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9,600 | Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. | To clarify the major features of the apical ballooning syndrome, we performed a systematic review of the existing literature.</AbstractText>Review of all relevant case series using the MEDLINE and EMBASE databases resulted in the identification of 14 studies. These studies suggest that the apical ballooning syndrome accounts for approximately 2.0% of ST-segment elevation infarcts, with most cases described in post-menopausal women. The most common clinical presentations are chest pain and dyspnoea, reported in 67.8 and 17.8% of the patients, respectively. Cardiogenic shock (4.2% of the patients) and ventricular fibrillation (1.5%) were not infrequent. ST-segment elevation was reported in 81.6% of the patients, T wave abnormalities in 64.3%, and Q waves in 31.8%. Cardiac biomarkers were usually mildly elevated, as reported in 86.2% of the patients. Typically, patients had left ventricular (LV) dysfunction on admission, with mean ejection fraction ranging from 20 to 49%. However, over a period of days to weeks, all patients experienced dramatic improvement in LV function. The onset of symptoms was often preceded by emotional (26.8%) or physical stress (37.8%). Norepinephrine concentration was elevated in 74.3% of the patients. Prognosis was generally excellent, with full recovery in most patients. In-hospital mortality was 1.1%. Only 3.5% of the patients experienced a recurrence.</AbstractText>Clinicians should consider this syndrome in the differential diagnosis of patients presenting with chest pain, especially in post-menopausal women with a recent history of emotional or physical stress.</AbstractText> |
9,601 | Impact of transforming growth factor-beta1 on atrioventricular node conduction modification by injected autologous fibroblasts in the canine heart. | Atrioventricular (AV) nodal ablation for management of atrial fibrillation (AF) is irreversible and requires permanent pacemaker implantation. We hypothesized that as an alternative, implantation of autologous fibroblasts in the perinodal region would focally modify AV nodal conduction and that this modulation would be enhanced by pretreatment with transforming growth factor-beta1 (TGF-beta1), a stimulant of fibroblasts.</AbstractText>Skin biopsies were taken from 12 mongrel dogs, and derived fibroblasts were dissociated and grown in culture for 2 weeks. Multiple injections (0.25 mL) were made through an 8F NOGA catheter along the fast/slow AV nodal pathways as guided by an electroanatomic mapping system. Seven dogs received fibroblasts alone (1x10(6) cells/mL), 7 dogs received TGF-beta1 (5 microg), 4 dogs received fibroblasts and TGF-beta1 (1x10(6) cells/mL+5 microg), and 4 dogs received saline only. AV node function was assessed at baseline and after 4 weeks. Saline (80 mL) with assigned therapy (0.25 mL per injection) was injected into the peri-AV nodal region in each dog. At baseline, the AH interval (66+/-3 ms) and the average RR interval (331+/-17 ms) in pacing-induced AF were similar in each cohort. The increase in AH interval in normal sinus rhythm was longer after fibroblast (23+/-4 versus 5+/-5 ms; P=0.05) and fibroblast plus TGF-beta1 (50+/-5 versus 5+/-5 ms; P<0.001) injections than with saline alone, with similar findings during high right atrium and distal coronary sinus pacing. The AH interval was not significantly increased after TGF-beta1 injections. The AH interval was significantly longer after fibroblast plus TGF-beta1 injections than with either therapy (TGF-beta1 or fibroblasts) alone. The RR interval during AF was increased in dogs that received fibroblasts alone (110+/-36 versus -41+/-34 ms) and to a greater extent with the addition of TGF-beta1 (294+/-108 versus -41+/-34 ms). No AV block was seen in any cohort at 4 weeks. Labeled fibroblasts that expressed vimentin were identified in all dogs that received cell injections at 4 weeks.</AbstractText>AV nodal modification can be achieved with injected fibroblasts without the creation of AV block. The effect on AV node conduction is substantially enhanced by pretreatment of fibroblasts with TGF-beta1. These data have therapeutic potential for the management of rapid ventricular rate during AF without pacemaker implantation.</AbstractText> |
