M. Prevention of ventricular fibrillation by cilostazol, an oral phosphodiesterase inhibitor, in a patient with Brugada syndrome. J Cardiovasc Electrophysiol. 2002;13:698–701.</Citation><ArticleIdList><ArticleId IdType="pubmed">12139296</ArticleId></ArticleIdList></Reference><Reference><Citation>van Den Berg MP, Wilde AA, Viersma TJW, Brouwer J, Haaksma J, van der Hout AH, Stolte-Dijkstra I, Bezzina TCR, Van Langen IM, Beaufort-Krol GC, Cornel JH, Crijns HJ. Possible bradycardic mode of death and successful pacemaker treatment in a large family with features of long QT syndrome type 3 and Brugada syndrome. J Cardiovasc Electrophysiol. 2001;12:630–636.</Citation><ArticleIdList><ArticleId IdType="pubmed">11405394</ArticleId></ArticleIdList></Reference><Reference><Citation>Vatta M, Dumaine R, Varghese G, Richard TA, Shimizu W, Aihara N, Nademanee K, Brugada R, Brugada J, Veerakul G, Li H, Bowles NE, Brugada P, Antzelevitch C, Towbin JA. Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome. Hum Mol Genet. 2002;11:337–345.</Citation><ArticleIdList><ArticleId IdType="pubmed">11823453</ArticleId></ArticleIdList></Reference><Reference><Citation>Weiss R, Barmada MM, Nguyen T, Seibel JS, Cavlovich D, Kornblit CA, Angelilli A, Villanueva F, McNamara DM, London B. Clinical and molecular heterogeneity in the Brugada syndrome. A novel gene locus on chromosome 3. Circulation. 2002;105:707–713.</Citation><ArticleIdList><ArticleId IdType="pubmed">11839626</ArticleId></ArticleIdList></Reference><Reference><Citation>Wichter T, Matheja P, Eckardt L, Kies P, Schafers K, Schulze-Bahr E, Haverkamp W, Borggrefe M, Schober 0, Breithardt G, Schafers M. Cardiac autonomic dysfunction in Brugada syndrome. Circulation. 2002;105:702–706.</Citation><ArticleIdList><ArticleId IdType="pubmed">11839625</ArticleId></ArticleIdList></Reference><Reference><Citation>Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG, Towbin JA. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Circulation. 2002a;106:2514–2519.</Citation><ArticleIdList><ArticleId IdType="pubmed">12417552</ArticleId></ArticleIdList></Reference><Reference><Citation>Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG, Towbin JA. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Eur Heart J. 2002b;23:1648–1654.</Citation><ArticleIdList><ArticleId IdType="pubmed">12448445</ArticleId></ArticleIdList></Reference><Reference><Citation>Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic Jwave. Circulation. 1996;93:372–379.</Citation><ArticleIdList><ArticleId IdType="pubmed">8548912</ArticleId></ArticleIdList></Reference><Reference><Citation>Yan GX, Antzelevitch C. Cellular basis for the Brugada Syndrome and other mechanisms of arrhythmogenesis associated with ST segment elevation. Circulation. 1999;100:1660–1666.</Citation><ArticleIdList><ArticleId IdType="pubmed">10517739</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610347</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal>Beta-blockers as antiarrhythmic agents.<Pagination><StartPage>235</StartPage><EndPage>266</EndPage><MedlinePgn>235-66</MedlinePgn></Pagination><Abstract><AbstractText>Drugs that suppress beta-adrenergic signaling by competitively inhibiting agonist binding to beta-adrenergic receptors ("beta-blockers") have important antiarrhythmic properties. They differ from most other antiarrhythmic agents by not directly modifying ion channel function; rather, they prevent the arrhythmia-promoting actions of beta-adrenergic stimulation. beta-Blockers are particularly useful in preventing sudden death due to ventricular tachyarrhythmias associated with acute myocardial ischemia, congenital long QT syndrome, and congestive heart failure. They are also quite valuable in controlling the ventricular rate in patients with atrial fibrillation. This chapter reviews the properties of beta-adrenoceptor signaling, the basic mechanisms of cardiac arrhythmias on which beta-blockers act, the ion channel mediators of beta-adrenergic responses, the evidence for clinical antiarrhythmic indications for beta-blocker therapy and the specific pharmacodynamic and pharmacokinetic properties of beta-blockers that differentiate the various agents of this class.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zicha</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Montreal Heart Institute, 5000 Belanger East, Montreal Quebec, HIT 1C8, Canada. stanley.nattel@icm-mhi.org</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsuji</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Shiroshita-Takeshita</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Nattel</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Handb Exp Pharmacol</MedlineTA><NlmUniqueID>7902231</NlmUniqueID><ISSNLinking>0171-2004</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000319">Adrenergic beta-Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020746">Calcium Channels, L-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018118">Chloride Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015221">Potassium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018342">Receptors, Adrenergic, beta-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018343">Receptors, Adrenergic, beta-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019831">Sodium-Calcium Exchanger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000319" MajorTopicYN="N">Adrenergic beta-Antagonists</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020746" MajorTopicYN="N">Calcium Channels, L-Type</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018118" MajorTopicYN="N">Chloride Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015221" MajorTopicYN="N">Potassium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018342" MajorTopicYN="N">Receptors, Adrenergic, beta-1</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018343" MajorTopicYN="N">Receptors, Adrenergic, beta-2</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019831" MajorTopicYN="N">Sodium-Calcium Exchanger</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>175</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>4</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610347</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610339</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2019</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal>History of arrhythmias. | Digoxin has traditionally been the drug of choice for ventricular rate control in patients with chronic atrial fibrillation (AF), with or without heart failure (HF) with systolic dysfunction. In patients with permanent AF, digoxin monotherapy is ineffective to control ventricular rate during exercise, but the combination of digoxin with a beta-blocker or a non-dihydropyridine calcium channel antagonist can control heart rate both at rest and during exercise. Only a few randomised, controlled studies have evaluated the adverse effects of digoxin in patients with AF in a systematic way and side effects requiring drug withdrawal have rarely been reported. When reported, the most frequent adverse effects were cardiac arrhythmias (ventricular arrhythmias, AV block of varying degrees and sinus pauses). This evidence suggested that, in contrast to other antiarrhythmic drugs, digoxin is a safe drug in patients with AF. However, this safety profile can be erroneous due to the short follow-up of the studies and patient selection. Because patients with HF have been excluded in most studies, the safety profile of digoxin in this population has not been directly addressed. Early recognition that an arrhythmia is related to digoxin intoxication as well as recognition of concomitant medications or medical conditions that may directly alter the pharmacokinetic profile of digoxin, or indirectly alter its cardiac effects by pharmacodynamic interactions remain essential for safe and effective use of digoxin in patients with AF.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tamargo</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, School of Medicine, Universidad Complutense, 28040 Madrid, Spain. jtamargo@med.ucm.es</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delpón</LastName><ForeName>Eva</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Caballero</LastName><ForeName>Ricardo</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Drug Saf</MedlineTA><NlmUniqueID>101163027</NlmUniqueID><ISSNLinking>1474-0338</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>73K4184T59</RegistryNumber><NameOfSubstance UI="D004077">Digoxin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001281" MajorTopicYN="N">Atrial Fibrillation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004077" MajorTopicYN="N">Digoxin</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004347" MajorTopicYN="N">Drug Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016903" MajorTopicYN="N">Drug Monitoring</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>113</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>10</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610972</ArticleId><ArticleId IdType="doi">10.1517/14740338.5.3.453</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610350</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2021</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Therapy for the Brugada syndrome.</ArticleTitle><Pagination><StartPage>305</StartPage><EndPage>330</EndPage><MedlinePgn>305-30</MedlinePgn></Pagination><Abstract>The Brugada syndrome is a congenital syndrome of sudden cardiac death first described as a new clinical entity in 1992. Electrocardiographically characterized by a distinct coved-type ST segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. The ECG manifestations of the Brugada syndrome are often dynamic or concealed and may be revealed or modulated by sodium channel blockers. The syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, and hypokalemia, as well as by alcohol and cocaine toxicity. An implantable cardioverter-defibrillator (ICD) is the most widely accepted approach to therapy. Pharmacological therapy aimed at rebalancing the currents active during phase 1 of the right ventricular action potential is used to abort electrical storms, as an adjunct to device therapy, and as an alternative to device therapy when use of an ICD is not possible. Isoproterenol and cilostazol boost calcium channel current, and drugs like quinidine inhibit the transient outward current, acting to diminish the action potential notch and thus suppress the substrate and trigger for ventricular tachycardia/fibrillation (VT/VF).</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Antzelevitch</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA. ca@mmrl.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fish</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL047678</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL47678</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Handb Exp Pharmacol</MedlineTA><NlmUniqueID>7902231</NlmUniqueID><ISSNLinking>0171-2004</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002037" MajorTopicYN="N">Bundle-Branch Block</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003645" MajorTopicYN="N">Death, Sudden</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017147" MajorTopicYN="N">Defibrillators, Implantable</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013577" MajorTopicYN="N">Syndrome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>4</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610350</ArticleId><ArticleId IdType="mid">NIHMS10275</ArticleId><ArticleId IdType="pmc">PMC1474239</ArticleId><ArticleId IdType="doi">10.1007/3-540-29715-4_12</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Aligs M, Wilde A. “Brugada” syndrome: clinical data and suggested pathophysiological mechanism. Circulation. 1999;99:666–673.</Citation><ArticleIdList><ArticleId IdType="pubmed">9950665</ArticleId></ArticleIdList></Reference><Reference><Citation>Alings M, Dekker L, Sadee A, Wilde A. Quinidine induced electrocardiographic normalization in two patients with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1420–1422.</Citation><ArticleIdList><ArticleId IdType="pubmed">11584468</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C. The Brugada syndrome: ionic basis and arrhythmia mechanisms. f Cardiovasc Electrophysiol. 2001a;12:268–272.</Citation><ArticleIdList><ArticleId IdType="pubmed">11232628</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C. The Brugada syndrome. Diagnostic criteria and cellular mechanisms. Eur Heart J. 2001b;22:356–363.</Citation><ArticleIdList><ArticleId IdType="pubmed">11207076</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada R. Fever and the Brugada syndrome. Pacing Clin Electrophysiol. 2002;25:1537–1539.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494608</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Shimizu W. Cellular mechanisms underlying the long QT syndrome. Curr Opin Cardiol. 2002;17:43–51.</Citation><ArticleIdList><ArticleId IdType="pubmed">11790933</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Sicouri S, Litovsky SH, Lukas A, Krishnan SC, Di Diego JM, Gintant GA, Liu DW. Heterogeneity within the ventricular wall: electrophysiology and pharmacology of epicardial, endocardial and M cells. Circ Res. 1991;69:1427–1449.</Citation><ArticleIdList><ArticleId IdType="pubmed">1659499</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Brugada J, Brugada R, Nademanee K, Towbin JA. The Brugada syndrome. In: Camm AJ, editor. Clinical approaches to tachyarrhythmias. Futura Publishing Company; Armonk: 1999a. pp. 1–99.</Citation></Reference><Reference><Citation>Antzelevitch C, Shimizu W, Yan GX, Sicouri S, Weissenburger J, Nesterenko V, Burashnikov A, Di Diego JM, Saffitz JE, Thomas GP. The M cell: Its contribution to the ECG and to normal and abnormal electrical function of the heart. J Cardiovasc Electrophysiol. 1999b;10:1124–1152.</Citation><ArticleIdList><ArticleId IdType="pubmed">10466495</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Brugada J, Brugada R, Shitmizu W, Gussak I, Perez Riera AR. Brugada syndrome: a decade of progress. Circ Res. 2002;91:1114–1118.</Citation><ArticleIdList><ArticleId IdType="pubmed">12480811</ArticleId></ArticleIdList></Reference><Reference><Citation>Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Riera ARP, Tan H, Shimizu W, Schulze-Bahr E, Wilde A. Brugada syndrome. Report of the Second Consensus Conference. Circulation. 2005;111:659–670.</Citation><ArticleIdList><ArticleId IdType="pubmed">15655131</ArticleId></ArticleIdList></Reference><Reference><Citation>Araki T, Konno T, Itoh H, Ino H, Shimizu M. Brugada syndrome with ventricular tachycardia and fibrillation related to hypokalemia. Circ J. 2003;67:93–95.</Citation><ArticleIdList><ArticleId IdType="pubmed">12520160</ArticleId></ArticleIdList></Reference><Reference><Citation>Ayerza MR, de Zutter M, Goethals M, Wellens F, Geelen P, Brugada P. Heart transplantation as last resort against Brugada syndrome. J Cardiovasc Electrophysiol. 2002;13:943–944.</Citation><ArticleIdList><ArticleId IdType="pubmed">12380937</ArticleId></ArticleIdList></Reference><Reference><Citation>Babaliaros VC, Hurst JW. Tricyclic antidepressants and the Brugada syndrome: an example of Brugada waves appearing after the administration of desipramine. Clin Cardiol. 2002;25:395–398.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6654619</ArticleId><ArticleId IdType="pubmed">12173907</ArticleId></ArticleIdList></Reference><Reference><Citation>Balser JR. The cardiac sodium channel: gating function and molecular pharmacology. J Mol Cell Cardiol. 2001;33:599–613.</Citation><ArticleIdList><ArticleId IdType="pubmed">11273715</ArticleId></ArticleIdList></Reference><Reference><Citation>Belardinelli L, Antzelevitch C, Vos MA. Assessing predictors of drug-induced torsade de pointes. Trends Pharmacol Sci. 2003;24:619–625.</Citation><ArticleIdList><ArticleId IdType="pubmed">14654302</ArticleId></ArticleIdList></Reference><Reference><Citation>Belhassen B, Viskin S. Pharmacologic approach to therapy of Brugada syndrome: quinidine as an alternative to ICD therapy. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Blackwell Futura; Oxford: 2004. pp. 202–211.</Citation></Reference><Reference><Citation>Belhassen B, Viskin S, Fish R, Glick A, Setbon I, Eldar M. Effects of electrophysiologic-guided therapy with Class IA antiarrhythmic drugs on the long-term outcome of patients with idiopathic ventricular fibrillation with or without the Brugada syndrome [see comments] J Cardiovasc Electrophysiol. 1999;10:1301–1312.</Citation><ArticleIdList><ArticleId IdType="pubmed">10515552</ArticleId></ArticleIdList></Reference><Reference><Citation>Belhassen B, Viskin S, Antzelevitch C. The Brugada syndrome: is ICD the only therapeutic option. Pacing Clin Electrophysiol. 2002;25:1634–1640.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494624</ArticleId></ArticleIdList></Reference><Reference><Citation>Bezzina C, Veldkamp MW, van Den Berg MP, Postma AV, Rook MB, Viersma JW, Van Langen IM, Tan-Sindhunata G, Bink-Boelkens MT, Der Hout AH, Mannens MM, Wilde AA. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ Res. 1999;85:1206–1213.</Citation><ArticleIdList><ArticleId IdType="pubmed">10590249</ArticleId></ArticleIdList></Reference><Reference><Citation>Bolognesi R, Tsialtas D, Vasini P, Conti M, Manca C. Abnormal ventricular repolarization mimicking myocardial infarction after heterocyclic antidepressant overdose. Am J Cardiol. 1997;79:242–245.</Citation><ArticleIdList><ArticleId IdType="pubmed">9193039</ArticleId></ArticleIdList></Reference><Reference><Citation>Bordachar P, Reuter S, Garrigue S, Cai X, Hocini M, Jais P, Haissaguerre M, Clementy J. Incidence, clinical implications and prognosis of atrial arrhythmias in Brugada syndrome. Eur Heart J. 2004;25:879–884.</Citation><ArticleIdList><ArticleId IdType="pubmed">15140537</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3. A marker for sudden death in patients without demonstrable structural heart disease. Circulation. 1998;97:457–460.</Citation><ArticleIdList><ArticleId IdType="pubmed">9490240</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada J, Brugada R, Brugada P. Pharmacological and device approach to therapy of inherited cardiac diseases associated with cardiac arrhythmias and sudden death. J Electrocardiol. 2000a;33(Suppl):41–47.</Citation><ArticleIdList><ArticleId IdType="pubmed">11265735</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada R, Brugada J, Geelen P. Use of the prophylactic implantable cardioverter defibrillator for patients with normal hearts. Am J Cardiol. 1999;83:98D–1OOD.</Citation><ArticleIdList><ArticleId IdType="pubmed">10089849</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada J, Brugada R. Arrhythmia induction by antiarrhythmic drugs. Pacing Clin Electrophysiol. 2000b;23:291–292.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750126</ArticleId></ArticleIdList></Reference><Reference><Citation>Brugada P, Brugada R, Antzelevitch C, Nademanee K, Towbin f, Brugada J. The Brugada syndrome. In: Gussak I, Antzelevitch C, editors. Cardiac repolarization. bridging basic and clinical sciences. Humana Press; Totowa: 2003. pp. 427–446.</Citation></Reference><Reference><Citation>Brugada P, Bartholomay E, Mont L, Brugada R, Brugada J. Treatment of Brugada syndrome with an implantable cardioverter defibrillator. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Blackwell Futura; Oxford: 2004. pp. 194–201.</Citation></Reference><Reference><Citation>Brugada R, Brugada J, Antzelevitch C, Kirsch GE, Potenza D, Towbin JA, Brugada P. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation. 2000c;101:510–515.</Citation><ArticleIdList><ArticleId IdType="pubmed">10662748</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, Potenza D, Moya A, Borggrefe M, Breithardt G, Ortiz-Lopez R, Wang Z, Antzelevitch C, O‘Brien RE, Schultze-Bahr E, Keating MT, Towbin JA, Wang Q. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature. 1998;392:293–296.