9,602 | Postischemic hyperoxia reduces hippocampal pyruvate dehydrogenase activity. | The pyruvate dehydrogenase complex (PDHC) is a mitochondrial matrix enzyme that catalyzes the oxidative decarboxylation of pyruvate and represents the sole bridge between anaerobic and aerobic cerebral energy metabolism. Previous studies demonstrating loss of PDHC enzyme activity and immunoreactivity during reperfusion after cerebral ischemia suggest that oxidative modifications are involved. This study tested the hypothesis that hyperoxic reperfusion exacerbates loss of PDHC enzyme activity, possibly due to tyrosine nitration or S-nitrosation. We used a clinically relevant canine ventricular fibrillation cardiac arrest model in which, after resuscitation and ventilation on either 100% O2 (hyperoxic) or 21-30% O2 (normoxic), animals were sacrificed at 2 h reperfusion and the brains removed for enzyme activity and immunoreactivity measurements. Animals resuscitated under hyperoxic conditions exhibited decreased PDHC activity and elevated 3-nitrotyrosine immunoreactivity in the hippocampus but not the cortex, compared to nonischemic controls. These measures were unchanged in normoxic animals. In vitro exposure of purified PDHC to peroxynitrite resulted in a dose-dependent loss of activity and increased nitrotyrosine immunoreactivity. These results support the hypothesis that oxidative stress contributes to loss of hippocampal PDHC activity during cerebral ischemia and reperfusion and suggest that PDHC is a target of peroxynitrite. |
9,603 | Evolving role of vasopressin in the treatment of cardiac arrest. | Sudden cardiac arrest is a major public heath problem, affecting more than 450,000 individuals annually. Response time and the initiation of cardiopulmonary resuscitation (CPR) remain the most important factors determining successful revival. During resuscitation, sympathomimetics are given to enhance cerebral and coronary perfusion pressures in an attempt to achieve restoration of spontaneous circulation. Epinephrine has been the preferred vasopressor since the inception of advanced cardiac life support, although the lack of definitive evidence regarding its effectiveness has created much controversy surrounding its use, including the optimum dosage. Vasopressin is an alternative vasopressor that, when given at high doses, causes vasoconstriction by directly stimulating smooth muscle V1 receptors. The 2000 American Heart Association (AHA) guidelines commented that vasopressin is a reasonable first-line vasopressor in patients with ventricular fibrillation or pulseless ventricular tachycardia. Since release of those guidelines, additional human studies support an expanded role for vasopressin, whereas other studies cast doubt regarding its efficacy compared with epinephrine. The AHA recently released revised guidelines for CPR and emergency cardiovascular care. The consensus was that vasopressors should remain a part of pulseless sudden cardiac arrest management, with epinephrine 1 mg every 3-5 minutes being the recommended adrenergic of choice. In these revised guidelines, the role of vasopressin expanded beyond previous recommendations, despite the recommendation being downgraded to class indeterminate. The guidelines comment that one dose of vasopressin 40 U may replace the first or second dose of epinephrine in all pulseless sudden cardiac arrest scenarios, including asystole and pulseless electrical activity. A consistent theme with all vasopressors in sudden cardiac arrest is that additional studies are necessary to clearly document greater efficacy compared with no treatment. Further evaluation is warranted to better assess the role of vasopressin in asystolic sudden cardiac arrest, as well as its use with epinephrine, and to determine its optimal timing of administration and potential synergistic effects. |
9,604 | Diabetes and impaired fasting glucose as predictors of morbidity and mortality in male coronary artery disease patients with reduced left ventricular function. | To evaluate the prognostic value of impaired fasting glucose and diabetes mellitus in male patients with coronary artery disease and poor left ventricular function.</AbstractText>From a prospective database on patients referred for gated myocardial perfusion imaging between 1998 and 2002 all male patients with a history of coronary artery disease and poor left ventricular function were selected. Poor function was defined as left ventricular ejection fraction < or = 40%. Subjects were classified as non-diabetics with fasting blood glucose levels < 110 mg/dL, non-diabetics with impaired fasting glucose (fasting blood glucose between 110 and 125 mg/dL) and diabetics. Median follow-up was 2.7years. End points were all-cause mortality, cardiac death and hospitalization for heart failure. One hundred and sixty patients were selected (age 65 +/- 9 years and left ventricular ejection fraction 29 +/- 8%). In univariate analysis atrial fibrillation, NYHA class, glycaemia and diabetes mellitus discriminated between survivors and non-survivors. In Cox multivariate regression analysis for all-cause mortality only NYHA class and diabetes mellitus remained significant. Kaplan Meier analysis showed that diabetics had the worst survival and non-diabetics with glucose < 110 mg/dL had the best survival. Non-diabetics with impaired fasting glucose had intermediate survival. Analysis for cardiac death/hospitalization for heart failure showed similar results.</AbstractText>In male patients with coronary artery disease and impaired left ventricular function diabetes mellitus and fasting glucose are strongly predictive of poor outcome. Diabetics have the worst prognosis but non-diabetics with impaired fasting glucose also are at higher risk compared to nondiabetics with low fasting blood glucose.</AbstractText> |
9,605 | [Successful resuscitation of intractable hyperkalemic cardiac arrest]. | We report on a 42-year-old oliguric uremic man on regular hemodialysis who developed sudden cardiac arrest, secondary to severe hyperkalemia, with a plasma potassium concentration of 9.7 mEq x l(-1). The cardiac arrest persisted after the initiation of cardiopulmonary resuscitation and intensive treatment for marked hyperkalemia for an hour and 55 minutes. Therefore a portable percutaneous cardiopulmonary support (PCPS) system had to be instituted while the patient had very prolonged refractory ventricular fibrillation. His cardiac rhythm was restored immediately after application of PCPS and he recovered without neurological sequelae. We therefore suggest that PCPS should be considered as a therapeutic option during cardiopulmonary resuscitation for life-threatening cardiac arrest secondary to severe hyperkalemia. |
9,606 | [A case of anaphylactic shock in an elderly man following protamine sulfate administration during emergent off-pump coronary artery bypass grafting]. | An 80-year-old diabetic man undergoing emergent off-pump coronary artery bypass grafting for acute myocardial infarction developed anaphylactic shock immediately following administering a small dose of protamine sulfate. Preoperative examination revealed atrial fibrillation, severe three-vessel coronary artery disease and impaired left ventricular function with ejection fraction of 40% and severe septal as well as apical hypokinesis and akinesis. After successful completion of coronary bypass grafting, a total of 40 mg of protamine sulfate was given through the central venous line. Three minutes after protamine administration, profound hypotension occurred. Pulmonary artery pressure was low and the left ventricle was almost empty by transesophageal echocardiography. Hypotension was refractory to rapid administration of 2 l of crystalloid and albumin, and repeated administrations of phenylephrine. Blood pressure finally returned towards baseline after infusion of norepinephrine 0.2 microg x kg(-1) x min(-1) and epinephrine 0.1 microg x kg(-1) x min(-1). Hemoconcentration and impaired oxygenation were also noted. The situation suggested anaphylactic shock due to protamine. He had diabetes mellitus for 20 years and been treated by protamine containing insulin. Postoperative interview revealed that the patient had experienced urticaria over the abdominal area with neutral protamine hagedorn (NPH) insulin administration. This history suggested that the patient had been sensitized by protamine before surgery. Although it is rare to experience anaphylactic shock due to protamine, it is important to elicit the detailed allergic history to insulin in diabetic patients. Because anaphylactic shock still carries high mortality even in a patient without cardiac disease, we were lucky to save this elderly patient with acute myocardial infarction and compromised left ventricular function. |