</Citation><ArticleIdList><ArticleId IdType="pubmed">9521325</ArticleId></ArticleIdList></Reference><Reference><Citation>Chinushi M, Aizawa Y, Ogawa Y, Shiba M, Takahashi K. Discrepant drug action of disopyramide on ECG abnormalities and induction of ventricular arrhythmias in a patient with Brugada syndrome. J Electrocardiol. 1997;30:133–136.</Citation><ArticleIdList><ArticleId IdType="pubmed">9141608</ArticleId></ArticleIdList></Reference><Reference><Citation>Di Diego JM, Cordeiro JM, Goodrow RJ, Fish JM, Zygmunt AC, Perez Gj, Scornik FS, Antzelevitch C. Ionic and cellular basis for the predominance of the Brugada syndrome phenotype in males. Circulation. 2002;106:2004–2011.</Citation><ArticleIdList><ArticleId IdType="pubmed">12370227</ArticleId></ArticleIdList></Reference><Reference><Citation>Dumaine R, Towbin JA, Brugada P, Vatta M, Nesterenko V, Nesterenko DV, Brugada J, Brugada R, Antzelevitch C. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 1999;85:803–809.</Citation><ArticleIdList><ArticleId IdType="pubmed">10532948</ArticleId></ArticleIdList></Reference><Reference><Citation>Dzielinska Z, Bilinska ZT, Szumowski L, Grzybowski J, Michalak E, Przybylski A, Lubiszewska B, Walczak P, Ruzyllo W. [Recurrent ventricular fibrillation during a febrile illness as the first manifestation of Brugada syndrome-a case report] Kardiol Pol. 2004;61:269–273.</Citation><ArticleIdList><ArticleId IdType="pubmed">15531939</ArticleId></ArticleIdList></Reference><Reference><Citation>Eckardt L, Kirchhof P, Johna R, Haverkamp W, Breithardt G, Borggrefe M. Wolff-Parkinson-White syndrome associated with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1423–1424.</Citation><ArticleIdList><ArticleId IdType="pubmed">11584469</ArticleId></ArticleIdList></Reference><Reference><Citation>Fish JM, Antzelevitch C. Role of sodium and calcium channel block in unmasking the Brugada syndrome. Heart Rhythm. 2004;1:210–217.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1524822</ArticleId><ArticleId IdType="pubmed">15851155</ArticleId></ArticleIdList></Reference><Reference><Citation>Fish JM, Extramiana F, Antzelevitch C. AVE0118, an Ito and IKur blocker, suppresses VT/VF in an experimental model of the Brugada syndrome. Circulation. 2004a;110:III–193.</Citation></Reference><Reference><Citation>Fish JM, Extramiana F, Antzelevitch C. Tedisamil abolishes the arrhythmogenic substrate responsible for VT/VF in an experimental model of the Brugada syndrome. Heart Rhythm. 2004b;1:S158. (abstr)</Citation></Reference><Reference><Citation>Fujiki A, Usui M, Nagasawa H, Mizumaki K, Hayashi H, Inoue H. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of Brugada syndrome [see comments] J Cardiovasc Electrophysiol. 1999;10:214–218.</Citation><ArticleIdList><ArticleId IdType="pubmed">10090224</ArticleId></ArticleIdList></Reference><Reference><Citation>Gasparini M, Priori SG, Mantica M, Napolitano C, Galimberti P, Ceriotti C, Simonini S. Flecainide test in Brugada syndrome: a reproducible but risky tool. Pacing Clin Electrophysiol. 2003;26:338–341.</Citation><ArticleIdList><ArticleId IdType="pubmed">12687841</ArticleId></ArticleIdList></Reference><Reference><Citation>Goldgran-Toledano D, Sideris G, Kevorkian JP. Overdose of cyclic antidepressants and the Brugada syndrome. N Engl J Med. 2002;346:1591–1592.</Citation><ArticleIdList><ArticleId IdType="pubmed">12015405</ArticleId></ArticleIdList></Reference><Reference><Citation>Gonzalez Rebollo G, Madrid H, Carcia A, Garcia de Casto A, Moro AM. Recurrent ventricular fibrillation during a febrile illness in a patient with the Brugada syndrome. Rev Esp Cardiol. 2000;53:755–757.</Citation><ArticleIdList><ArticleId IdType="pubmed">10816181</ArticleId></ArticleIdList></Reference><Reference><Citation>Gussak I, Antzelevitch C, Bjerregaard P, Towbin JA, Chaitman BR. The Brugada syndrome: clinical, electrophysiological and genetic aspects. J Am Coll Cardiol. 1999;33:5–15.</Citation><ArticleIdList><ArticleId IdType="pubmed">9935001</ArticleId></ArticleIdList></Reference><Reference><Citation>Haissaguerre M, Extramiana F, Hocini M, Cauchemez B, Jais P, Cabrera JA, Farre G, Leenhardt A, Sanders P, Scavee C, Hsu LF, Weerasooriya R, Shah DC, Frank R, Maury P, Delay M, Garrigue S, Clementy J. Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes. Circulation. 2003;108:925–928.</Citation><ArticleIdList><ArticleId IdType="pubmed">12925452</ArticleId></ArticleIdList></Reference><Reference><Citation>Hermida JS, Denjoy I, Clerc J, Extramiana F, Jarry G, Milliez P, Guicheney P, Di Fusco S, Rey JL, Cauchemez B, Leenhardt A. Hydroquinidine therapyin Brugada syndrome. J Am Coll Cardiol. 2004;43:1853–1860.</Citation><ArticleIdList><ArticleId IdType="pubmed">15145111</ArticleId></ArticleIdList></Reference><Reference><Citation>Hong K, Berruezo-Sanchez A, Poungvarin N, Oliva A, Vatta M, Brugada J, Brugada P, Towbin JA, Dumaine R, Pinero-Galvez C, Antzelevitch C, Brugada R. Phenotypic characterization of a large European family with Brugada syndrome displaying a sudden unexpected death syndrome mutation in SCN5A. J Cardiovasc Electrophysiol. 2004;15:64–69.</Citation><ArticleIdList><ArticleId IdType="pubmed">15028074</ArticleId></ArticleIdList></Reference><Reference><Citation>Horigome H, Shigeta 0, Kuga K, Isobe T, Sakakibara Y, Yamaguchi I, Matsui A. Ventricular fibrillation during anesthesia in association with J waves in the left precordial leads in a child with coarctation of the aorta. J Electrocardiol. 2003;36:339–343.</Citation><ArticleIdList><ArticleId IdType="pubmed">14661171</ArticleId></ArticleIdList></Reference><Reference><Citation>Kalla H, Yan GX, Marinchak R. Ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a Brugada syndrome variant. J Cardiovasc Electrophysiol. 2000;11:95–98.</Citation><ArticleIdList><ArticleId IdType="pubmed">10695469</ArticleId></ArticleIdList></Reference><Reference><Citation>Kasanuki H, Ohnishi S, Ohtuka M, Matsuda N, Nirei T, Isogai R, Shoda M, Toyoshimna Y, Hosoda S. Idiopathic ventricular fibrillation induced with vagal activity in patients with out obvious heart disease. Circulation. 1997;95:2277–2285.</Citation><ArticleIdList><ArticleId IdType="pubmed">9142005</ArticleId></ArticleIdList></Reference><Reference><Citation>Kies P, Wichter T, Schafers M, Paul M, Schafers KP, Eckardt L, Stegger L, Schulze-Bahr E, Rimoldi 0, Breithardt G, Schober 0, Camici PG. Abnormal myocardial presynaptic norepinephrine recycling in patients with Brugada syndromel. Circulation. 2004;110:3017–3022.</Citation><ArticleIdList><ArticleId IdType="pubmed">15520312</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Antzelevitch C. Sodium channel blockade produces opposite electrophysiologic effects in canine ventricular epicardium and endocardium. Circ Res. 1991;69:277–291.</Citation><ArticleIdList><ArticleId IdType="pubmed">1650294</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Antzelevitch C. Flecainide-induced arrhythmia in canine ventricular epicardium: phase 2 reentry. Circulation. 1993;87:562–572.</Citation><ArticleIdList><ArticleId IdType="pubmed">8425300</ArticleId></ArticleIdList></Reference><Reference><Citation>Krishnan SC, Josephson ME. ST segment elevation induced by class IC antiarrhythmic agents: underlying electrophysiologic mechanisms and insights into drug-induced proarrhythmia. J Cardiovasc Electrophysiol. 1998;9:1167–1172.</Citation><ArticleIdList><ArticleId IdType="pubmed">9835260</ArticleId></ArticleIdList></Reference><Reference><Citation>Kum L, Fung JWH, Chan WWL, Chan GK, Chan YS, Sanderson JE. Brugada syndrome unmasked by febrile illness. Pacing Clin Electrophysiol. 2002;25:1660–1661.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494630</ArticleId></ArticleIdList></Reference><Reference><Citation>Kurita T, Shimizu W, Inagaki M, Suyama K, Taguchi A, Satomi K, Aihara N, Kamakura S, Kobayashi J, Kosakai Y. The electrophysiologic mechanism of ST-segment elevation in Brugada syndrome. J Am Coil Cardiol. 2002;40:330–334.</Citation><ArticleIdList><ArticleId IdType="pubmed">12106940</ArticleId></ArticleIdList></Reference><Reference><Citation>Litovsky SH, Antzelevitch C. Differences in the electrophysiological response of canine ventricular subendocardium and subepicardium to acetylcholine and isoproterenol. A direct effect of acetylcholine in ventricular myocardium. Circ Res. 1990;67:615–627.</Citation><ArticleIdList><ArticleId IdType="pubmed">2397572</ArticleId></ArticleIdList></Reference><Reference><Citation>Littmann L, Monroe MH, Svenson RH. Brugada-type electrocardiographic pattern induced by cocaine. Mayo Clin Proc. 2000;75:845–849.</Citation><ArticleIdList><ArticleId IdType="pubmed">10943241</ArticleId></ArticleIdList></Reference><Reference><Citation>Lukas A, Antzelevitch C. Phase 2 reentry as a mechanism of initiation of circus movement reentry in canine epicardium exposed to simulated ischemia. The antiarrhythmic effects of 4-aminopyridine. Cardiovasc Res. 1996;32:593–603.</Citation><ArticleIdList><ArticleId IdType="pubmed">8881520</ArticleId></ArticleIdList></Reference><Reference><Citation>Madle A, Kratochvil Z, Polivkova A. [The Brugada syndrome] Vnitr Lek. 2002;48:255–258.</Citation><ArticleIdList><ArticleId IdType="pubmed">11968588</ArticleId></ArticleIdList></Reference><Reference><Citation>Matana A, Goldner V, Stanic K, Mavric Z, Zaputovic L, Matana Z. Unmasking effect of propafenone on the concealed form of the Brugada phenomenon. Pacing Clin Electrophysiol. 2000;23:416–418.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750149</ArticleId></ArticleIdList></Reference><Reference><Citation>Matsuo K, Shimizu W, Kurita T, Inagaki M, Aihara N, Kamakura S. Dynamic changes of 12-lead electrocardiograms in a patient with Brugada syndrome. J Cardiovasc Electrophysiol. 1998;9:508–512.</Citation><ArticleIdList><ArticleId IdType="pubmed">9607459</ArticleId></ArticleIdList></Reference><Reference><Citation>Miyasaka Y, Tsuji H, Yamada K, Tokunaga S, Saito D, Imuro Y, Matsumoto N, Iwasaka T. Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan. J Am Coll Cardiol. 2001;38:771–774.</Citation><ArticleIdList><ArticleId IdType="pubmed">11527631</ArticleId></ArticleIdList></Reference><Reference><Citation>Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa Y, Ogawa S. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome. J Am Coll Cardiol. 1996;27:1061–1070.</Citation><ArticleIdList><ArticleId IdType="pubmed">8609322</ArticleId></ArticleIdList></Reference><Reference><Citation>Mizumaki K, Fujiki A, Tsuneda T, Sakabe M, Nishida K, Sugao M, Inoue H. Vagal activity modulates spontaneous augmentation of ST elevation in daily life of patients with Brugada syndrome. J Cardiovasc Electrophysiol. 2004;15:667–673.</Citation><ArticleIdList><ArticleId IdType="pubmed">15175062</ArticleId></ArticleIdList></Reference><Reference><Citation>Mok NS, Chan NY, Chi-Suen CA. Successful use of quinidine in treatment of electrical storm in Brugada syndrome. Pacing Clin Electrophysiol. 2004;27:821–823.</Citation><ArticleIdList><ArticleId IdType="pubmed">15189543</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita H, Kusano-Fukushima K, Nagase S, Fujimoto Y, Hisamatsu K, Fujio H, Haraoka K, Kobayashi M, Morita ST, Nakamura K, Emori T, Matsubara H, Hina K, Kita T, Fukatani M, Ohe T. Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome. J Am Coll Cardiol. 2002;40:1437.</Citation><ArticleIdList><ArticleId IdType="pubmed">12392834</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita H, Fukushima-Kusano K, Nagase S, Miyaji K, Hiramatsu S, Banba K, Nishii N, Watanabe A, Kakishita M, Takenaka-Morita S, Nakamura K, Saito H, Emori T, Ohe T. Sinus node function in patients with Brugada-type ECG. Circ J. 2004;68:473–476.</Citation><ArticleIdList><ArticleId IdType="pubmed">15118291</ArticleId></ArticleIdList></Reference><Reference><Citation>Nademanee K, Veerakul G, Nimmannit S, Chaowakul V, Bhuripanyo K, Likittanasombat K, Tunsanga K, Kuasirikul S, Malasit P, Tansupasawadikul S, Tatsanavivat P. Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation. 1997;96:2595–2600.</Citation><ArticleIdList><ArticleId IdType="pubmed">9355899</ArticleId></ArticleIdList></Reference><Reference><Citation>Nimmannit S, Malasit P, Chaovakul V, Susaengrat W, Vasuvattakul S, Nilwarangkur S. Pathogenesis of sudden unexplained nocturnal death (lai tai) and endemic distal renal tubular acidosis. Lancet. 1991;338:930–932.</Citation><ArticleIdList><ArticleId IdType="pubmed">1681278</ArticleId></ArticleIdList></Reference><Reference><Citation>Noda T, Shimizu W, Taguchi A, Satomi K, Suyama K, Kurita T, Aihara N, Kamakura S. ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome. J Am Coll Cardiol. 2002;40:1841–1847.</Citation><ArticleIdList><ArticleId IdType="pubmed">12446069</ArticleId></ArticleIdList></Reference><Reference><Citation>Nogami A, Nakao M, Kubota S, Sugiyasu A, Doi H, Yokoyama K, Yumoto K, Tamaki T, Kato K, Hosokawa N, Sagai H, Nakamura H, Nitta J, Yamauchi Y, Aonuma K. Enhancement of J-ST-segment elevation by the glucose and insulin test in Brugada syndrome. Pacing Clin Electrophysiol. 2003;26:332–337.</Citation><ArticleIdList><ArticleId IdType="pubmed">12687840</ArticleId></ArticleIdList></Reference><Reference><Citation>Ortega-Carnicer J, Bertos-Polo J, Gutierrez-Tirado C. Aborted sudden death, transient Brugada pattern, and wide QRS dysrhythmias after massive cocaine ingestion. J Electrocardiol. 2001;34:345–349.</Citation><ArticleIdList><ArticleId IdType="pubmed">11590577</ArticleId></ArticleIdList></Reference><Reference><Citation>Ortega-Carnicer J, Benezet J, Ceres F. Fever-induced ST-segment elevation and T-wave alternans in a patient with Brugada syndrome. Resuscitation. 2003;57:315–317.</Citation><ArticleIdList><ArticleId IdType="pubmed">12804811</ArticleId></ArticleIdList></Reference><Reference><Citation>Pastor A, Nunez A, Cantale C, Cosio FG. Asymptomatic Brugada syndrome case unmasked during dimenhydrinate infusion. J Cardiovasc Electrophysiol. 2001;12:1192–1194.</Citation><ArticleIdList><ArticleId IdType="pubmed">11699532</ArticleId></ArticleIdList></Reference><Reference><Citation>Pitzalis MV, Anaclerio M, Iacoviello M, Forleo C, Guida P, Troccoli R, Massari F, Mastropasqua F, Sorrentino S, Manghisi A, Rizzon P. QT-interval prolongation in right precordial leads: an additional electrocardiographic hallmark of Brugada syndrome. J Am Coil Cardiol. 2003;42:1632–1637.</Citation><ArticleIdList><ArticleId IdType="pubmed">14607451</ArticleId></ArticleIdList></Reference><Reference><Citation>Porres JM, Brugada J, Urbistondo V, Garcia F, Reviejo K, Marco P. Fever unmasking the Brugada syndrome. Pacing Clin Electrophysiol. 2002;25:1646–1648.</Citation><ArticleIdList><ArticleId IdType="pubmed">12494626</ArticleId></ArticleIdList></Reference><Reference><Citation>Potet F, Mabo P, Le Coq G, Probst V, Schott Jf, Airaud F, Guihard G, Daubert JC, Escande D, Le Marec H. Novel Brugada SCNSA mutation leading to ST segment elevation in the inferior or the right precordial leads. J Cardiovasc Electrophysiol. 2003;14:200–203.</Citation><ArticleIdList><ArticleId IdType="pubmed">12693506</ArticleId></ArticleIdList></Reference><Reference><Citation>Priori SG, Napolitano C, Gasparini M, Pappone C, Della BP, Brignole M, Giordano U, Giovannini T, Menozzi C, Bloise R, Crotti L, Terreni L, Schwartz PJ. Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome: a prospective evaluation of 52 families. Cfrculation. 2000;102:2509–2515.</Citation><ArticleIdList><ArticleId IdType="pubmed">11076825</ArticleId></ArticleIdList></Reference><Reference><Citation>Priori SG, Napolitano C, Gasparini M, Pappone C, Della BP, Giordano U, Bloise R, Giustetto C, De Nardis R, Grillo M, Ronchetti E, Faggiano G, Nastoli J. Natural history of Brugada syndrome: insights for risk stratification and management. Circulation. 2002;105:1342–1347.</Citation><ArticleIdList><ArticleId IdType="pubmed">11901046</ArticleId></ArticleIdList></Reference><Reference><Citation>Proclemer A, Facchin D, Feruglio GA, Nucifora R. Recurrent ventricular fibrillation, right bundle-branch block and persistent ST segment elevation in V1-V3: a new arrhythmia syndrome? A clinical case report [see comments] G Ital Cardiol. 1993;23:1211–1218.</Citation><ArticleIdList><ArticleId IdType="pubmed">8174872</ArticleId></ArticleIdList></Reference><Reference><Citation>Rolf S, Bruns HJ, Wichter T, Kirchhof P, Ribbing M, Wasmer K, Paul M, Breithardt G, Haverkamp W, Eckardt L. The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. Eur Heart J. 2003;24:1104–1112.</Citation><ArticleIdList><ArticleId IdType="pubmed">12804924</ArticleId></ArticleIdList></Reference><Reference><Citation>Rouleau F, Asfar P, Boulet S, Dube L, Dupuis JM, Alquier P, Victor J. Transient ST segment elevation in right precordial leads induced by psychotropic drugs: relationship to the Brugada syndrome. J Cardiovasc Electrophysiol. 2001;12:61–65.</Citation><ArticleIdList><ArticleId IdType="pubmed">11204086</ArticleId></ArticleIdList></Reference><Reference><Citation>Sangwatanaroj S, Prechawat S, Sunsaneewitayakul B, Sitthisook S, Tosukhowong P, Tungsanga K. New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives. Eur Heart J. 2001;22:2290–2296.</Citation><ArticleIdList><ArticleId IdType="pubmed">11728150</ArticleId></ArticleIdList></Reference><Reference><Citation>Saura D, Garcia-Alberola A, Carrillo P, Pascual D, Martinez-Sanchez J, Valdes M. Brugada-like electrocardiographic pattern induced by fever. Pacing Clin Electrophysiol. 2002;25:856–859.</Citation><ArticleIdList><ArticleId IdType="pubmed">12049381</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W. Acquired forms of Brugada syndrome. In: Antzelevitch C, Brugada P, Brugada J, Brugada R, editors. The Brugada syndrome: from bench to bedside. Black-well Futura; Oxford: 2004. pp. 166–177.</Citation></Reference><Reference><Citation>Shimizu W, Antzelevitch C, Suyama K, Kurita T, Taguchi A, Aihara N, Takaki H, Sunagawa K, Kamakura S. Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome. J Cardiovasc Electrophysiol. 2000a;11:1320–1329.</Citation><ArticleIdList><ArticleId IdType="pubmed">11196553</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W, Matsuo K, Takagi M, Tanabe Y, Aiba T, Taguchi A, Suyama K, Kurita T, Aihara N, Kamakura S. Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms. J Cardiovasc Electrophysiol. 2000b;11:396–404.</Citation><ArticleIdList><ArticleId IdType="pubmed">10809492</ArticleId></ArticleIdList></Reference><Reference><Citation>Shimizu W, Aiba T, Kurita T, Kamakura S. Paradoxic abbreviation of repolarization in epicardium of the right ventricular outflow tract during augmentation of Brugada-type ST segment elevation. J Cardiovasc Electrophysiol. 2001;12:1418–1421.</Citation><ArticleIdList><ArticleId IdType="pubmed">11798001</ArticleId></ArticleIdList></Reference><Reference><Citation>Smits JP, Eckardt L, Probst V, Bezzina CR, Schott JJ, Remme CA, Haverkamp W, Breithardt G, Escande D, Schulze-Bahr E, LeMarec H, Wilde AA. Genotype-phenotype relationship in Brugada syndrome: electrocardiographic features differentiate SCN5A-related patients from non-SCN5A-related patients. J Am Coll Cardiol. 2002;40:350–356.</Citation><ArticleIdList><ArticleId IdType="pubmed">12106943</ArticleId></ArticleIdList></Reference><Reference><Citation>Suzuki H, Torigoe K, Numata 0, Yazaki S. Infant case with a malignant form of Brugada syndrome. J Cardiovasc Electrophysiol. 2000;11:1277–1280.</Citation><ArticleIdList><ArticleId IdType="pubmed">11083249</ArticleId></ArticleIdList></Reference><Reference><Citation>Tada H, Nogami A, Shimizu W, Naito S, Nakatsugawa M, Oshima S, Taniguchi K. ST segment and T wave alternans in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2000;23:413–415.</Citation><ArticleIdList><ArticleId IdType="pubmed">10750148</ArticleId></ArticleIdList></Reference><Reference><Citation>Tada H, Sticherling C, Oral H, Morady F. Brugada syndrome mimicked by tricyclic antidepressant overdose. J Cardiovasc Electrophysiol. 2001;12:275.</Citation><ArticleIdList><ArticleId IdType="pubmed">11232630</ArticleId></ArticleIdList></Reference><Reference><Citation>Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, Kikuchi K. A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill. J Intern Med. 2004;255:137–142.