9,607 | [Emergent coronary artery bypass grafting for a patient with cardiopulmonary arrest]. | A 59-year-old man was admitted to our hospital due to sudden onset of unconsciousness caused by myocardial infarction with ventricular fibrillation. Emergent coronary angiography under intraaortic balloon pumping revealed 90% stenosis of the left main trunk and left anterior descending artery (LAD), and complete obstruction of the left circumflex artery (Cx) and right coronary artery (RCA). Emergent coronary artery bypass grafting (CABG) to LAD, Cx, and RCA was performed. During the postoperative course, the patient developed ventricular tachycardia/fibrillation. After implantation of an implantable cardioverter defibrillator (ICD), he was discharged on the postoperative day 36. The patient has now resumed normal daily life. |
9,608 | [Life-threatening ventricular tachycardia during flecainide treatment for symptomatic atrial fibrillation in a patient with a structural cardiac disorder]. | A 37-year-old man with symptomatic acute atrial fibrillation and a low-voltage electrocardiogram was treated with flecainide intravenously. Instead of conversion to sinus rhythm, he developed a wide-complex tachycardia suggestive of ventricular tachycardia. The patient recovered following electric cardioversion. First-choice therapy for symptomatic atrial fibrillation of recent onset (duration < 48 hours) is chemical conversion with a class IC antiarrhythmic drug (e.g. flecainide, propafenone). However, in patients with structural heart disorders, these drugs may induce ventricular tachycardia. A low-voltage electrocardiogram is suggestive of left ventricular damage. For these patients, electric cardioversion is a better alternative. |
9,609 | Cardiac stress MR imaging with dobutamine. | Stress testing for detection of ischemia-induced wall-motion abnormalities has become a mainstay for noninvasive diagnosis and risk stratification of patients with suspected coronary artery disease (CAD). Recent technical developments in magnetic resonance imaging (MRI), including the adoption of balanced steady-state free precession (b-SSFP) sequences-preferentially in combination with parallel imaging techniques-have led to a significant reduction of imaging time and improved patient safety. The stress protocol includes application of high-dose dobutamine (up to 40 microg/kg/min) combined with fractionated atropine (up to a maximal dose of 1.0 mg). High-dose dobutamine stress MRI revealed good sensitivity (83-96%) and specificity (80-100%) for detection of significant CAD. Myocardial tagging methods have been shown to further increase sensitivity for CAD detection. Severe complications (sustained tachycardia, ventricular fibrillation, myocardial infarction, cardiogenic shock) are rare but may be expected in 0.1-0.3% of patients. Dobutamine stress MRI has emerged as a reliable and safe clinical alternative for noninvasive assessment of CAD. New pulse sequences, such as real-time imaging, might obviate the need for breath holding and electrocardiogram (ECG) triggering in patients with severe dyspnoea and cardiac arrhythmias, which may further improve the clinical impact and acceptance of stress MRI in the future. |
9,610 | B-type natriuretic peptide levels in patients with paroxysmal lone atrial fibrillation. | To investigate the levels of B-type natriuretic peptide (BNP) in patients with atrial fibrillation (AF) but without structural heart disease, we measured plasma BNP concentration in 61 consecutive AF patients and in 61 age- and sex-matched healthy subjects. Plasma BNP concentration in the AF group was significantly higher than in the control group (121+/-32 vs 41+/-12 pg/ml, P<0.001). Logistic regression analysis showed that age (r=0.66, P<0.001), left atrial diameter (r=0.59, P<0.01), and a history of AF (r=0.72, P<0.001) were independent predictors of elevated BNP. We concluded that BNP was elevated in patients with paroxysmal lone AF. The clinical significance of BNP elevation in these patients requires further investigation. |
9,611 | Adrenomedullin acts via nitric oxide and peroxynitrite to protect against myocardial ischaemia-induced arrhythmias in anaesthetized rats. | 1. The overall aim of this study was to determine if adrenomedullin (AM) protects against myocardial ischaemia (MI)-induced arrhythmias via nitric oxide (NO) and peroxynitrite. 2. In sham-operated rats, the effects of in vivo administration of a bolus dose of AM (1 nmol kg-1) was assessed on arterial blood pressure (BP), ex vivo leukocyte reactive oxygen species generation and nitrotyrosine deposition (a marker for peroxynitrite formation) in the coronary endothelium. 3. In pentobarbitone-anaesthetized rats subjected to ligation of the left main coronary artery for 30 min, the effects of a bolus dose of AM (1 nmol kg-1, i.v.; n=19) or saline (n=18) given 5 min pre-occlusion were assessed on the number and incidence of cardiac arrhythmias. In a further series of experiments, some animals received infusions of the NO synthase inhibitor N(G)-nitro-L-arginine (LNNA) (0.5 mg kg-1 min-1) or the peroxynitrite scavenger N-mercaptopropionyl-glycine (MPG) (20 mg kg-1 h-1) before AM. 4. AM treatment significantly reduced mean arterial blood pressure (MABP) and increased ex vivo chemiluminescence (CL) generation from leukocytes in sham-operated animals. AM also enhanced the staining for nitrotyrosine in the endothelium of coronary arteries. 5. AM significantly reduced the number of total ventricular ectopic beats that occurred during ischaemia (from 1185+/-101 to 520+/-74; P<0.05) and the incidences of ventricular fibrillation (from 61 to 26%; P<0.05). AM also induced a significant fall in MABP prior to occlusion. AM-induced cardioprotection was abrogated in animals treated with the NO synthase inhibitor LNNA and the peroxynitrite scavenger MPG. 6. This study has shown that AM exhibits an antiarrhythmic effect through a mechanism that may involve generation of NO and peroxynitrite. |
9,612 | From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. | Therapeutic hypothermia has been recommended for postcardiac arrest coma due to ventricular fibrillation. However, no studies have evaluated whether therapeutic hypothermia could be effectively implemented in intensive care practice and whether it would improve the outcome of all comatose patients with cardiac arrest, including those with shock or with cardiac arrest due to nonventricular fibrillation rhythms.</AbstractText>Retrospective study.</AbstractText>Fourteen-bed medical intensive care unit in a university hospital.</AbstractText>Patients were 109 comatose patients with out-of-hospital cardiac arrest due to ventricular fibrillation and nonventricular fibrillation rhythms (asystole/pulseless electrical activity).</AbstractText>We analyzed 55 consecutive patients (June 2002 to December 2004) treated with therapeutic hypothermia (to a central target temperature of 33 degrees C, using external cooling). Fifty-four consecutive patients (June 1999 to May 2002) treated with standard resuscitation served as controls. Efficacy, safety, and outcome at hospital discharge were assessed. Good outcome was defined as Glasgow-Pittsburgh Cerebral Performance category 1 or 2.</AbstractText>In patients treated with therapeutic hypothermia, the median time to reach the target temperature was 5 hrs, with a progressive reduction over the 18 months of data collection. Therapeutic hypothermia had a major positive impact on the outcome of patients with cardiac arrest due to ventricular fibrillation (good outcome in 24 of 43 patients [55.8%] of the therapeutic hypothermia group vs. 11 of 43 patients [25.6%] of the standard resuscitation group, p = .004). The benefit of therapeutic hypothermia was also maintained in patients with shock (good outcome in five of 17 patients of the therapeutic hypothermia group vs. zero of 14 of the standard resuscitation group, p = .027). The outcome after cardiac arrest due to nonventricular fibrillation rhythms was poor and did not differ significantly between the two groups. Therapeutic hypothermia was of particular benefit in patients with short duration of cardiac arrest (<30 mins).</AbstractText>Therapeutic hypothermia for the treatment of postcardiac arrest coma can be successfully implemented in intensive care practice with a major benefit on patient outcome, which appeared to be related to the type and the duration of initial cardiac arrest and seemed maintained in patients with shock.</AbstractText> |
9,613 | Trans-fatty acids and sudden cardiac death. | Sudden cardiac death (SCD) is usually due to ventricular fibrillation and can occur as a first manifestation of heart disease. Prevention of ventricular fibrillation and SCD with n-3 polyunsaturated fatty acids is well documented. Trans-fatty acids (TFA) in the diet and cell membranes might affect the risk of SCD as well. We review evidence from an observational study that high levels of trans-18:2 (9 cis-, 12 trans- and 9 trans-, 12 cis-isomers of linoleic acid) in red blood cell membranes are associated with markedly higher risk of SCD. In contrast, cell membrane levels of trans-18:1 (trans-isomers of oleic acid), the major TFA in foods, do not appear associated with higher risk of SCD. While further studies are needed to investigate possible effects of trans-18:2 on arrhythmia, it would be prudent to limit dietary intake of trans-18:2. |