</Citation><ArticleIdList><ArticleId IdType="pubmed">14687250</ArticleId></ArticleIdList></Reference><Reference><Citation>Takenaka S, Emori T, Koyama S, Morita H, Fukushima K, Ohe T. Asymptomatic form of Brugada syndrome. Pacing Clin Electrophysiol. 1999;22:1261–1263.</Citation><ArticleIdList><ArticleId IdType="pubmed">10461307</ArticleId></ArticleIdList></Reference><Reference><Citation>Tan HL, Bezzina CR, Smits JP, Verkerk AO, Wilde AA. Genetic control of sodium channel function. Cardiovasc Res. 2003;57:961–973.</Citation><ArticleIdList><ArticleId IdType="pubmed">12650874</ArticleId></ArticleIdList></Reference><Reference><Citation>Tanaka H, Kinoshita 0, Uchikawa S, Kasai H, Nakamura M, Izawa A, Yokoseki 0, Kitabayashi H, Takahashi W, Yazaki Y, Watanabe N, Imamura H, Kubo K. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1293–1294.</Citation><ArticleIdList><ArticleId IdType="pubmed">11523620</ArticleId></ArticleIdList></Reference><Reference><Citation>Tsuchiya T, Ashikaga K, Honda T, Arita M. Prevention of ventricular fibrillation by cilostazol, an oral phosphodiesterase inhibitor, in a patient with Brugada syndrome. J Cardiovasc Electrophysiol. 2002;13:698–701.</Citation><ArticleIdList><ArticleId IdType="pubmed">12139296</ArticleId></ArticleIdList></Reference><Reference><Citation>van Den Berg MP, Wilde AA, Viersma TJW, Brouwer J, Haaksma J, van der Hout AH, Stolte-Dijkstra I, Bezzina TCR, Van Langen IM, Beaufort-Krol GC, Cornel JH, Crijns HJ. Possible bradycardic mode of death and successful pacemaker treatment in a large family with features of long QT syndrome type 3 and Brugada syndrome. J Cardiovasc Electrophysiol. 2001;12:630–636.</Citation><ArticleIdList><ArticleId IdType="pubmed">11405394</ArticleId></ArticleIdList></Reference><Reference><Citation>Vatta M, Dumaine R, Varghese G, Richard TA, Shimizu W, Aihara N, Nademanee K, Brugada R, Brugada J, Veerakul G, Li H, Bowles NE, Brugada P, Antzelevitch C, Towbin JA. Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome. Hum Mol Genet. 2002;11:337–345.</Citation><ArticleIdList><ArticleId IdType="pubmed">11823453</ArticleId></ArticleIdList></Reference><Reference><Citation>Weiss R, Barmada MM, Nguyen T, Seibel JS, Cavlovich D, Kornblit CA, Angelilli A, Villanueva F, McNamara DM, London B. Clinical and molecular heterogeneity in the Brugada syndrome. A novel gene locus on chromosome 3. Circulation. 2002;105:707–713.</Citation><ArticleIdList><ArticleId IdType="pubmed">11839626</ArticleId></ArticleIdList></Reference><Reference><Citation>Wichter T, Matheja P, Eckardt L, Kies P, Schafers K, Schulze-Bahr E, Haverkamp W, Borggrefe M, Schober 0, Breithardt G, Schafers M. Cardiac autonomic dysfunction in Brugada syndrome. Circulation. 2002;105:702–706.</Citation><ArticleIdList><ArticleId IdType="pubmed">11839625</ArticleId></ArticleIdList></Reference><Reference><Citation>Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG, Towbin JA. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Circulation. 2002a;106:2514–2519.</Citation><ArticleIdList><ArticleId IdType="pubmed">12417552</ArticleId></ArticleIdList></Reference><Reference><Citation>Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG, Towbin JA. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Eur Heart J. 2002b;23:1648–1654.</Citation><ArticleIdList><ArticleId IdType="pubmed">12448445</ArticleId></ArticleIdList></Reference><Reference><Citation>Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic Jwave. Circulation. 1996;93:372–379.</Citation><ArticleIdList><ArticleId IdType="pubmed">8548912</ArticleId></ArticleIdList></Reference><Reference><Citation>Yan GX, Antzelevitch C. Cellular basis for the Brugada Syndrome and other mechanisms of arrhythmogenesis associated with ST segment elevation. Circulation. 1999;100:1660–1666.</Citation><ArticleIdList><ArticleId IdType="pubmed">10517739</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610347</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Beta-blockers as antiarrhythmic agents.</ArticleTitle><Pagination><StartPage>235</StartPage><EndPage>266</EndPage><MedlinePgn>235-66</MedlinePgn></Pagination><Abstract>Drugs that suppress beta-adrenergic signaling by competitively inhibiting agonist binding to beta-adrenergic receptors ("beta-blockers") have important antiarrhythmic properties. They differ from most other antiarrhythmic agents by not directly modifying ion channel function; rather, they prevent the arrhythmia-promoting actions of beta-adrenergic stimulation. beta-Blockers are particularly useful in preventing sudden death due to ventricular tachyarrhythmias associated with acute myocardial ischemia, congenital long QT syndrome, and congestive heart failure. They are also quite valuable in controlling the ventricular rate in patients with atrial fibrillation. This chapter reviews the properties of beta-adrenoceptor signaling, the basic mechanisms of cardiac arrhythmias on which beta-blockers act, the ion channel mediators of beta-adrenergic responses, the evidence for clinical antiarrhythmic indications for beta-blocker therapy and the specific pharmacodynamic and pharmacokinetic properties of beta-blockers that differentiate the various agents of this class.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zicha</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Montreal Heart Institute, 5000 Belanger East, Montreal Quebec, HIT 1C8, Canada. stanley.nattel@icm-mhi.org</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsuji</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Shiroshita-Takeshita</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Nattel</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Handb Exp Pharmacol</MedlineTA><NlmUniqueID>7902231</NlmUniqueID><ISSNLinking>0171-2004</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000319">Adrenergic beta-Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020746">Calcium Channels, L-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018118">Chloride Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015221">Potassium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018342">Receptors, Adrenergic, beta-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018343">Receptors, Adrenergic, beta-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019831">Sodium-Calcium Exchanger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000319" MajorTopicYN="N">Adrenergic beta-Antagonists</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020746" MajorTopicYN="N">Calcium Channels, L-Type</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018118" MajorTopicYN="N">Chloride Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015221" MajorTopicYN="N">Potassium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018342" MajorTopicYN="N">Receptors, Adrenergic, beta-1</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018343" MajorTopicYN="N">Receptors, Adrenergic, beta-2</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019831" MajorTopicYN="N">Sodium-Calcium Exchanger</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>175</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>4</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>4</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16610347</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16610339</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2019</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0171-2004</ISSN><JournalIssue CitedMedium="Print"><Issue>171</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Handbook of experimental pharmacology</Title><ISOAbbreviation>Handb Exp Pharmacol</ISOAbbreviation></Journal><ArticleTitle>History of arrhythmias.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>39</EndPage><MedlinePgn>1-39</MedlinePgn></Pagination><Abstract>A historical overview is given on the techniques to record the electrical activity of the heart, some anatomical aspects relevant for the understanding of arrhythmias, general mechanisms of arrhythmias, mechanisms of some specific arrhythmias and nonpharmacological forms of therapy. The unravelling of arrhythmia mechanisms depends, of course, on the ability to record the electrical activity of the heart. It is therefore no surprise that following the construction of the string galvanometer by Einthoven in 1901, which allowed high-fidelity recording of the body surface electrocardiogram, the study of arrhythmias developed in an explosive way. Still, papers from McWilliam (1887), Garrey (1914) and Mines (1913, 1914) in which neither mechanical nor electrical activity was recorded provided crucial insights into re-entry as a mechanism for atrial and ventricular fibrillation, atrioventricular nodal re-entry and atrioventricular re-entrant tachycardia in hearts with an accessory atrioventricular connection. The components of the electrocardiogram, and of extracellular electrograms directly recorded from the heart, could only be well understood by comparing such registrations with recordings of transmembrane potentials. The first intracellular potentials were recorded with microelectrodes in 1949 by Coraboeuf and Weidmann. It is remarkable that the interpretation of extracellular electrograms was still controversial in the 1950s, and it was not until 1962 that Dower showed that the transmembrane action potential upstroke coincided with the steep negative deflection in the electrogram. For many decades, mapping of the spread of activation during an arrhythmia was performed with a "roving" electrode that was subsequently placed on different sites on the cardiac surface with a simultaneous recording of another signal as time reference. This method could only provide reliable information if the arrhythmia was strictly regular. When multiplexing systems became available in the late 1970s, and optical mapping in the 1980s, simultaneous registrations could be made from many sites. The analysis of atrial and ventricular fibrillation then became much more precise. The old question whether an arrhythmia is due to a focal or a re-entrant mechanism could be answered, and for atrial fibrillation, for instance, the answer is that both mechanisms may be operative. The road from understanding the mechanism of an arrhythmia to its successful therapy has been long: the studies of Mines in 1913 and 1914, microelectrode studies in animal preparations in the 1960s and 1970s, experimental and clinical demonstrations of initiation and termination of tachycardias by premature stimuli in the 1960s and 1970s, successful surgery in the 1980s, the development of external and implantable defibrillators in the 1960s and 1980s, and finally catheter ablation at the end of the previous century, with success rates that approach 99% for supraventricular tachycardias. |
9,730 | [Obstructive sleep apnea-related cardiovascular disease]. | The clinical spectrum of obstructive sleep apnea-(OSA-)related cardiovascular disease (CVD) comprises systemic arterial hypertension (prevalence: 40-60%), pulmonary hypertension (20-30%), coronary artery disease (20-30%), congestive heart failure (5-10%), and stroke (5-10%). During sleep, heart rhythm disorders such as atrioventricular blocks, sinus arrests and atrial fibrillation can be induced by OSA. OSA-related CVD mainly affects those patients with an apnea-hypopnea index > 30/h and, if left untreated, is linked to increased mortality. Epidemiologic data have clearly shown that cardiovascular risk is increased in OSA independent of confounding factors such as obesity and concomitant metabolic disease. In recent years, the pathophysiology of OSA-related CVD has been further elucidated showing that apart from the well-known sympathetic activation, increased oxidative stress and pro-inflammatory changes seem to play major roles. Furthermore, studies using high resolution ultrasonography have demonstrated endothelial dysfunction and enhanced atherosclerosis in these patients. Finally, animal models of OSA have delineated that daytime arterial hypertension is the consequence of the OSA-associated chronic intermittent hypoxia. Therapy of OSA by continuous positive airway pressure (CPAP) ventilation exerts cardioprotective effects. It has been shown to rectify the vascular micromilieu, restore endothelium-dependent vasodilation, lower 24-h blood pressure, eliminate nocturnal heart rhythm disorders, and improve left ventricular function. Furthermore, long-term CPAP therapy leads to a reduction in important clinical endpoints such as the rates of myocardial infarction and stroke. |
9,731 | Predictive impact of the inducibility of ventricular fibrillation in patients with Brugada-type ECG. | The natural history of asymptomatic individuals with a Brugada-type electrocardiogram (ECG) is still controversial. In this study, we evaluated ventricular fibrillation (VF) inducibility in Brugada-type ECG patients and compared it with other risk factors to clarify the significance of these data on their prognosis. The study population consisted of 38 patients who presented with a typical ST-segment elevation in the precordial leads and underwent an electrophysiological study (EPS). The patients were divided into 3 groups; group A: patients with spontaneous ventricular fibrillation (VF) (n = 5), group B: patients without clinical VF but with inducible VF in EPS (n = 16), and group C: patients with neither clinical nor inducible VF (n = 17). The clinical features, diagnostic results, and prognosis were compared among these groups. During the follow-up period of 26 +/- 19 months, 2/5 (group A), 1/16 (group B), and 0/17 (group C) patients suffered fatal arrhythmic events. None of the clinical features showed any significant difference, although the incidence of positive results in a drug challenge test was higher in groups A and B than in group C (P < 0.05). On the other hand, VF inducibility was higher in patients with positive results in the drug challenge test than in patients with negative results (59% versus 13%; P < 0.05). No VF episodes were observed in patients without VF induction, although one was observed in 1 of 16 patients with VF induction in asymptomatic Brugada syndrome. The drug challenge test appears to be useful for predicting VF inducibility even though it is a noninvasive test. |
9,732 | A biventricular ICD system with biventricular defibrillation. | We describe the case of a 59-year-old gentleman with severe dilated cardiomyopathy requiring implantation of a dual-chamber biventricular implantable cardioverter-defibrillator (ICD). High defibrillation thresholds (DFT) were encountered at implant with an inadequate defibrillation safety margin. Testing of all possible shock vectors/polarities with and without the SVC coil and optimization of the distal RV coil position all proved inadequate. A satisfactory defibrillation safety margin was achieved following placement of a second lead in the coronary sinus to enable biventricular defibrillation. This case highlights an additional strategy for combating high DFTs and is an option even in dual-chamber biventricular ICD systems. |
9,733 | Late-phase 3 EAD. A unique mechanism contributing to initiation of atrial fibrillation. | Early (EAD) and delayed (DAD) afterdepolarizations-induced triggered activity is capable of initiating and maintaining cardiac arrhythmias. EAD-induced triggered responses are traditionally thought to be involved in the generation of ventricular arrhythmias under long QT conditions and are precipitated by bradycardia or long pauses. In contrast, DAD-induced triggered activity commonly underlies arrhythmias precipitated by tachycardia. Spontaneous release of calcium from the sarcoplasmic reticulum (SR) secondary to cellular calcium overload induces DADs and some forms of EADs. Recent studies from our laboratory have uncovered a novel mechanism giving rise to triggered activity, termed "late-phase 3 EAD," which combines properties of both EAD and DAD, but has its own unique character. Late-phase 3 EAD-induced triggered extrasystoles represent a new concept of arrhythmogenesis in which abbreviated repolarization permits "normal SR calcium release" to induce an EAD-mediated closely coupled triggered response, particularly under conditions permitting intracellular calcium loading. This review briefly describes the mechanisms and properties of late-phase 3 EADs, how they differ from conventional EADs and DADs, as well as their role in the initiation of cardiac arrhythmias, such as atrial fibrillation. |
9,734 | Antiinflammatory effects of cardiac resynchronization therapy in patients with chronic heart failure. | Cardiac resynchronization therapy (CRT) pacing has been proposed as an additional treatment to medical therapy to improve heart failure patients with left ventricular asynchrony. The aim of this study was to evaluate the influence of CRT treatment on proinflammatory cytokines in patients with heart failure.</AbstractText>Twenty patients, with a mean age 64 +/- 2 years, with severe chronic heart failure NYHA class II-IV (mean ejection fraction 25 +/- 2%), were included in the study. Patients were treated with CRT pacing, after failure of optimal therapy. Blood samples were taken at baseline, 3 months after pacing therapy, and after a subsequent 3-month period of no pacing for the assessment of proinflammatory cytokines TNF-alpha and its receptors (sTNFR-I, sTNFR-II), IL-6, adhesion molecules sICAM-1 and sVCAM-1, and the apoptotic indices sFas and sFas-Ligand.</AbstractText>Levels of TNF-alpha, sTNFR-I, and sTNFR-II were reduced at the end of 3 months of CRT therapy and further reduced at the end of the no pacing period (P < 0.05, compared to baseline). Levels of IL-6 also declined after 3 months of CRT pacing (from 8.9 +/- 2.5 pg/mL to 4.7 +/- 1.3 pg/mL, P < 0.05) and this was maintained during the no pacing period (3.9 +/- 1.1 pg/mL P < 0.05 compared to baseline). The adhesion molecule sICAM-1 levels also reduced (from 265 +/- 17 ng/mL to 235 +/- 12, P < 0.05) after 3 months of CRT pacing and remained unchanged at the end of the no pacing period (219 +/- 12 ng/mL, P < 0.05 compared to baseline values).</AbstractText>Major proinflammatory cytokines and the adhesion molecule sICAM-1 are reduced with CRT therapy and this effect is maintained for at least 3 months after discontinuation of pacing.</AbstractText> |
9,735 | Reduction of right ventricular pacing in patients with dual-chamber ICDs. | Unnecessary right ventricular (RV) pacing in patients with implantable cardioverter defibrillators (ICD) may adversely affect heart failure morbidity and total mortality. Inhibition of Unnecessary RV Pacing with AV Search Hysteresis in ICDs (INTRINSIC RV) is a prospective, multicenter, randomized trial evaluating outcomes in ICD recipients programmed to single-chamber pacing (VVI) versus dual-chamber (DDDR) pacing with AV search hysteresis (AVSH).</AbstractText>Patients underwent ICD implant (for standard indications). The ICD was programmed to DDDR with AVSH regardless of any need for pacing. Rate-adaptive pacing was set at 60-130 ppm with dynamic AV delay from 200 to 90 ms. AVSH was programmed to search every 32 intervals and extend the AV delay by 50%. One week post-implant patients with ICDs were interrogated to assess the percentage of RV pacing with the expectation that most would have <20% RV pacing and would be randomized into INTRINSIC RV. Early analysis showed that targets for randomization were not met. AVSH parameters were modified under a protocol amendment to increase AV delay extension to 100%. We report findings related to this programming change based upon analyses of (nonrandomized) data pre- and post-amendment.</AbstractText>Twenty-one percent of patients (n = 314) were enrolled pre-amendment and 79% (n = 1,216) were enrolled post-amendment. The mean percentage of RV pacing at the 1-week visit was 41.4 +/- 29.6% pre-amendment and 14.7 +/- 22.6% post-amendment (P < 0.0001). The proportion of patients eligible for randomization (RV pacing <20% at the 1-week visit) was 31.2% pre-amendment and 76.8% post-amendment (P < 0.0001).</AbstractText>AVSH can dramatically reduce the percentage of RV pacing among ICD recipients.</AbstractText> |