9,614 | [Myocardial disease mortality in children and young adults. A population-based observational study]. | Few studies have investigated death due to myocardial disease in children and young adults. The aim of this study was to analyze the epidemiological, clinical, and pathologic characteristics of death in these cases.</AbstractText>Population-based observational study of all deaths in individuals aged 1-35 years in the Spanish province of Biscay over a period of 12 years.</AbstractText>Forty deaths from myocardial disease occurred in 29 males and 11 females (mean age 25.3 years): 30 sudden and 10 non-sudden deaths. The mortality rate was 0.64 per 100,000 persons-year. The relative risk of sudden death was significantly greater than that of non-sudden death, particularly in adolescents and young males. The cause of death was myocarditis in 12 cases (83.3% sudden death), dilated cardiomyopathy in 10 (80% non-sudden death), arrhythmogenic cardiomyopathy in seven, hypertrophic cardiomyopathy in six, and idiopathic concentric left ventricular hypertrophy in five (100% sudden death). Myocardial disease was diagnosed before sudden death in only three cases. Ten subjects had symptoms and electrocardiogram abnormalities but their cardiomyopathy had not been diagnosed. Six individuals had a comorbid condition (morbid obesity in four), six had prodromal symptoms, and 11 had arrhythmic triggering factors (sporting activity in seven). Ventricular fibrillation was frequently observed during cardiopulmonary resuscitation.</AbstractText>Mortality due to myocardial disease in children and young adults is uncommon. Most deaths are sudden. However, some may be preventable. Preventative measures should be aimed at sudden death in adolescents and young males. There was a noticeable association between arrhythmogenic cardiomyopathy and sporting activity.</AbstractText> |
9,615 | High-efficiency multiplex capillary electrophoresis single strand conformation polymorphism (multi-CE-SSCP) mutation screening of SCN5A: a rapid genetic approach to cardiac arrhythmia. | Mutations in the SCN5A gene coding for the alpha-subunit of the cardiac Na(+) ion channel cause long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, sick sinus node syndrome, progressive conduction disease, dilated cardiomyopathy and atrial standstill. These diseases exhibit variable expressivity, and identification of gene carriers is clinically important, particularly in sudden infant and adult death syndromes. The SCN5A gene comprises 28 exons distributed over 100 kbp of genomic sequence at chromosome 3p21. Disease-causing mutations are private and scattered over the DNA sequence, making it difficult to screen for specific mutations. We developed a multiplex capillary-electrophoresis single-strand conformation polymorphism (Multi-CE-SSCP) mutation screening protocol on the ABI 3100 platform and applied it to 10 previously slab-gel SSCP identified mutations and SNPs and used it to identify one novel deletion. The method is highly efficient, with a turnover of 23 patients per 24 h and a false positive rate of 0.5% of the analyzed amplicons. Each variant has a particular elution pattern, and all 20 carriers of the H558R polymorphism out of 57 persons were correctly identified. We suggest that the method could become part of routine work-up of patients with suspicious syncope and of members of families with sudden unexplained death. |
9,616 | [Catheter ablation of atrial fibrillation]. | In patients with drug-refractory atrial fibrillation, left-atrial catheter ablation represents a new curative therapeutic option. Segmental ostial or circumferential pulmonary vein isolation can achieve stable sinus rhythm in some 70% of patients with paroxysmal atrial fibrillation but no severe structural heart disease. In patients with chronic atrial fibrillation, complex left-atrial linear, or substrate-oriented ablation strategies may additionally be applied. In patients with cardiac insufficiency or more severe systolic left-ventricular dysfunction, restoration of a stable sinus rhythm through the use of left-atrial catheter ablation can improve the left-ventricular ejection fraction and reduce the severity of cardiac failure. Potential complications of ablation include, in particular, pulmonary veins stenosis, iatrogenic left-atrial tachycardia, thromboembolic events and fatal atrio-esophageal fistulas. |