9,736 | Long-term performance of active-fixation pacing leads: a prospective study. | Despite the increasingly widespread use of active-fixation leads, long-term clinical follow-up of pacing lead outcomes is lacking. The aim was to analyze pacing parameters over a 2-year follow-up. We performed a prospective observational study of consecutive new pacemaker implants using the 1488T St. Jude (100) and the Medtronic 5076 (100) active-fixation leads. Detailed analysis of pacing parameters was collected at implant, day 1, and 1, 3, 6, 12, 18, and 24 months.</AbstractText>One hundred patients underwent implantation of 100 dual-chamber pacemakers. Initial pacing parameters in the ventricle were threshold 0.7 +/- 0.2 V, R wave 12.0 +/- 6.5 mV, and impedance 879 +/- 224 Omega. Threshold increased significantly from day 1 (0.7 +/- 0.2 V) to month 1 (0.9 +/- 0.6 V, P < 0.01) and remained stable over the long term. Four of the 100 patients had a threshold >2 V (mean 3.3 +/- 0.9 V) all between day 1 and month 3. For all patients, R wave remained stable, but impedance declined significantly from day 1 (879 +/- 184 Omega) to month 1 (677 +/- 122 Omega, P < 0.01). There were no ventricular lead complications. Initial pacing parameters in the atrium were threshold 0.9 +/- 0.3 V, P wave 3.3 +/- 2.4 mV, and impedance 606 +/- 144 Omega. Threshold remained stable over the long-term follow-up. One of 100 patients had a rise in threshold >2 V (2.2 V) between day 1 and month 1. No patients underwent lead repositioning. Sensing and impedance remained stable over the long term. Patient follow-up was completed in 94% (6 unrelated deaths). There was an 8% incidence of atrial fibrillation.</AbstractText>Active-fixation leads are generally associated with stable long-term pacing parameters.</AbstractText> |
9,737 | Nonequilibrium ribbon model of twisted scroll waves. | We formulate a reduced model to analyze the motion of the core of a twisted scroll wave. The model is first shown to provide a simple description of the onset and nonlinear evolution of the helical state appearing in the sproing bifurcation of scroll waves. It then serves to examine the experimentally studied case of a medium with spatially varying excitability. The model shows the role of sproing in this more complex setting and highlights the differences between the convective and absolute sproing instabilities. |
9,738 | Control of electrical alternans in canine cardiac purkinje fibers. | Alternation in the duration of consecutive cardiac action potentials (electrical alternans) may precipitate conduction block and the onset of arrhythmias. Consequently, suppression of alternans using properly timed premature stimuli may be antiarrhythmic. To determine the extent to which alternans control can be achieved in cardiac tissue, isolated canine Purkinje fibers were paced from one end using a feedback control method. Spatially uniform control of alternans was possible when alternans amplitude was small. However, control became attenuated spatially as alternans amplitude increased. The amplitude variation along the cable was well described by a theoretically expected standing wave profile that corresponds to the first quantized mode of the one-dimensional Helmholtz equation. These results confirm the wavelike nature of alternans and may have important implications for their control using electrical stimuli. |
9,739 | Characterization of repolarization alternans during ischemia: time-course and spatial analysis. | T-wave alternans (TWA) has been linked to increased vulnerability to ventricular fibrillation in different settings including myocardial ischemia. In this study, we propose a methodology for the characterization of TWA induced by transient, regional ischemia. We studied the prevalence, magnitude and spatio-temporal relationship between TWA and ischemia in 95 patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Two electrocardiogram records of each patient, a control recording before PTCA and the PTCA record, were analyzed using a robust, recently proposed method for TWA analysis. The detected episodes were characterized in terms of their time-course, lead distribution and alternans waveform. One third of the patients (33.7%) showed TWA episodes during PTCA. The highest prevalence (51.7%) and amplitude were found in patients with left anterior descendent artery occlusion. The onset of TWA was detected after the first 1-2 min of occlusion, suggesting that some level of ischemia must be attained before TWA arises, while disappearance of TWA following reperfusion was much more rapid. The TWA lead distributions and waveforms showed distinct distributions according to the occluded artery reflecting the regional nature of the TWA phenomenon. |
9,740 | Prospects for the prevention of stroke. | We are currently fighting a battle against a stroke epidemic. Implementation of new treatment strategies could save many patients in the future. The control of blood pressure is a major objective; however, choosing specific antihypertensive therapy (e.g. an agent blocking the renin-angiotensin system) is also important. The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study demonstrates potential benefits beyond blood pressure reduction of prescribing an angiotensin II receptor blocker (ARB) compared with more established therapy in patients with left ventricular hypertrophy (LVH). Losartan-based therapy brought about regression of LVH and reduced incidences of fatal and non-fatal stroke by 25%, new-onset diabetes by 25% and atrial fibrillation by 30% more than atenolol-based therapy for a similar blood pressure control and better tolerability. The Study on COgnition and Prognosis in the Elderly (SCOPE) study, although difficult to interpret, does not contradict an ARB benefit beyond blood pressure lowering in primary prevention linked to targeting the angiotensin type 1 receptor. The findings of the MOrbidity and mortality after Stroke, Eprosartan compared with nitrendipine in Secondary prevention (MOSES) trial suggest clear-cut ARB benefits independent of blood pressure lowering in secondary stroke prevention. Experimental findings and other clinical evidence further support the benefits of ARBs in stroke prevention. Telmisartan is an ARB with a particularly interesting profile for stroke; given the 24-hour efficacy with more pronounced protection against the morning blood pressure surge and peroxisome proliferator-activated receptor-gamma activity at clinical doses. The unique properties of telmisartan for secondary stroke prevention are being tested in the Prevention Regimen For Effectively avoiding Second Strokes (PRoFESS) study. |
9,741 | Cardiac connexins as candidate genes for idiopathic atrial fibrillation. | Atrial fibrillation is the most common sustained cardiac arrhythmia and may cause significant morbidity. Current management strategies offer only modest success and may be associated with intolerable drug side effects or risk of procedural complications. As with other cardiac arrhythmias, the identification of genetic determinants predisposing to atrial fibrillation may provide novel molecular targets for drug development. This review discusses the role of cardiac connexins in the heart and suggests that genetic defects in cardiac connexins may predispose to arrhythmia vulnerability.</AbstractText>Animal models deficient in cardiac connexins demonstrate abnormalities in myocardial tissue conduction and vulnerability to re-entrant arrhythmias, including ventricular tachycardia and atrial fibrillation. Atrial tissue analyses from human patients with atrial fibrillation consistently demonstrate alterations in connexin distribution and protein levels, suggesting a role of connexins in the perpetuation of the arrhythmia. Most recently, genetic studies of Cx43 and Cx40 indicate that genetic variations in these genes may predispose to arrhythmia vulnerability in humans.</AbstractText>Current data support the critical role of cardiac connexins in mediating coordinated electrical activation and conduction through myocardial tissue. Alterations in the tissue distribution or function of cardiac connexins may predispose to cardiac arrhythmias, supporting a previously proposed hypothesis that cardiac connexins should be considered a major therapeutic target in the management of atrial fibrillation.</AbstractText> |
9,742 | Ventricular fibrillation waveform characteristics are different in ischemic heart failure compared with structurally normal hearts. | For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration.</AbstractText>Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency).</AbstractText>All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001).</AbstractText>VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.</AbstractText> |
9,743 | [Indication for cardiac resynchronization therapy: Consensus 2005]. | The indication for cardiac resynchronization therapy (CRT) using biventricular pacing or ICD systems has to be highly differentiated to optimize the proportion of patients who derive significant symptomatic benefit from this therapy, on the one hand, and to avoid this invasive treatment in patients with a low probability of clinical success of CRT, on the other hand. As a consensus in 2005, it can be put forward that there is sufficient evidence for an indication for CRT from clinical studies for the following characteristics: 1) Heart failure in NYHA functional class III or IV (if cardiac recompensation to class III is at least temporarily successful), 2) left ventricular ejection fraction < or =35%, 3) QRS duration >130 ms, particularly if left bundle branch block is present, 4) sinus rhythm. In addition, available data also suggest an indication for CRT in patients with atrial fibrillation if the other criteria listed above are met. The indication for CRT is unclear in patients with other intraventricular conduction delay (particularly right bundle branch block) while patients with left bundle branch block and a QRS duration of 120-130 ms seem to benefit if echocardiographic criteria demonstrate ventricular dyssynchrony. Since a multiplicity of echocardiographic criteria of ventricular dyssynchrony exists which is neither standardized nor evaluated in large-scale randomized trials, ventricular dyssynchrony on echocardiography alone cannot be regarded as an established indication for CRT without a QRS complex > or =120 ms. Similarly, whether heart failure in functional state NYHA II should be regarded as a CRT indication is currently being investigated in the randomized RAFT and MADIT-CRT trials. |
9,744 | [Cardiac resynchronization therapy for heart failure - from experimental pacing to evidence-based therapy]. | Within the last decade, cardiac resynchronization therapy (CRT) has become an evidence-based cornerstone for a subset of patients with chronic heart failure. For those, who suffer from ischemic or non-ischemic cardiomyopathies at NYHA III or IV, have sinus rhythm, a left bundle branch block and a left ventricular ejection fraction below 35%, CRT has evolved as an important treatment option with promising results. Numerous studies have shown that in these patients pacemaker-mediated correction of intra- and interventicular conduction disturbances can improve not only clinical symptoms, exercise tolerance and the frequency of hospitalizations, but even more important the overall mortality. These clinical results are due to several functional aspects. In the failing heart characteristic intra- and interventricular alterations in electrical conduction result in mechanical asynchrony that leads to an abnormal contraction of the left ventricle with delayed activation of the lateral wall, a paradoxical septal movement, a reduced diastolic filling and a mitral regurgitation due to dyssynchrony of papillary muscle activation. It is conceivable that these functional changes have fatal consequences for the failing heart. AV-optimized left- or biventricular stimulation by modern pacemakers can correct the pathological dyssynchrony, thereby improving cardiac function and clinical outcome in these patients. Although tremendous progress in cardiac resynchronization therapy has been made during the last decade, a couple of questions still need to be resolved. Critical issues are the identification of patients, who will predictably benefit from CRT, the value of CRT-pacemakers versus CRT-ICDs, and the usefullness of CRT in patients with atrial fibrillation. |
9,745 | Stress cardiomyopathy mimicking acute coronary syndrome: case presentation and review of the literature. | Stress cardiomyopathy is a novel clinical syndrome affecting predominantly elderly female patients. It is characterized by severe reversible left ventricular dysfunction demonstrating a peculiar pattern of extensive apical wall motion abnormality known as "apical ballooning". The syndrome is typically precipitated by acute severe emotional, psychological or physical stress. It mimics acute coronary syndrome exhibiting typical clinical and electrocardiographic features of acute myocardial infarction. At angiography, however, significant coronary artery disease is invariably excluded. In the acute phase, the syndrome may be complicated by cardiogenic shock or ventricular fibrillation. Clinical data indicate that the disease is associated with an extensive increase of endogenous cathecholamine levels which may exhibit a direct toxic effect on the myocytes causing non-ischemic myocardial "stunning". This mechanism may have important implications for the management of patients in the acute phase of the disease. The prognosis of stress cardiomyopathy, however, seems favorable with recovery of global and regional myocardial function within a few weeks in the vast majority of patients. Yet, long-term outcome data in larger patient populations are lacking. We report the case of a female patient presenting with stress cardiomyopathy and review the current knowledge of the disease. |
9,746 | Coronary artery spasm of the native right coronary artery during off-pump coronary surgery of the left coronary artery system. | Native coronary artery spasm is a very rare complication during off-pump coronary artery bypass grafting. We report the case of a 74-year-old man who experienced angiographically documentated right coronary artery spasm while undergoing off-pump coronary artery bypass grafting on the diseased left coronary system. Despite two episodes of ventricular fibrillation and persistent ST segment elevation of the posterior wall, the off-pump procedure was successfully completed by grafting the left internal thoracic artery to the left anterior descending artery and a saphenous vein graft to the Ramus intermedius. The immediate postoperatively performed coronary angiography demonstrated patent anastomoses and two areas of significant spasticity within the course of the right coronary artery. Intracoronary nitroglycerin infusion into the ostium of the right coronary artery resolved the spasms of this nondiseased vessel as well as the associated ST segment elevations. |
9,747 | Application of normothermic cardiac arrest algorithms to hypothermic cardiac arrest in a canine model. | International guidelines (2000) do not recommend vasopressor and antiarrhythmic medications during ventricular fibrillation (VF) with a core temperature below 30 degrees C. The efficacy of normothermic AHA algorithms using standard doses of epinephrine (EPI) (adrenaline) followed by amiodarone (AMIO) in hypothermic VF is uncertain.</AbstractText>To determine the effects of EPI followed by the combination of EPI/AMIO in the treatment of VF in a canine model of severe hypothermia.</AbstractText>An un-blinded, placebo controlled experiment using 21 mechanically ventilated dogs. Coronary perfusion pressure (CPP), temperature, and electrocardiogram (ECG) were monitored. Animals were cooled to 22 degrees C or the onset of spontaneous VF. VF was induced if necessary. Animals in the treatment group received EPI (0.01 mg/kg IV) and defibrillation. This was followed by EPI (0.01 mg/kg IV), AMIO (10 mg/kg IV) and defibrillation if there was no sustained return of spontaneous circulation (ROSC) for 15 min.</AbstractText>Mean CPP in the treatment group increased after the administration of EPI/AMIO (24.7+/-13.3 mmHg to 46.6+/-7.7 mmHg, p<0.004). Cumulatively, the administration of EPI followed by EPI/AMIO achieved ROSC after defibrillation in 10 of 11 animals compared to 3 of 10 in the control group (91% versus 30%, n=21, p=0.0075).</AbstractText>In this model of severe hypothermia, the use of standard 2000 protocols for VF resulted in a significant increase of CPP, and, a higher ROSC rate compared to placebo controls. This study suggests that AHA normothermic algorithms may be beneficial in severe hypothermia.</AbstractText> |
9,748 | Cardiac mast cell-derived renin promotes local angiotensin formation, norepinephrine release, and arrhythmias in ischemia/reperfusion. | Having identified renin in cardiac mast cells, we assessed whether its release leads to cardiac dysfunction. In Langendorff-perfused guinea pig hearts, mast cell degranulation with compound 48/80 released Ang I-forming activity. This activity was blocked by the selective renin inhibitor BILA2157, indicating that renin was responsible for Ang I formation. Local generation of cardiac Ang II from mast cell-derived renin also elicited norepinephrine release from isolated sympathetic nerve terminals. This action was mediated by Ang II-type 1 (AT1) receptors. In 2 models of ischemia/reperfusion using Langendorff-perfused guinea pig and mouse hearts, a significant coronary spillover of renin and norepinephrine was observed. In both models, this was accompanied by ventricular fibrillation. Mast cell stabilization with cromolyn or lodoxamide markedly reduced active renin overflow and attenuated both norepinephrine release and arrhythmias. Similar cardioprotection was observed in guinea pig hearts treated with BILA2157 or the AT1 receptor antagonist EXP3174. Renin overflow and arrhythmias in ischemia/reperfusion were much less prominent in hearts of mast cell-deficient mice than in control hearts. Thus, mast cell-derived renin is pivotal for activating a cardiac renin-angiotensin system leading to excessive norepinephrine release in ischemia/reperfusion. Mast cell-derived renin may be a useful therapeutic target for hyperadrenergic dysfunctions, such as arrhythmias, sudden cardiac death, myocardial ischemia, and congestive heart failure. |
9,749 | Kir3-based inward rectifier potassium current: potential role in atrial tachycardia remodeling effects on atrial repolarization and arrhythmias. | We previously characterized a novel K+ current (IKH) with properties of constitutively active acetylcholine-related current in dog atrium. I(KH) is sensitive to tertiapin-Q (IC50 approximately 10 nmol/L), a highly selective Kir3 current blocker. This study assessed the role of IKH in atrial tachycardia (AT)-remodeled canine left atrium (LA) with the use of tertiapin-Q as a probe.</AbstractText>Dogs were subjected to 7 to 13 days of AT (400 bpm). Coronary-perfused LA preparations were studied intact or subjected to cardiomyocyte isolation. IKH was recorded with patch-clamp methods. AT pacing increased time-dependent hyperpolarization-activated current (IKH) at -110 mV from -1.8+/-0.3 (control) to -3.4+/-0.5 pA/pF (AT) and the 100-nmol/L tertiapin-sensitive component from -1.5+/-0.4 (control) to -3.3+/-0.6 pA/pF (AT). Prolonged atrial tachyarrhythmias could be induced with single extrastimuli in AT-remodeled, but not control, preparations, reflecting the atrial fibrillation-promoting effects of AT remodeling. In AT-remodeled preparations, tachyarrhythmia duration averaged 11.0+/-5.2 seconds, with a cycle length of 108+/-6 ms. Tertiapin-Q decreased tachyarrhythmia duration (to 0.6+/-0.1 second; P<0.001) and increased tachyarrhythmia cycle length (to 175+/-10 ms; P<0.001). Atrial action potential duration (APD) was increased 65+/-6% by tertiapin in AT-remodeled hearts versus 19+/-2% (P<0.001) in control. In 2 AT-remodeled preparations, tachyarrhythmia lasted uninterrupted for >20 minutes; tertiapin-Q slowed and then terminated arrhythmia in both. Tertiapin had no effect on left ventricular cardiomyocyte currents or APD.</AbstractText>AT remodeling increases IKH, and a highly selective Kir3 current antagonist, tertiapin-Q, increases APD and suppresses atrial tachyarrhythmias in AT-remodeled preparations without affecting ventricular electrophysiology. Constitutive acetylcholine-related K+ current contributes to AT-remodeling effects in dogs and is a potentially interesting antiarrhythmic target.</AbstractText> |
9,750 | Effects of gap geometry on conduction through discontinuous radiofrequency lesions. | Gaps of sufficient cross-sectional dimensions within linear radiofrequency (RF) lesions may allow conduction through the lesion. The purpose of this study was to examine the effects of different gap geometries on conduction through discontinuous RF lesions.</AbstractText>Radiofrequency lesions were created in isolated, perfused rabbit right ventricular (RV) free wall preparations to produce gaps with 3 different lesion geometries: straight, bifurcated, and angled (n=10 each group). Angled preparations contained 2 right angles within the conduction path. Optical mapping was used to assess bidirectional conduction through the myocardium before and after gap formation during pacing at 1000-, 400-, and 200-ms cycle lengths. Histological analysis was performed on each preparation after optical mapping. After lesion formation, 9 of 10 straight gap preparations and 1 of 10 angled gap preparations demonstrated bidirectional conduction (P<0.001) at all cycle lengths. Nine of 10 bifurcated gap preparations demonstrated bidirectional conduction and 1 demonstrated unidirectional conduction at all cycle lengths. Two bifurcated gap preparations showed rate-dependent unidirectional 2:1 conduction. All unidirectional and rate-dependent block occurred during impulse propagation in the direction of diverging arms of the bifurcation. The occurrence of bidirectional conduction in the gaps was associated with the gap geometry (P<0.0001). Histological analysis confirmed the continuity of viable myocardium transmurally throughout the length of the gap in each preparation. The sites of conduction block were demonstrated to be just after the first angle in the conduction path for angled gaps and at the branch point of a bifurcated gap. The predominant myofiber orientation was changed relative to the conduction path at angulations of the gaps. Flecainide (0.1 micromol/L) produced bidirectional conduction block in straight and bifurcated gap preparations with bidirectional conduction at baseline.</AbstractText>Conduction through discontinuities in RF lesions is associated with gap geometry. Complex gap geometry may allow for unidirectional and/or rate-dependent block. Gaps within RF lesions are susceptible to pharmacological blockade.</AbstractText> |
9,751 | [Ventricular fibrillation in a patient with three accessory pathways, Ebstein anomaly and intermittent long QT interval. RF ablation and electrophysiologic considerations]. | We present a case of a 19-year old man with minor Ebstein's anomaly, intermittent long QT interval and WPW syndrome in whom atrial fibrillation, degenerating into ventricular fibrillation was the first symptom. QRS complex morphologies during atrial fibrillation revealed the presence of three accessory pathways (septal, right inferior paraseptal and antero-inferior). Immediately after resuscitation the patient was treated with amiodarone, which resulted in a significant prolongation of QT interval to 700 ms. After RF ablation of accessory pathways patient remains asymptomatic during 6-month follow up, however QTc interval is about 500 ms. |
9,752 | [Myocardial infarction after butane inhalation in a 14-year-old boy]. | Myocardial infarction is a rare disease in children. Among many reasons the toxic damage of myocardium should be taken into consideration. The authors present the case of a 14-year-old boy with sudden cardiac arrest due to ventricular fibrillation and myocardial infarction as a result of butane gas inhalation. Coronary angiography revealed normal coronary arteries. Cardioverter-defibrillator was implanted as a secondary prophylaxis of sudden cardiac death. |
9,753 | "Tombstoning" of ST segment in acute myocardial infarction -- effect on clinical course. | There are many reports evaluating the effects of the amplitude of ST segment elevation in acute myocardial infarction with ST segment elevation (STEMI) on infarction zone and course. There are, however, few publications dealing with the effects of ST segment elevation shape in STEMI patients on their clinical course and prognosis.</AbstractText>Assessment of the rate of "tombstoning" of ST segment (TOMB-ST) in STEMI patients and the effects on their clinical outcome.</AbstractText>The study involved 207 consecutive patients with STEMI hospitalised in the period 2000-2002 analysed with respect to the in-hospital complication rate.</AbstractText>On admission, TOMB-ST was observed in 55 (26.1%) subjects. TOMB-ST was more common in anterior MI (39.8%) than in inferior MI (10.6%). Patients with TOMB-ST compared to non-TOMB-ST ones had a significantly higher mortality rate (38.2% vs 9.9%, p <0.001), heart failure (45.6% vs 28.3%, p <0.026), ventricular fibrillation (18.1% vs 6.4%, p <0.016), and lower left ventricular ejection fraction (40.9% vs 48.6%, p <0.001). The sum of amplitudes of ST segment deviations (SigmaST) >20 mm was indicative for the subgroup of patients with TOMB-ST and trend towards higher mortality (40% vs 30%, NS). However, in patients without TOMB-ST, SigmaST >20 mm identified two subgroups with significantly different mortality rates (20% vs 4%, p=0.001).</AbstractText>TOMB-ST was observed in one fourth of patients with STEMI. This abnormality was associated with an increased mortality rate, higher incidence of heart failure and ventricular fibrillation as well as decreased left ventricular ejection fraction. In the population with TOMB-ST, increased mortality was independent of the total amplitude of ST segment displacement; this relation was, however, observed in patients with STEMI without TOMB-ST.</AbstractText> |
9,754 | Cardioversion in patients with left ventricular thrombus is not associated with increased thromboembolic risk. | The purpose of the study was to define the incidence of systemic embolism after cardioversion in patients with left ventricular (LV) thrombus.</AbstractText>The risk of systemic embolization after cardioversion in patients with an atrial thrombus is well known. However, data on thromboembolic events after cardioversion in patients with LV thrombus are limited because of hesitance to perform cardioversion in this population.</AbstractText>Transthoracic and transesophageal echocardiograms acquired between January 1996 and October 2001 at our institution were reviewed for presence of LV thrombus in two orthogonal apical views. A total of 413 patients had echocardiographic evidence of LV thrombus. Medical records were reviewed for cardioversion performed within 3 weeks of the echocardiogram.</AbstractText>A total of 21 patients, age 66 +/- 10 years and ejection fraction 22 +/- 10% were identified. Cardioversion was indicated for atrial fibrillation in 8 (38%) and ventricular tachyarrhythmia in 13 (62%) patients, and was performed emergently in 5 (24%), electively in 8 (38%), and during electrophysiology study in 8 (38%) patients. The time interval between diagnostic echocardiographic study and cardioversion was 6 +/- 5 (range 1-18) days. All thrombi were located in the apical LV and were described as laminated (71%) and protruding (29%), and measured 0.7 +/- 0.4 x 1.6 +/- 0.8 cm. Before cardioversion, 17 (81%) patients were anticoagulated with warfarin or heparin. During clinical follow-up of up to 1 year (153 +/- 150 days) anticoagulation with warfarin was given to 15 (71%) patients. No patient had clinically apparent embolic event, including stroke, during hospitalization or during outpatient follow-up.</AbstractText>Embolism after cardioversion in patients with echocardiographic evidence of LV thrombus was not observed. Cardioversion seems to be safe and further prospective studies are needed to address this.</AbstractText> |
9,755 | The prevalence of cardiac ectopy in elderly patients with echocardiographically normal hearts is not increased by significant coronary artery disease. | A higher frequency of abnormal heart rhythms has previously been shown in elderly subjects with overtly normal hearts as demonstrated by noninvasive testing. However, no prior study on elderly patients with echocardiographically structurally normal hearts has distinguished cardiac dysrhythmia incidence based on the presence or absence of angiographically documented coronary artery disease (CAD).</AbstractText>We performed 24-hour ambulatory monitoring on patients with no coronary stenosis of greater than 30% and normal left ventricular (LV) systolic function by angiography. This group was then compared with a group of elderly patients with normal LV systolic function and at least one major coronary artery stenosis of 70% or greater. All patients had echocardiographically normal LV wall thickness and systolic function and no significant valvular disease.</AbstractText>The experimental group was composed of 15 patients with CAD aged 71 +/- 6 years. The control group without significant CAD was composed of 20 patients aged 73 +/- 4 years (P = not significant [NS]). There was no difference with respect to prevalence of hypertension, use of calcium-channel blockers, and history of smoking. There was no difference between the groups with regard to the number of premature atrial contractions (467 +/- 759 [experimental] vs 672 +/- 1789 [control]; P = NS); premature ventricular contractions (359 +/- 599 [experimental] vs 290 +/- 858 [control]; P = NS); and prevalence of ventricular couplets, ventricular tachycardia, paroxysmal atrial fibrillation, and supraventricular tachycardia (all P = NS).</AbstractText>These findings indicate that the prevalence of cardiac dysrhythmias in elderly patients with echocardiographically normal hearts is not influenced by the presence of angiographically significant CAD.</AbstractText> |
9,756 | Vagal nerve-mediated vasospasm-induced lethal ventricular fibrillation. | We report a case of variant angina complicated by lethal ventricular fibrillation. Serial ambulatory electrocardiogram monitoring revealed high-frequency spectra reflecting augmented vagal nerve activity preceding the vasospastic episodes. Our case suggests that heart rate variability analysis can help identify potential unexpected sudden cardiac death in patients with variant angina. |
9,757 | [Effect of the class III antiarrhythmic drug nibentan in vagotonic atrial fibrillation]. | Nibentan, the class III antiarrhythmic drug, was experimentally investigated in anaesthetized dogs using the model of vagotonic atrial fibrillation. Under the conditions of vagus nerve stimulation, nibentan retained the ability to prolong the ventricular repolarization and increase the effective refractory periods and to maintain the frequency-independent action on the effective refractory periods of the atrium. At the same time, nibentan did not affect conduction via the His-Purkinje system and prevented bradycardia induced by vagus stimulation. The drug was found to depress the conduction in atrium, this effect being retained on the background of vagus nerve stimulation. Nibentan has proved to be effective in preventing the vagotonic atrial fibrillation. |
9,758 | Intermediate-term results of 505 consecutive minithoracotomy mitral valve procedures. | : Patient demand for less invasive surgery and interest in avoiding sternotomy has led to the increased use of the minithoracotomy for mitral valve surgery. Although the feasibility of this approach has been established, few data are available regarding intermediate-term results.</AbstractText>: A total of 505 consecutive minithoracotomy mitral valve procedures performed between 1996 and 2004 were analyzed. Procedures were mitral replacement (191/505, 38%) and repair (314/505, 62%). Concomitant cardiac procedures were performed in 78 cases (13%) (maze 36, tricuspid 29, atrial septal defect/patent foramen ovale 13) and reoperation in 92 cases (18%). Arterial cannulation was ascending aorta in 403 cases (80%), femoral in 101 cases (20%), and axillary in 1 case (<1%). An endoluminal aortic clamp was used in 406 cases (80%), an external clamp was used in 19 cases (4%), and 80 procedures (16%) were performed with ventricular fibrillation. Robotic assistance was used in 12 cases (2%).</AbstractText>: Mean patient age was 58.7 years (range 18-90 years). Median follow-up was 3.1 years. Operative mortality was 4 of 505 cases (<1%). Major complications included stroke in 7 cases (1%) and reoperation for bleeding in 18 cases (4%); there were no cases of mediastinitis. Late complications included chronic aortic dissection in 1 case (<1%) and mitral reoperation in 13 cases (3%) (subacute bacterial endocarditis 6, failed repair 2, other 5). Five-year survival was (83% ± 2%) and freedom from mitral reoperation was (96% ± 1%). Follow-up echocardiograms were available in 246 of 314 cases (78%) mitral repairs and mean mitral regurgitation grade was 1 ± 1. Mitral regurgitation was grade 3-4+ in 14 of 246 cases (6%) (subacute bacterial endocarditis 4, low ejection fraction 5, other 5). Five-year freedom from 3-4+ mitral regurgitation was 89% ± 3%.</AbstractText>: Mitral valve surgery via minithoracotomy can be performed safely with a low perioperative complication rate. A durable technical result and excellent long-term survival can be expected.</AbstractText> |
9,759 | Early repolarization syndrome: is it always benign? | Early repolarization syndrome is a well-recognized idiopathic electrocardiographic phenomenon characterized by prominent J wave and ST-segment elevation predominantly in left precordial leads. The syndrome shares remarkable cellular, ionic, and electrocardiographic similarities with the Brugada syndrome and idiopathic ventricular fibrillation (a variant of the Brugada syndrome with ST-segment elevation in inferior leads). Although early repolarization syndrome is considered a benign entity, its arrhythmogenic potential still remains unknown. We report the case of a 39-year-old male with a family history of sudden death and an electrocardiogram consistent with early repolarization syndrome. Diagnostic dilemmas are discussed. |
9,760 | [Non-pharmacological treatment of hypertrophic obstructive cardiomyopathy guided by echocardiography]. | As a relevant cause of symptoms and adverse clinical prognosis, left ventricular obstruction should be regarded as an important therapeutic target in patients with hypertrophic obstructive cardiomyopathy. The surgical approach (including septal myectomy or mitral valve surgery) and percutaneous transluminal septal myocardial ablation offer a non-pharmacological option for the treatment of symptomatic left ventricular obstruction and symptoms unresponsive to medical treatment. The surgical approach is established as an effective strategy for relieving symptoms from dynamic obstruction. Percutaneous septal ablation, on the other hand, has only recently been introduced into clinical practice and, despite its efficacy as an obstructive abolisher, little is known about the prognostic long-term impact of procedural-induced myocardial damage. Due to its accuracy and diagnostic versatility, including intraprocedural use, Doppler echocardiography provides essential information for the planning and monitoring of non-pharmacological therapy in patients with hypertrophic obstructive cardiomyopathy. |
9,761 | Using the superior sagittal sinus for emergency venous access in an infant. Case report. | Emergency venous access in an infant suffering from multiple trauma and shock can be difficult. Peripheral venous access and central line placement are not always successful. Death following underresuscitation due to the lack of adequate access occurs, although it is not often reported in the literature. The author presents a case in which successful resuscitation was achieved by injecting blood into the superior sagittal sinus through an open fontanelle in a 2-week-old infant who presented in shock and with ventricular fibrillation after nonaccidental trauma. |
9,762 | Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node. | In the mammalian heart, gap junction channels between electrically coupled cardiomyocytes are necessary for impulse propagation and coordinated contraction of atria and ventricles. Recently, mouse connexin30.2 (Cx30.2) was shown to be expressed in the cardiac conduction system, predominantly in sinoatrial and atrioventricular (AV) nodes. The corresponding gap junctional channels expressed in HeLa cells exhibit the lowest unitary conductance (9 pS) of all connexin channels. Here we report that Cx30.2 slows down the propagation of excitation through the AV node. Mice expressing a LacZ reporter gene instead of the Cx30.2 coding region (Cx30.2(LacZ/LacZ)) exhibit a PQ interval that is approximately 25% shorter than in WT littermates. By recording atrial, His, and ventricular signals with intracardiac electrodes, we show that this decrease is attributed to significantly accelerated conduction above the His bundle (atrial-His interval: 27.9 +/- 5.1 ms in Cx30.2(LacZ/LacZ) versus 37.1 +/- 4.1 ms in Cx30.2(+/+) mice), whereas HV conduction is unaltered. Atrial stimulation revealed an elevated AV-nodal conduction capacity and faster ventricular response rates during induced episodes of atrial fibrillation in Cx30.2(LacZ/LacZ) mice. Our results show that Cx30.2 contributes to the slowdown of impulse propagation in the AV node and additionally limits the maximum number of beats conducted from atria to ventricles. Thus, it is likely to be involved in coordination of atrial and ventricular contraction and to fulfill a protective role toward pathophysiological states such as atrial tachyarrhythmias (e.g., atrial fibrillation) by preventing rapid conduction to the ventricles potentially associated with hemodynamic deterioration. |
9,763 | Ventricular fibrillation in pediatric cardiac arrest. | After activating 9-1-1 for out-of-hospital cardiac arrest (CA), guidelines for children 1 year and older have evolved to include immediate automated external defibrillator (AED) use for witnessed arrest, and two minutes of cardiopulmonary resuscitation (CPR) followed by AED use for unwitnessed arrests. The best approach to resuscitation in a two-tiered emergency medical services (EMS) system depends in part on how likely the patient is to present with ventricular fibrillation (VF). Therefore, the authors evaluated the frequency of VF with respect to age and other characteristics to further elucidate the role of the AED among pediatric CAs.</AbstractText>The investigation was a retrospective cohort study of EMS-treated, nontraumatic, out-of-hospital CA among persons aged 1-18 years in King County, Washington, between April 1, 1976, and December 31, 2003. The primary goal was to identify the proportion of patients presenting to EMS in VF, according to age. The association between other characteristics and the likelihood of VF was also evaluated. Finally, hospital survival according to cardiac rhythm at EMS arrival was evaluated.</AbstractText>Ventricular fibrillation was the presenting rhythm in 17.6% of cases (48/272). The proportion presenting with VF was 7.6% (10/131) among children aged 1-7 years and 27.0% (38/141) among children aged 8-18 years (p < 0.001). In multivariable models, VF was independently associated with age 8 years and older compared with 1-7 years (odds ratio, 3.19; 95% confidence interval [CI] = 1.46 to 6.97), witnessed arrest (odds ratio, 3.33; 95% CI = 1.63 to 6.82), and cardiac etiology (odds ratio, 2.89; 95% CI = 1.32 to 6.34). Survival was 31.3% (15/48) for VF and 10.7% (24/224) for nonshockable rhythm CAs.</AbstractText>The proportion of children aged younger than 8 years presenting with VF is low compared with older children. The greatest increase in VF proportion occurs in children older than 12 years. Based on these results, the best approach for initial EMS resuscitation in a two-tiered EMS system, CPR versus AED use, is uncertain among younger children. Inclusion of witness status into the decision process for younger children may more efficiently allocate AED use, a finding in accordance with 2005 guidelines.</AbstractText> |