9,617 | [Spectral parameters of heart rate variability and frequency of detection of autoantibodies to beta(1)-adrenoreceptors in patients with tachyarrhythmias: idiopathic and at the background of primary myocardial diseases]. | In order to assess parameters of heart rate variability (HRV) and prevalence of autoantibodies against the beta(1)-adrenoreceptors in patients with cardiac arrhythmias we studied 42 patients with arrhythmias and 20 healthy control subjects. Thirty one patients with idiopathic arrhythmias were included in group I: with paroxysmal atrial fibrillation or flutter (n=13), paroxysmal atrial tachycardia (n=2) and paroxysmal ventricular tachycardia (n=16). Group II was formed of 11 patients with paroxysmal ventricular tachycardia and dilated cardiomyopathy or chronic myocarditis. ab1-AR were determined in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of ab1-AR second loop was used as antigen. Groups I (54.8%) and II (63.6%) showed similar prevalence of ab1-AR, which was significantly higher than in control subjects (10%) (p<0.005). HRV parameters in I group were lower in ab1-AR-positive compared with ab1-AR-negative patients. At the same time HRV parameters in ab1-AR-positive patients were significantly different from those in controls (p<0.05). In group II HRV parameters of ab1-AR-positive and ab1-AR-negative patients were significantly lower than in control subjects (p<0.05). We suppose, that ab1-AR could participate in dysfunction of chronotropic heart regulation and contribute to development of arrhythmias in patients with structurally normal hearts. |
9,618 | Beta1-Adrenergic receptor antagonism abrogates cardioprotective effects of intermittent hypoxia.<Pagination><StartPage>436</StartPage><EndPage>446</EndPage><MedlinePgn>436-46</MedlinePgn></Pagination><Abstract><AbstractText>Adaptation to hypoxia lessens myocardial ischemic injury. This study tested whether hypoxia-induced beta-adrenergic activity mobilizes mechanisms that protect myocardium during subsequent ischemia and reperfusion. Dogs were intermittent hypoxia conditioned (IHC) by a 20 days program of 5-8 daily, 5-10 min cycles of normobaric hypoxia (FIO2 = 9.5-10%), or sham conditioned with normoxic air, and metoprolol (beta1-adrenoceptor antagonist) was administered throughout the IHC program. Twenty-four hours after the last IHC session, the left anterior descending coronary artery (LAD) was occluded for 60 min, and then reperfused for 5 h. Area at risk (AAR) and infarct size (IS) were measured. IHC lowered IS/AAR from 38+/-6% in sham-conditioned dogs to 1.1+/-0.3%, and eliminated ventricular tachycardia (VT) and fibrillation (VF) that occurred in 14 of 17 non-conditioned dogs. Metoprolol blunted IHC-evoked cardioprotection (IS/AAR=27+/-3%), and VT and/or VF occurred in 5 of 6 dogs. Metoprolol did not exacerbate ischemic injury in sham-conditioned dogs (IS/AAR=38+/-2%). Neither IHC nor metoprolol affected hematocrit or LAD collateral blood flow. A single IHC session failed to protect ischemic myocardium (IS/AAR = 36+/-8%), and protection was incomplete after 10 days of IHC (IS/AAR = 13+/-5%), suggesting that de novo protein synthesis was required for protection. Thus, episodic beta1-adrenergic activation during IHC evokes progressive development of powerful resistance to myocardial ischemia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>Robert T</ForeName><Initials>RT</Initials><AffiliationInfo><Affiliation>Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA. malletr@hsc.unt.