9,764 | Ventricular arrhythmias after acute myocardial infarction: a 20-year community study. | Although myocardial infarction (MI) severity is declining, the occurrence of ventricular arrhythmia (VA) after MI and its effect on outcome is unknown. This study was undertaken to examine the frequency and timing of VA and the effect of VA on mortality after MI.</AbstractText>Myocardial infarctions recorded between 1979 and 1998 were validated. Baseline characteristics, occurrence of VA, and survival were determined. Ventricular arrhythmias were categorized as primary ventricular fibrillation (VF), nonprimary VF, and ventricular tachycardia (VT). Logistic regression was used to analyze associations between VA and baseline characteristics. Temporal trends were assessed with the Mantel-Haenszel chi2. Survival was analyzed with the Kaplan-Meier method. Proportional hazards regression was used to examine the association between death and occurrence of VA.</AbstractText>Among 2317 persons with incident MI, 7.5% experienced VA (3.6% nonprimary VF, 2.1% primary VF, 1.8% VT). Ventricular arrhythmia-associated factors were younger age, female sex, higher Killip class, ST elevation, and atrial fibrillation. Ventricular arrhythmias were associated with increased risk of death at 30 days.</AbstractText>Ventricular arrhythmias after MI are relatively common, particularly among persons with more severe MI and no prior history of coronary disease. Over time, the incidence of VF declined, whereas VT did not change. Ventricular arrhythmia after MI was associated with a 6-fold increase in morality. Thus, identification of high-risk MI survivors and prevention of VA could markedly improve outcomes. Further studies are needed to determine the cause of the shift in distribution of VA subtype.</AbstractText> |
9,765 | Drug Insight: angiotensin-converting-enzyme inhibitors and atrial fibrillation--indications and contraindications. | Large clinical trials have demonstrated that angiotensin-converting-enzyme (ACE) inhibitors are associated with beneficial outcomes in patients with arterial hypertension, heart failure, coronary artery disease, or a combination of these conditions. Other reports have suggested that ACE inhibitors prevent the development or recurrence of atrial fibrillation (AF), a common arrhythmia. In the TRACE trial, in patients with reduced left ventricular function after myocardial infarction, trandolapril reduced the frequency of AF. In the SOLVD trial, a 78% reduction in the frequency of AF after infarction was noted with enalapril compared with placebo. Studies in patients with persistent AF undergoing cardioversion suggest that ACE inhibitors improve outcomes and prevent AF recurrences. The mechanism of AF prevention by ACE inhibitors is unclear, but experimental data show prevention or attenuation of pacing-induced atrial remodeling with ACE inhibitor use. ACE inhibitors decrease angiotensin II concentration; angiotension II stimulates mitogen-activated protein kinases, which in turn activate fibrosis formation and lead to conduction heterogeneity and induction of AF. On the other hand, AF induces atrial dilatation, atrial stretch and atrial secretion of ACE. Among other properties, ACE inhibitors have a sympatholytic effect and increase baroreceptor sensitivity. This review discusses the current data on the use of ACE inhibitors for AF prevention. Although these drugs represent a promising therapeutic option for AF patients, the data so far seem only supportive rather than definitive. Prospective trials are required to validate the benefit of ACE inhibitors and to investigate which patients are most likely to benefit from this pharmacological therapy. |
9,766 | Equivalent arrhythmic risk in patients recently diagnosed with dilated cardiomyopathy compared with patients diagnosed for 9 months or more. | The Centers for Medicare and Medicaid Services (CMS) recently expanded coverage for implantable cardioverter-defibrillators (ICDs) in patients with left ventricular ejection fraction < or =35% and nonischemic dilated cardiomyopathy for > or =9 months. To investigate the ramifications of these criteria, the ICD registry from Tufts-New England Medical Center was analyzed for arrhythmic events and death in patients with newly diagnosed (<9 months) vs late-diagnosed (> or =9 months) nonischemic dilated cardiomyopathy.</AbstractText>The purpose of this study was to analyze the arrhythmic risk in patients with recent vs late diagnosis of nonischemic dilated cardiomyopathy.</AbstractText>One hundred thirty-one patients with nonischemic dilated cardiomyopathy were divided into two cohorts (<9 or > or =9 months of symptoms) and analyzed for any occurrence of treated ventricular arrhythmia, potentially lethal arrhythmias defined as ventricular flutter rates > or =230 bpm, and ventricular fibrillation. Patients with documented sustained ventricular tachycardias (included in prior CMS coverage) were excluded.</AbstractText>In the study group, the mean age was 58.1 +/- 15 years and ejection fraction 20.6% +/- 8%. In a follow-up period of 25.3 +/- 24 months, the 52 patients with a recent diagnosis (1.4 +/- 2 months) had no difference in the occurrence of ventricular arrhythmias (P = .49) and malignant ventricular arrhythmias (P = .16) compared with the 79 patients diagnosed > or =9 months (mean 58.1 +/- 39 months).</AbstractText>Patients with nonischemic dilated cardiomyopathy experienced equivalent occurrences of treated and potentially lethal arrhythmias irrespective of diagnosis duration. These findings suggest that the 9-month time qualifier used in the CMS guidelines for ICD reimbursement may not reliably discriminate patients at high risk for sudden cardiac death in this selected population.</AbstractText> |
9,767 | Electrocardiographic changes with segmental akinesia after chloral hydrate overdose. | We report a case of deliberate ingestion of 12.5 g chloral hydrate in a 25-year-old psychiatric patient. Coma and life-threatening ventricular dysrhythmias were observed soon after ingestion. Repeated electrocardiographic examination was consistent with ischemic changes appearing on day 3. They were associated with segmental abnormal left ventricular wall motion by echocardiography. A coronary angiogram was performed and was normal. Toxic metabolites of chloral hydrate, trichloroethanol and trichloroacetic acid were found in the urine until day 7. This case illustrates that with halogenated aliphatic hydrocarbons, sustained changes in cardiac contractility may occur in addition to early life-threatening ventricular dysrhythmias. |
9,768 | An unusual case of 4-aminopyridine toxicity. | 4-aminopyridine (4-AP) is an orphan drug in the United States. It enhances neuronal conduction at synapses and is indicated in the treatment of selected neuromuscular disorders, including multiple sclerosis and myasthenia gravis, among others. Its documented toxicity generally has been limited to central nervous system (CNS) hyperexcitation and gastrointestinal upset. In this case, a 56-year-old man accidentally overdosed on an unknown amount of generic 4-AP. This history was unknown by his family and unavailable to initial providers. Approximately 1 h after ingestion, his son found him diaphoretic, vomiting, and having unintelligible speech. In the ensuing 2-3 h, the patient became moderately hypothermic (32.8 degrees C; 91 degrees F), developed atrial fibrillation with a rapid ventricular response, and had neurological changes that were confused with an acute cerebrovascular accident. After a 36-h stay in the intensive care unit that included mechanical ventilation, cardioversion, passive rewarming, and an extensive medical workup, the patient recovered without sequelae. After extubation he stated that he thought he may have ingested too much 4-AP after rubbing a large amount of it against a sore tooth to take advantage of its local analgesic properties. This case of 4-AP overdose resulting in atrial fibrillation with rapid ventricular response, hypothermia, and acute neurological changes mistaken for an acute cerebrovascular accident is an unusual one. This case shows that overdose of 4-AP can cause or mimic several serious medical conditions, and that a detailed history and physical examination are essential for uncovering unusual diagnoses. |
9,769 | Insular involvement in brain infarction increases risk for cardiac arrhythmia and death. | Brain injuries may induce cardiac dysrhythmias and sudden cardiac death.</AbstractText>We analyzed 12-lead electrocardiograms of 493 consecutive patients with brain infarction (BI) proved by an magnetic resonance imaging and 493 control subjects matched for age, sex, and center. Insular involvement (insula (+/-)) was assessed by two independent readings of the magnetic resonance imaging scans. Cases were followed for 5 years.</AbstractText>Acute BI was independently associated with heart rate (< or = 64 beats/min), abnormal repolarization, atrial fibrillation, and ventricular and supraventricular ectopic beats. Lower heart rate in BI patients was due to an interaction with smoking (p for interaction = 0.004). Insula(+) group was significantly associated with abnormal repolarization with no interaction with infarct side. Atrial fibrillation by history was also more frequent in the insula(+) than in the insula(-) group (p = 0.07). After adjustment for age, sex, cardiovascular history, and handicap at admission, right insula(+) BI was significantly associated with 2-year all-cause death (hazard ratio, 2.11; 95% confidence interval, 1.27-3.52) and with vascular death (hazard ratio, 2.00; 95% confidence interval, 1.00-3.93). In multivariate analysis including age, sex, cardiovascular history, handicap at admission, and lesion side, increased QTc interval and left bundle branch block were independent predictors of all-cause and vascular mortality at 2 years in right insula(+) patients.</AbstractText>These findings support the notion that right insular involvement may lead to electrocardiographic abnormalities with potential prognostic implications. This could be important for optimal care in patients with right insular infarct.</AbstractText> |
9,770 | Comparison of nifekalant and lidocaine for the treatment of shock-refractory ventricular fibrillation. | Although nifekalant is a class III antiarrhythmic agent without negative inotropic activity, its effect in patients with shock-refractory ventricular fibrillation remains unclear.</AbstractText>Patients who had an out-of-hospital cardiac arrest with ventricular fibrillation that persisted after 3 shocks from an external defibrillator, intravenous epinephrine, and another shock were retrospectively studied. The patients received lidocaine from January 1997 through June 2001 and nifekalant from July 2001 through December 2004. Short-term survival rates (survival to hospital admission and 24-h survival) were compared between the groups. The study group comprised 120 patients (mean age: 62+/-16 years): 55 received nifekalant and 65 received lidocaine. Age, sex, history of ischemic heart disease, whether arrest was witnessed or not and time to arrival at the hospital did not differ significantly between the groups. As compared with lidocaine, nifekalant was associated with significantly higher rates of survival to hospital admission (67% vs 37%, p<0.001) and 24-h survival (53% vs 31%, p=0.01). Multivariate analysis showed that treatment with nifekalant and early initiation of cardiopulmonary resuscitation were independent predictors of 24-h survival.</AbstractText>As compared with lidocaine, nifekalant may improve short-term survival in patients with out-of-hospital cardiac arrest due to shock-refractory ventricular fibrillation.</AbstractText> |
9,771 | Alternans and spiral breakup in a human ventricular tissue model. | Ventricular fibrillation (VF) is one of the main causes of death in the Western world. According to one hypothesis, the chaotic excitation dynamics during VF are the result of dynamical instabilities in action potential duration (APD) the occurrence of which requires that the slope of the APD restitution curve exceeds 1. Other factors such as electrotonic coupling and cardiac memory also determine whether these instabilities can develop. In this paper we study the conditions for alternans and spiral breakup in human cardiac tissue. Therefore, we develop a new version of our human ventricular cell model, which is based on recent experimental measurements of human APD restitution and includes a more extensive description of intracellular calcium dynamics. We apply this model to study the conditions for electrical instability in single cells, for reentrant waves in a ring of cells, and for reentry in two-dimensional sheets of ventricular tissue. We show that an important determinant for the onset of instability is the recovery dynamics of the fast sodium current. Slower sodium current recovery leads to longer periods of spiral wave rotation and more gradual conduction velocity restitution, both of which suppress restitution-mediated instability. As a result, maximum restitution slopes considerably exceeding 1 (up to 1.5) may be necessary for electrical instability to occur. Although slopes necessary for the onset of instabilities found in our study exceed 1, they are within the range of experimentally measured slopes. Therefore, we conclude that steep APD restitution-mediated instability is a potential mechanism for VF in the human heart. |
9,772 | Combined off-pump coronary artery bypass grafting surgery and ablative therapy for atrial fibrillation: early and mid-term results. | The aim of this study was to evaluate the feasibility of off-pump coronary artery bypass grafting combined with radiofrequency ablation and to compare outcomes between patients with permanent and paroxysmal atrial fibrillation (AF) in terms of restoring sinus rhythm.</AbstractText>Thirty-three patients underwent the combined procedure. Mean age was 62.34 +/- 8.20 years; there were 12 female and 21 male patients. Twenty-one patients were diagnosed as permanent AF (group A) and 12 had paroxysmal AF (group B). After the off-pump revascularization patients underwent pulmonary vein ablation. Rhythm was evaluated at discharge and at 6 and 12 months' follow-up. Patients in stable sinus rhythm underwent transthoracic echocardiographic examination to evaluate atrial contractility at 6 and 12 months.</AbstractText>There was no operative mortality or major complications. The mean ablation time was 11 +/- 3.4 minutes, including multiple applications. At the end of the procedure 84.5% of patients were free of AF. Sinus rhythm was established in 56% (group A, 52%; group B, 58.3%), 70.5% (group A, 58%; group B, 83.3%), and 71% (group A, 59%; group B, 83.3%) of patients at discharge and at 6 and 12 months, respectively (p = 0.249). Biatrial contractility was detected in 71% of group A and 76% of group B patients at 6 months' follow-up. More patients in group A returned to AF during follow-up when compared with group B (p = 0.016). Female sex (odds ratio, 2.1), chronic lung disease (odds ratio, 1.40), left ventricular disfunction (p = 0.016), and hypertension (odds ratio, 2.57) emerged as risk factors for AF recurrence after ablation.</AbstractText>Concomitant off-pump coronary artery bypass grafting and bipolar radiofrequency ablation was safe and effective. These patients should be considered for adjunctive treatment at the time of off-pump revascularization.</AbstractText> |
9,773 | Prognostic value of routine preoperative electrocardiography in patients undergoing noncardiac surgery. | Electrocardiography is commonly performed as part of preoperative cardiovascular risk assessment in patients undergoing noncardiac surgery. However, the prognostic value of such electrocardiography is still not clear. This study retrospectively studied 23,036 patients who underwent 28,457 surgical procedures at Erasmus Medical Center from 1991 to 2000. Patients were screened before surgery by type of surgery, cardiovascular risk factors (history of coronary heart disease, heart failure, diabetes mellitus, renal dysfunction, and stroke), and preoperative electrocardiography. Electrocardiographic (ECG) results showing atrial fibrillation, left or right bundle branch block, left ventricular hypertrophy, premature ventricular complexes, pacemaker rhythm, or Q-wave or ST-segment changes were classified as abnormal. Multivariate logistic regression was applied to evaluate the relation between ECG abnormalities and cardiovascular death. In-hospital cardiovascular death was observed in 199 of 28,457 patients (0.7%). Patients with abnormal ECG findings had a greater incidence of cardiovascular death than those with normal ECG results (1.8% vs 0.3%; adjusted odds ratio 4.5, 95% confidence interval 3.3 to 6.0). Adding ECG data to clinical risk factors and the type of surgery resulted in an improved C index for the prediction of cardiovascular death (0.79 vs 0.72). However, in patients who underwent low-risk or low- to intermediate-risk surgery, the absolute difference in the incidence of cardiovascular death between those with and without ECG abnormalities was only 0.5%. In conclusion, preoperative electrocardiography provides prognostic information in addition to clinical characteristics and the type of surgery. However, the usefulness of its routine use in lower risk surgery is questionable. |
9,774 | A public access defibrillation programme in non-inpatient hospital areas. | Automatic external defibrillators (AED) have proven to be valuable and life saving for out of hospital cardiac arrests. Their use in hospital arrests is less well documented, but they offer the opportunity to improve survival in the hospital setting also.</AbstractText>The implementation of a public access defibrillation (PAD) programme at a tertiary care hospital is described, with reference specifically to targeting areas where time from arrest to arrival of defibrillation would be greater than 3 min.</AbstractText>Nine AEDs were placed in areas of the hospital distant from inpatient or outpatient floors. The locations of the AEDs were chosen based on a 3 min walk from currently available defibrillators to all areas of the hospital, including parking garages and walkways from building to building. In this programme AED use in non-inpatient hospital locations resulted in the resuscitation of a patient in ventricular fibrillation.</AbstractText>PAD in non-inpatient hospital settings can be life saving and similar programmes should be considered for other hospitals.</AbstractText> |
9,775 | A randomized comparison of manual, mechanical and high-impulse chest compression in a porcine model of prolonged ventricular fibrillation. | Elevated coronary perfusion pressure (CPP) during CPR is associated with return of spontaneous circulation (ROSC). We compared CPP achieved with three methods of chest compression: manual (MAN), mechanical (MECH) and high-impulse mechanical (HI) in a porcine model of prolonged ventricular fibrillation (VF). We hypothesized that HI (very rapid acceleration of the down-stroke) would produce greater CPPs than MAN or MECH, and that HI would also produce a higher rate of ROSC.</AbstractText>Twenty-eight domestic swine (mean 27.8 kg) were randomly assigned to three methods of chest compression. Animals were instrumented under anesthesia, and VF was induced and untreated for 8 min. After 2 min of CPR, epinephrine (adrenaline) (0. 1 mg/kg), vasopressin (40 U) and propranolol (1.0 mg) were administered. CPR continued for three more minutes, after which up to three rescue shocks were delivered. CPP was determined in an automated fashion by measuring the difference between aortic and right atrial pressures 0.1s prior to the down-stroke of each compression (i.e. end-relaxation). ROSC was defined as a systolic pressure greater than 80 mmHg sustained for at least 1 min. We analyzed CPP and ROSC using repeated measures ANOVA and Fisher's exact test.</AbstractText>Over the 5 min of CPR, CPP increased more with HI compression than with MAN compression (p=0.017). ROSC was attained in 4/9 MAN, 6/9 MECH and 10/10 HI (HI versus MAN p=0.01).</AbstractText>Over the course of CPR, HI compression increased CPP more than MAN compression. HI compression produced a significantly higher rate of ROSC than MAN, but not MECH compression.</AbstractText> |
9,776 | Adherence to CPR guidelines during perioperative cardiac arrest in a developing country. | BACKGROUND AND GOAL OF STUDY: Cardiopulmonary resuscitation (CPR) is an integral part of anaesthetic training. In Nigeria, these skills are taught mainly during medical school and postgraduate training. International guidelines were introduced in 2000 and new guidelines were produced in November 2005. The study sought to assess how closely anaesthetists in a Nigerian teaching hospital abide by the 2000 guidelines.</AbstractText>All perioperative cardiac arrests in adults that occurred in a 1-year-period were studied prospectively. All patients <15 years and cardiac arrests occurring outside the direct supervision of the anaesthetists were excluded. Time and duration of arrest, cardiac arrest rhythm and management were documented along with immediate outcome.</AbstractText>Thirteen cardiac arrests occurred in 2147 perioperative cases (incidence: 6/1000). Seven patients had non ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) rhythms. The mean age of patients was 30.23+/-11.06 years. Orotracheal intubation, manual ventilation with 100% O(2) and external chest compressions were instituted in all cases. The mean duration of arrest was 25.66+/-13.34 min. All patients received adrenaline (epinephrine) and atropine. The median interval between adrenaline doses was 7.5 min. Only one cycle of defibrillation was given to patients in VF/VT. Immediate survival occurred in five patients (38.46%).</AbstractText>Anaesthetists in our hospital are not applying proper resuscitation guidelines. The lack of organised simulation practice resulted in deficient knowledge and skills. There is a need for continuing training in basic and advanced resuscitation for all anaesthetists according to the guidelines.</AbstractText> |
9,777 | The frequency ratio: an improved method to estimate ventricular fibrillation duration based on Fourier analysis of the waveform. | CPR prior to defibrillation improves survival from prolonged ventricular fibrillation (VF) by over 10%, based on recent studies. Waveform analysis could identify those patients with VF of over 5 to 7-min duration who should receive CPR first. A method based on the changes in the Fourier-derived frequency spectrum over time could improve the ability to identify prolonged VF.</AbstractText>The Fourier frequency spectra were calculated on 5-s epochs of VF from 45 swine for 12.5 min. The average power at each frequency shows a marked loss of frequencies above 8 Hz occurring at 5 min accompanied by an increase in the power in frequency spectra from 3 to 5 Hz. A measure termed the frequency ratio is defined as the ratio of the power in the high frequency band from 8 to 24 Hz compared to the power in the low frequency band from 3 to 5 Hz. The frequency ratio is shown to detect 90% of epochs with VF less than 5 min while allowing selection of 74% of those epochs over 5 min. When the frequency ratio is set to detect 90% of episodes of VF under 7 min, it is able to select 88% of those traces with VF over 7 min. The receiver operating curve (ROC) for the frequency ratio has an area under the curve of 0.91 at 5 min and 0.95 at 7 min of VF duration.</AbstractText>The frequency ratio is an improved frequency-based measure of VF duration. Waveform analysis techniques could determine which patients should receive shock first and which should receive a period of CPR prior to shock, thereby increasing probability of survival.</AbstractText> |
9,778 | Effects of amiodarone on electrical and structural remodeling induced in a canine rapid pacing-induced persistent atrial fibrillation model. | Structural in addition to electrical remodeling may be induced by persistent atrial fibrillation per se and make atrial fibrillation refractory to antiarrhythmic drug therapy. Matrix metalloproteinases (MMPs) contribute to structural remodeling in the interstitial space. Amiodarone is effective in treating persistent atrial fibrillation compared with other antiarrhythmic drugs. In mongrel dogs, right atrial pacing at 540 beats/min (bpm) was performed along with ventricular pacing at 100 bpm for 6 weeks after atrioventricular node ablation. Right atrial pacing at 400 bpm was continued for 4 weeks with (n=5) or without (n=5) oral amiodarone (30 mg/kg/day). In sham dogs, only ventricular pacing was done with (n=4) or without (n=6) amiodarone. In atrial pacing without amiodarone group, electrical remodeling characterized by monophasic action potential duration shortening, loss of action potential duration-rate adaptation and depressed conduction velocity and structural remodeling characterized by slightly but significantly increased interstitial fibrosis and enhanced MMP-2 activity compared with sham group were observed, and sustained atrial fibrillation was easily induced. In atrial pacing with amiodarone group, both electrical and structural remodeling were reversed and sustained atrial fibrillation was not induced. In sham group with amiodarone, action potential duration prolongation and depressed conduction velocity compared with sham without amiodarone were observed, but either increased fibrosis or enhanced MMP-2 activity was not observed. Not only electrical but structural remodeling were induced in a canine persistent atrial fibrillation model. Amiodarone reversed both of them, which may be related to its high efficacy in preventing recurrence of persistent atrial fibrillation. |
9,779 | Cost effectiveness of biventricular pacemakers in heart failure patients. | Biventricular pacemakers have been shown to reduce mortality and hospitalizations in heart failure (HF) patients and are indicated for those with a New York Heart Association functional class of III or IV and a QRS interval of >130 ms. However, these devices currently cost in the region of dollar US 33,500 and require replacement upon battery depletion. Therefore, determination of the cost effectiveness of resynchronization therapy is important, although little data have been published to date on this topic.</AbstractText>A cost-utility analysis from the healthcare perspective was performed using HF patients who received a biventricular pacing device in the Cleveland Clinic Foundation. The comparator was a similarly profiled group of patients who did not receive the device but were treated medically. A Markov model was used to investigate the cost effectiveness at 1 and 5 years. Second-order Monte-Carlo simulation was used to determine the variability in results, using probabilistic sensitivity analysis. Medical treatment was dominated by biventricular pacemaker treatment at both 1 and 5 years of follow-up.</AbstractText>Biventricular device insertion is an economically attractive treatment option for clinically indicated HF patients.</AbstractText> |
9,780 | [Disseminated coronary occlusions and massive pulmonary embolism in a 40-year-old woman]. | A 40-year-old woman was admitted to the emergency room because of severe angina pectoris and dyspnoe at rest. She developed ventricular fibrillation a few minutes later from which she had to be resuscitated . After intubation and controlled ventilation immediate angiocardiography was performed while she was still in cardiogenic shock. Coronary angiography ten days before had been unremarkable.</AbstractText>The second coronary angiogram revealed severe thrombotic lesion at the origin of the left anterior descending branch (LAD) and total occlusions of the peripheral LAD and of the first marginal branch. After intracoronary application of 10 mg abciximab and coronary stent implantation in the origin of the LAD the patient had good clinical improvement. Massive pulmonary embolism two days later, despite of effective heparinization and inhibition of platelet aggregation (as measured by partial thromboplastin time), was treated successfully by regional injection of 100 mg tissue plasminogen activator (t-PA). Tests for possible hypercoagulability showed no detectable changes in the clotting and fibrinolytic system with a normal platelet count. In a standardized aggregation test of platelets hyperaggregation in response to ADP and epinephrine, also at low test doses, revealed the presence of a sticky platelet syndrome.</AbstractText>This case history suggests that enhanced platelet aggregation associated with sticky platelet syndrome may provoke myocardial infarction even in angiographically normal coronary arteries.</AbstractText> |
9,781 | Clinical and echocardiographic features of Ebstein's malformation in Sudanese patients. | Ebstein's malformation is a rare congenital cardiac malformation, accounting for about 0.5% of all congenital cardiac lesions. We report our experience with the anomaly as encountered at the Sudan Heart Centre from July 2004 to April 2005. Diagnosis was based on the echocardiographic demonstration of displacement of the septal leaflet of the tricuspid valve towards the ventricular apex by greater than 8 millimetres per metre squared.</AbstractText>In a period of 10 months, we identified 12 patients with the malformation, this number constituting 2% of all patients seen with congenital cardiac disease. The age ranged from 2 weeks to 35 years. Of the patients, half were asymptomatic, while the other half presented with congestive cardiac failure, 4 of these having cyanosis in addition to heart failure. Associated diseases included chronic renal failure, impaired hearing, stunted growth, and developmental delay. Electrocardiographic abnormalities included peaked and tall P waves, seen in four-fifths, an Rsr pattern, first degree atrioventricular block, atrial fibrillation, and Wolf-Parkinson-White syndrome, including the Mahaim pattern of pre-excitation. Associated abnormalities diagnosed echocardiographically included atrial septal defects, prolapse of the leaflets of the mitral valve, left ventricular dysfunction, atrial septal aneurysm, pulmonary valvar stenosis, and pericardial effusion.</AbstractText>Ebstein's malformation was seen four times more frequently at the Sudan Heart Centre when compared to the average frequency reported in the Western literature. Many of the associated diseases encountered in Sudan had not previously been reported.</AbstractText> |
9,782 | Drug treatment and thrombolytics during cardiopulmonary resuscitation. | During cardiopulmonary resuscitation, no specific drug therapy has been shown to improve survival to hospital discharge after cardiac arrest, and only few drugs have a proven benefit for short-term survival. This article reviews recent experimental and clinical data about vasopressor, antiarrhythmic and thrombolytic agents.</AbstractText>General use of high-dose epinephrine (>1 mg) can not be recommended, whereas it should be considered during prolonged cardiopulmonary resuscitation. No catecholamine superior to epinephrine has been identified. Arginine vasopressin has been shown to be as effective as epinephrine in patients with ventricular fibrillation and pulseless electrical activity, and may be more effective in patients presenting with asystole or as the second vasopressor (after epinephrine) in refractory cardiac arrest. Sodium bicarbonate should not be 'blindly' administered during cardiopulmonary resuscitation unless an arterial blood gas analysis can be obtained, or after prolonged unsuccessful cardiopulmonary resuscitation. Amiodarone should be preferred over lidocaine, since it may improve short-term survival. Thrombolytic therapy during cardiopulmonary resuscitation may be beneficial if a pulmonary embolism or acute myocardial infarction is suggested to be the cause of the cardiac arrest.</AbstractText>Epinephrine still represents the first-line vasopressor during cardiopulmonary resuscitation. Arginine vasopressin may be considered in patients presenting with asystole or who are unresponsive to initial treatment with epinephrine. Amiodarone should be preferred to other antiarrythmic agents in patients with cardiac arrest. Thrombolytic therapy during cardiopulmonary resuscitation is a promising new therapeutic option, but its general use in cardiac arrest cannot be recommended until the results of a large multicentre trial become available.</AbstractText> |
9,783 | Altered electrical activity of fibrillation process following thrombolytic therapy in out-of-hospital cardiac arrest patients with sustained ventricular fibrillation. | The likelihood of successful defibrillation in patients with sustained ventricular fibrillation (VF) is increased after administering thrombolytics during cardiopulmonary resuscitation (CPR). While dissolution of coronary artery thrombosis resolves the underlying cause of myocardial infarction in the majority of patients, improved microcirculatory reperfusion and alteration of the electrical activity of the fibrillation process may increase the likelihood of restoring spontaneous circulation in cardiac arrest patients. Electrocardiography is a sensitive means of displaying current myocardial perfusion in VF using changes in the frequency and amplitude of fibrillation. Our hypothesis postulates that thrombolytic therapy during CPR increases fibrillation frequency, fibrillation amplitude and amplitude spectrum area, thus improving ventricular fibrillation status and the chance of successful defibrillation. |
9,784 | [Electrophysiologic study and ablation therapy in idiopathic paroxystic atrial fibrillation]. | To analyze the results of radiofrequency catheter ablation (RFCA) of the pulmonary veins (PV) in patients with paroxysmal atrial fibrillation (PAF).</AbstractText>We describe 4 patients (38 +/- 12 years, interval 8-52; 11 men) with symptomatic PAF, refractory to antiarrhythmic drugs. Special mapping catheters were used and ablation was performed at the ostium/antrum of those veins with abnormal electrical activity (AEA).</AbstractText>AEA in one or more PV was identified in 13 patients (86%); in one patient AEA was also found in the superior vena cava (6.6%). One procedure was complicated by unstable ventricular tachycardia and was notfinished. Success was accomplished in 10, in 5 after the first ablation, in 4 after the second, and in one after a third procedure. One patient had pericarditis with a small pericardial effusion that did not require intervention.</AbstractText>RFCA is a useful and relatively safe procedure for the treatment of PAF and the only one with curative potential. The long-term rate of success (with or without antiarrhythmics) in this series was 71%. These results justify catheter ablation in selected patients with symptomatic PAF unresponsive to medical treatment.</AbstractText> |
9,785 | [Implantation of a re-synchronization device in a patient with persistent left superior vena cava-a case report]. | We report an implantation of a cardiac re-synchronization system in a patient with persistent left superior vena cava. This anomaly occurs in 0.3 to 0.5% of healthy individuals and remains usually asymptomatic. Variations of the superior vena cava should be considered in venous catheterization and other procedures such as implantation of pacemaker and ICD systems as well as port catheter insertion. In re-synchronization systems, persistent left superior vena cava can be an obstacle for cannulation of the coronary sinus and placement of a transvenous left ventricular lead. |
9,786 | Experience with coronary sinus lead implantations for cardiac resynchronization therapy in 244 patients. | Cardiac resynchronization therapy (CRT) using coronary sinus (CS) leads is a new method for the therapy of congestive heart failure (CHF). Because the intervention is more complex than regular pacemaker implantations, information on the feasibility and side effects of this method are of interest.</AbstractText>From 1999 to June 2005, CRT implantations were attempted in 244 patients (pts; mean age 64+/-12 years, range 14-90 years), 82% were male, 44% had coronary artery disease, 29% were in atrial fibrillation, 71 had preexisting pacemakers.</AbstractText>In 97% of the pts the intervention was successful (27% of the systems with defibrillation capabilities). In 285 interventions, 255 CS leads were positioned according to CS vein anatomy in 130 posterolateral, 97 anterolateral and 28 anterior side branches (16 patients received 2 CS leads). Over-the-wire leads were used in 88%, 71% were additionally preshaped. We observed no mortality but 37 complications (12.5%): CS dissection in 9, CS perforation in 1, ventricular fibrillation in 4, asystole in 5, pulmonary edema in 1, pneumothorax in 2, need for early CS lead revision in 19 (dislodgement n=7, phrenic nerve stimulation n=12) and infection with explantation in 2 cases. An improvement in NYHA functional class was found in 88% of pts (only 55% if anterior lead position).</AbstractText>Perioperative complications during CS lead implantation occur in 10-15% of cases. Most patients responded well to CRT. Patients should be informed about the possible need for a reoperation. During implantation, immediate defibrillation and stimulation capabilities must be available. Anterior lead positions should be avoided.</AbstractText> |
9,787 | A continued role for beta-blocker therapy in heart failure. | The number of patients with newly diagnosed heart failure continues to grow worldwide, to some extent reflecting the increase in survival after acute coronary syndromes and the aging of the population. The search for new and effective therapies for this condition remains a priority in the 21st century. The use of beta-blockers is now well established in the clinical context of mild and moderate systolic heart failure. The effects of beta-blockade on mortality are additive to those with angiotensin-converting enzyme inhibitor therapy. Recently completed, large, randomized trials provided strong evidence for the use of beta-blockers in severe (NYHA functional class IV) heart failure and in asymptomatic patients with left ventricular systolic dysfunction and recent myocardial infarction. Obviously, patient selection still remains the key to the safe use of beta-blockers in patients with heart failure. Further data from clinical trials have emerged to support similar benefits in terms of mortality and morbidity, a good safety record, and tolerability in patients at extremes of age (children and adults >70 years of age) and in specific clinical circumstances (including diabetes, chronic obstructive airways disease, renal failure, and atrial fibrillation). Recent use of beta-blockers with vasodilatory properties in patients with heart failure and preserved systolic function (so-called diastolic heart failure) appears promising but will require large-scale, long-term trials prior to widespread clinical use. |
9,788 | Isolated heart function after ischemia and reperfusion in sucrose-fed rats: influence of gender and treatment. | Sucrose-fed rats (HTG) develop hypertension, hypertriglyceridemia, and other features of the metabolic syndrome. This condition, nowadays a world epidemic, is more prevalent in males and increases the risk of cardiovascular diseases. Weanling male and female rats were given either tap water in control (C) or 30% sucrose solution in HTG groups and commercial rat chow for 3, 5, or 8 months. We studied possible variations in cardiac function, due to gender and length of treatment, in isolated heart after ischemia-reperfusion, since an impaired performance may be more easily detected under stress. Together, sucrose treatment and age affected all cardiac variables. Gender had significant effect on coronary vascular resistance and postischemic levels of the enzyme CK-MB; the percentages of retained cardiac enzymes after ischemia were higher in C and HTG females. C and HTG males had a higher incidence of arrhythmias than females, but only HTG males suffered lethal ventricular fibrillation. |
9,789 | The use of automated external defibrillators and public access defibrillators in the mountains: official guidelines of the international commission for mountain emergency medicine ICAR-MEDCOM. | In this article we propose guidelines for rational use of automated external defibrillators and public access defibrillators in the mountains. In cases of ventricular fibrillation and pulseless ventricular tachycardia, early defibrillation is the most effective therapy. Easy access to mountainous areas permits visitation by persons with high risks for sudden cardiac death, and medical trials show the benefit of exercising in moderate altitude. The introduction of public access defibrillators in popular areas in the mountains may lead to a reduction of fatal outcome of cardiac arrest. Public access defibrillators should be placed with priority in popular ski areas, in busy mountain huts and restaurants, at mass-participation events, and in remote but often-visited locations that do not have medical coverage. Automated external defibrillators should be available to first-responder groups and mountain-rescue teams. It is important that people know how to perform cardiopulmonary resuscitation and how to use public access defibrillators and automated external defibrillators. |
9,790 | Problems and complications with cold-water rescue. | A case description is presented of a 9-member rowing team whose scull swamped on a small lake in Victoria, Canada, because of a sudden winter storm, which immersed them in 4 degrees C water for 50 minutes until a small rescue boat found them in darkness. Another 13 minutes of cold exposure in 6.7 degrees C air occurred during boat transport to waiting ambulance paramedics. Two rowers died, one from severe hypothermia and the other from drowning as a consequence of cold incapacitation and hypothermia. The 2 coldest rowers, who were transported 8 km to a major hospital, arrived with rectal temperatures of 23.4 degrees C and 25 degrees C; the first was asystolic and the second was unconscious and in sinus bradycardia. Analysis of all the circumstances of this incident provided an opportunity to observe a continuum of responses in a heterogeneous group of rowers at risk of severe hypothermia. Several practical lessons concerning cold-water survival, rescue, and treatment can be learned. The effects of low body mass were associated with greater cooling rate. Diminished neuromuscular performance in the periphery appeared to be independent of body mass. Rough handling during moving of patients with marked hypothermia introduces the risk of producing ventricular fibrillation or cardiac arrest. Unconscious, nonshivering hypothermia victims who are rescued and insulated from cold could have a further afterdrop of 3 degrees C to 4 degrees C. During transport to a hospital, the use of heating devices concentrating on core regions may increase the chance of successful treatment in the hospital. Cardiopulmonary bypass may be indicated for severely hypothermic patients in asystole. |
9,791 | Predictors of mortality in end-stage renal disease patients with mitral annulus calcification. | Mitral annulus calcification (MAC) is an independent predictor of cardiovascular mortality in the general population. The purpose of the current historical cohort study is to assess risk factors for long-term mortality in end-stage renal disease (ESRD) patients with MAC (n = 30; age, 62 +/- 2 yr), as compared to ESRD patients without MAC (n = 30; age, 63 +/- 2 yr). Additional analysis compared ESRD patients with MAC to non-ESRD patients with MAC (n = 32; age, 66 +/- 2 yr).</AbstractText>The groups included age-matched male patients followed at a single center. Long-term survival was assessed by Kaplan-Meier analysis. Regular and stepwise Cox proportional hazards models were used to determine risk factors for mortality.</AbstractText>There was a similarly high prevalence of cardiovascular complications, including hypertension, coronary artery disease, left ventricular hypertrophy, atrial fibrillation, and congestive heart failure, in all three groups. Median survival time was significantly longer in non-ESRD patients (90 months), compared with the ESRD with MAC (45 months) and ESRD without MAC (45 months) patients (log-rank test; P < 0.001). With stepwise Cox proportional hazards model, including ESRD patients with MAC and ESRD patients without MAC, increased calcium x phosphate product, decreased serum creatinine concentration, and the presence of coronary artery disease and lower extremity amputations were independent predictors of mortality for patients with ESRD. With stepwise Cox proportional hazards model, including ESRD patients with MAC and non-ESRD patients with MAC, the presence of ESRD, atrial fibrillation, diabetes, aortic valve calcification, coronary artery disease, and tricuspid regurgitation were independent predictors of mortality.</AbstractText>The mortality rate was high in ESRD patients, approximately 15% per year. After accounting for baseline cardiovascular disease and traditional risk factors, the presence of MAC did not confer additional risk for mortality.</AbstractText> |
9,792 | 123I-metaiodo-benzylguanidine myocardial scintigraphy in the Brugada-type ECG. | The degree of ST-segment elevation and amplitude of J waves, which may change in patients with the Brugada-type electrocardiogram (ECG) over time, are influenced by autonomic nervous activity and the administration of antiarrhythmic drugs. In the present study, we evaluated whether the shape of ST-segment elevation in patients with a Brugada-type ECG might alter the parameters of an 123I-MIBG myocardial scintigraphy and body surface signal-averaged ECG (SAECG). The subjects consisted of 12 patients with a Brugada-type ECG and 15 healthy volunteers (N group). The patients with a Brugada-type ECG were classified into the following 2 groups based on the type of ST-segment elevation: 6 patients with the coved type ST-segment elevation (C group), and 6 patients with the saddle-back type ST-segment elevation (S group). Planar and SPECT images were obtained 15 minutes (early images) and 3 hours (delayed images) after the administration of 123I-MIBG, respectively. In addition, the washout rate (% WR) of 123I-MIBG was obtained in a bull's eye map of the SPECT image. There were no significant differences in the early H/M ratio between the C and S groups. In the C group, however, there were some patients who showed a decreased accumulation or defect of 123I-MIBG in the planar and SPECT images. Furthermore, in contrast to the N and S groups, the C group showed a decreased delayed H/M ratio and increased % WR. SAECG did not show any significant differences between the S and C groups. These results of the present study suggest that the shape of ST-segment elevation may be associated with myocardial autonomic nervous function. In addition, the electric heterogeneity of the action potential in the right ventricular epicardial myocardium, which is frequently influenced by autonomic nervous activity, is closely associated with the development of Brugada syndrome. |
9,793 | Dimethyl lithospermate B, an extract of Danshen, suppresses arrhythmogenesis associated with the Brugada syndrome. | Dimethyl lithospermate B (dmLSB) is an extract of Danshen, a traditional Chinese herbal remedy, which slows inactivation of INa, leading to increased inward current during the early phases of the action potential (AP). We hypothesized that this action would be antiarrhythmic in the setting of Brugada syndrome.</AbstractText>The Brugada syndrome phenotype was created in canine arterially perfused right ventricular wedge preparations with the use of either terfenadine or verapamil to inhibit INa and ICa or pinacidil to activate IK-ATP. AP recordings were simultaneously recorded from epicardial and endocardial sites together with an ECG. Terfenadine, verapamil, and pinacidil each induced all-or-none repolarization at some epicardial sites but not others, leading to ST-segment elevation as well as an increase in both epicardial and transmural dispersions of repolarization (EDR and TDR, respectively) from 12.9+/-9.6 to 107.0+/-54.8 ms and from 22.4+/-8.1 to 82.2+/-37.4 ms, respectively (P<0.05; n=9). Under these conditions, phase 2 reentry developed as the epicardial AP dome propagated from sites where it was maintained to sites at which it was lost, generating closely coupled extrasystoles and ventricular tachycardia and fibrillation. Addition of dmLSB (10 micromol/L) to the coronary perfusate restored the epicardial AP dome, reduced EDR and TDR to 12.4+/-18.1 and 24.4+/-26.7 ms, respectively (P<0.05; n=9), and abolished phase 2 reentry-induced extrasystoles and ventricular tachycardia and fibrillation in 9 of 9 preparations.</AbstractText>Our data suggest that dmLSB is effective in eliminating the arrhythmogenic substrate responsible for the Brugada syndrome and that it deserves further study as a pharmacological adjunct to implanted cardioverter/defibrillator usage.</AbstractText> |
9,794 | Failure of cilostazol in the prevention of ventricular fibrillation in a patient with Brugada syndrome. | The ECG appearance in Brugada syndrome is caused by failure of the dome of the action potential to develop. Increased activity of the I(to) current in epicardial cells generates a transmural gradient with repolarization dispersion between the epicardium and the endocardium in the right ventricular wall, thus favoring the development of VF by a phase 2 reentry mechanism. The efficacy of cilostazol for the management of these arrhythmias has been reported. This drug is a phosphodiesterase inhibitor with positive chronotropic properties, thus blocking outward potassium currents I(to) in the myocardial tissue. We present a patient with Brugada syndrome with an implantable cardioverter defibrillator (ICD), who suffered multiple ICD discharges due to VF during therapy with this drug. |
9,795 | Use of fast fourier transform analysis of atrial electrograms for rapid characterization of atrial activation-implications for delineating possible mechanisms of atrial tachyarrhythmias. | Different analysis techniques have been developed to help understand and characterize the mechanisms responsible for atrial arrhythmias. We tested the hypothesis that Fast Fourier Transform (FFT) analysis of recorded atrial electrograms (AEGs) will rapidly and accurately identify regular and irregular patterns of atrial activation, and, thereby, may provide evidence suggestive of underlying mechanisms of atrial tachyarrhythmias.</AbstractText>During induced atrial tachyarrhythmias in both the canine sterile pericarditis model and canine rapid ventricular pacing-induced congestive heart failure model; 380-404 AEGs were recorded simultaneously from epicardial electrodes on both atria. From AEGs, atrial activation sequences were determined during atrial flutter (AFL), focal atrial tachycardia (AT), and atrial fibrillation (AF). Four-second recording segments of each AEG were subjected to FFT analysis. Frequencies found during FFT analyses in all studies precisely corresponded to the cycle lengths of the AEGs. In AFL and AT, one dominant frequency peak was found throughout both atria. In AF due to multiple unstable reentry circuits, multiple and broad frequency peaks were found in both atria. In AF due to a stable rapid rhythm (driver) in the left atrium with fibrillatory conduction to the rest of the atria, one dominant frequency peak in areas with 1:1 conduction from the driver, and multiple and/or broad frequency peaks in areas with fibrillatory conduction produced by the driver were found. Computation time for all FFT analyses took <5 minutes.</AbstractText>FFT analysis accurately and rapidly identifies global atrial activation patterns during AFL, AT, and AF, thereby assisting in determining arrhythmia mechanisms.</AbstractText> |
9,796 | Chronic myocardial infarction is a substrate for bradycardia-induced spontaneous tachyarrhythmias and sudden death in conscious animals. | Patients with bradycardia can have severe tachyarrhythmias but it is unclear whether bradycardia alone can induce arrhythmias or whether an additional substrate is necessary. While several animal models of ventricular tachycardia (VT) exist, no model has been reported to mimic the clinical condition of spontaneous VT and sudden cardiac death (SCD) in the presence of bradycardia and chronic myocardial infarction (MI) in large animals without manipulation of the autonomic nervous system. We tested the hypothesis that MI and bradycardia cause more spontaneous sustained VT than does bradycardia alone.</AbstractText>Sheep (42-56 kg) underwent atrioventricular (AV) node catheter ablation alone (n = 5) or AV node ablation and 150 minutes of angioplasty balloon occlusion of the left anterior descending coronary artery (n = 9). An implantable cardioverter defibrillator delivered rescue shocks and demand pacing at 90 beats per minute for the first week and at 40 beats per minute thereafter. Electrograms were continuously radiotelemetered and recorded for 6 weeks. Acute post-MI VT disappeared by day 4. The sudden bradycardia on day 8 triggered numerous premature ventricular contractions (PVCs) and episodes of sustained VT lasting >30 seconds during the next 5 weeks. There were 43 episodes of sustained VT and no spontaneous ventricular fibrillation (VF) with bradycardia alone. However, in the presence of both MI and bradycardia there were 970 episodes of VT/VF (P < 0.05) and three deaths at days 13, 15, and 34. The average 24-hour count of PVCs was similar at day 7 between the two groups but by days 11 and 40, the PVC counts were 35 times and 4 times greater, respectively, in the presence of bradycardia and chronic MI compared to bradycardia alone. No significant difference in the incidence of PVCs was detected because of large individual variation between the two groups (P = 0.21). A high PVC count did not appear to predict SCD.</AbstractText>The combination of MI and bradycardia secondary to AV node ablation in sheep produces a higher incidence of VT than bradycardia alone, suggesting that this preparation can serve as a model for the study of VT and sudden cardiac death.</AbstractText> |
9,797 | Proarrhythmia of circumferential left atrial lesions for management of atrial fibrillation. | After circumferential ablation for atrial fibrillation, new onset left atrial flutter (LA Flr) may occur. This study assessed the relationship between induced and clinical episodes of LA Flr, the rate of spontaneous resolution of LA Flr, and the proarrhythmic effect of circumferential ablation.</AbstractText>A total 112 patients underwent circumferential LA ablation for atrial fibrillation. Immediately after completion of the ablation, LA Flr was induced in 43 of 112 (38%) patients, but was not targeted for ablation. During follow-up (14 +/- 4 months), new onset LA Flr occurred in 28 of 112 (25%) patients; however, the presence of inducible LA Flr did not identify those patients with clinical LA Flr (P = 0.6). In comparison to episodes of atrial fibrillation occurring before circumferential ablation, LA Flr was associated with a faster ventricular rate (124 +/- 19 beats/min vs 91 +/- 16 beats/min, P < 0.001), and was more likely to be persistent requiring cardioversion (86% vs 32%, P = 0.01). By >or=4 months postcircumferential ablation, clinical LA Flr resolved in 18 of 28 patients (64%). A second ablation procedure for LA Flr was performed in 9 of 10 patients. Of the 17 morphologies, 16 (94%) LA Flr circuits were successfully ablated.</AbstractText>(1) LA Flrs that are induced immediately after circumferential ablation for atrial fibrillation do not identify those patients who require a second ablation procedure for clinical LA Flr; (2) Since the majority of clinical LA Flrs spontaneously resolve, ablation of LA Flr should be postponed several months; and (3) new onset LA Flr after ablation for atrial fibrillation is likely a manifestation of the proarrhythmic effect of ablation lines in the LA.</AbstractText> |
9,798 | Intraoperative testing of the implantable cardioverter-defibrillator: how much is enough? | Defibrillation testing of the implantable cardioverter-defibrillator (ICD) is considered a standard and required practice at the time of implantation. How much testing, if any in some cases, should be performed, however, remains unknown.</AbstractText>Included in this retrospective analysis were 835 patients (77% men; age 65 +/- 13 years) who received transvenous ICDs between January 1996 and December 2003. One hundred twenty-nine (15.5%) had intraoperative defibrillation threshold (DFT) testing, 503 (60.2%) had limited defibrillation safety margin testing, and 203 (24.3%) had no defibrillation testing. We compared the outcome (success of ICD therapies against spontaneous VT/VF events and survival) of the three groups of patients, who in some respects had important clinical differences. The success of the first delivered shocks against VT/VF was similar for DFT (91%), safety margin testing (91%), and no-testing (92%) groups; and the second shocks terminated the remaining episodes in all three groups. Sudden-death-free survival rates were similar in the three groups, however, the overall long-term survival rate was significantly lower in the no-testing group (58%) than in the DFT (74%) and safety margin testing (69%) groups (P < 0.0005). Multivariate analysis found no strong predictors of sudden death, but there were several independent predictors of overall mortality including lack of ICD testing (HR: 2.031, CI: 1.253-3.290, P = 0.004).</AbstractText>In this select patient cohort, success of ICD therapies and sudden-death-free survival were similar in patients who had DFT, safety margin testing, and no testing, but overall survival was significantly lower in the no-testing group. Thus in the absence of prospective mortality data, a minimum of safety margin ICD testing should remain standard practice.</AbstractText> |
9,799 | Age-related changes in human left and right atrial conduction. | Advancing age is an independent risk factor for atrial fibrillation (AF), which is considered to be initiated by ectopic triggers and maintained by an arrhythmogenic substrate. It is not known whether substrate changes produce this age-related increase in propensity toward AF. We addressed the hypothesis that advancing age is associated with changes in biatrial electrophysiology even in patients with no history of atrial arrhythmias.</AbstractText>Patients with left-sided accessory pathways and requiring routine electrophysiological studies were recruited. Electroanatomic mapping was performed in the left and right atria of 23 patients (age ranging from 17 to 75 years) with structurally normal hearts and no history of AF during sinus rhythm and pacing. Unlike previous studies, a trigonometric method was used to quantify wavefront propagation velocities (WPV) precisely in the direction of propagation. Refractoriness was measured at 2 cycle lengths, at three different atrial sites. Both right (r =-0.77, P < 0.0001) and left (r =-0.79, P < 0.001) atrial WPV demonstrated strongly inverse correlation with age. Furthermore, left and right WPVs were highly correlated (r = 0.66, P < 0.01), with velocities being 6.4 +/- 2.2 cm/sec higher in the right atria (P < 0.01). Refractoriness was significantly correlated with increasing age only at the septum (r = 0.53, P < 0.01). Left atrial wavelength was inversely correlated with increasing age (r =-0.56, P = 0.03). P wave duration was associated with age (r = 0.42, P = 0.04) and left atrial size (r = 0.44, P = 0.04) but not atrial WPV.</AbstractText>Aging human atria demonstrate progressive decline in WPV and increase in septal refractoriness. These age-related changes in biatrial electrophysiology are likely to be important factors in the age-related increase in AF prevalence.</AbstractText> |
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