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ryou</LastName><ForeName>Myoung-Gwi</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Arthur G</ForeName><Initials>AG</Initials><Suffix>Jr</Suffix></Author><Author ValidYN="Y"><LastName>Howard</LastName><ForeName>Linda</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Downey</LastName><ForeName>H Fred</ForeName><Initials>HF</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL 071684</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>05</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Basic Res Cardiol</MedlineTA><NlmUniqueID>0360342</NlmUniqueID><ISSNLinking>0300-8428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058671">Adrenergic beta-1 Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000319">Adrenergic beta-Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006454">Hemoglobins</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D058671" MajorTopicYN="Y">Adrenergic beta-1 Receptor Antagonists</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000319" MajorTopicYN="N">Adrenergic beta-Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003097" MajorTopicYN="N">Collateral Circulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003326" MajorTopicYN="N">Coronary Circulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006400" MajorTopicYN="N">Hematocrit</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006454" MajorTopicYN="N">Hemoglobins</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019157" MajorTopicYN="Y">Ischemic Preconditioning, Myocardial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>3</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>4</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>2</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>5</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16705468</ArticleId><ArticleId IdType="doi">10.1007/s00395-006-0599-y</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16705224</PMID><DateCompleted><Year>2006</Year><Month>07</Month><Day>17</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>133</Issue><PubDate><Year>2006</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal>[Heart arrhythmias and congestive heart failure]. | Adaptation to hypoxia lessens myocardial ischemic injury. This study tested whether hypoxia-induced beta-adrenergic activity mobilizes mechanisms that protect myocardium during subsequent ischemia and reperfusion. Dogs were intermittent hypoxia conditioned (IHC) by a 20 days program of 5-8 daily, 5-10 min cycles of normobaric hypoxia (FIO2 = 9.5-10%), or sham conditioned with normoxic air, and metoprolol (beta1-adrenoceptor antagonist) was administered throughout the IHC program. Twenty-four hours after the last IHC session, the left anterior descending coronary artery (LAD) was occluded for 60 min, and then reperfused for 5 h. Area at risk (AAR) and infarct size (IS) were measured. IHC lowered IS/AAR from 38+/-6% in sham-conditioned dogs to 1.1+/-0.3%, and eliminated ventricular tachycardia (VT) and fibrillation (VF) that occurred in 14 of 17 non-conditioned dogs. Metoprolol blunted IHC-evoked cardioprotection (IS/AAR=27+/-3%), and VT and/or VF occurred in 5 of 6 dogs. Metoprolol did not exacerbate ischemic injury in sham-conditioned dogs (IS/AAR=38+/-2%). Neither IHC nor metoprolol affected hematocrit or LAD collateral blood flow. A single IHC session failed to protect ischemic myocardium (IS/AAR = 36+/-8%), and protection was incomplete after 10 days of IHC (IS/AAR = 13+/-5%), suggesting that de novo protein synthesis was required for protection. Thus, episodic beta1-adrenergic activation during IHC evokes progressive development of powerful resistance to myocardial ischemia.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>Robert T</ForeName><Initials>RT</Initials><AffiliationInfo><Affiliation>Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA. malletr@hsc.unt.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ryou</LastName><ForeName>Myoung-Gwi</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Arthur G</ForeName><Initials>AG</Initials><Suffix>Jr</Suffix></Author><Author ValidYN="Y"><LastName>Howard</LastName><ForeName>Linda</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Downey</LastName><ForeName>H Fred</ForeName><Initials>HF</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL 071684</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>05</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Basic Res Cardiol</MedlineTA><NlmUniqueID>0360342</NlmUniqueID><ISSNLinking>0300-8428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058671">Adrenergic beta-1 Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000319">Adrenergic beta-Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006454">Hemoglobins</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D058671" MajorTopicYN="Y">Adrenergic beta-1 Receptor Antagonists</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000319" MajorTopicYN="N">Adrenergic beta-Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003097" MajorTopicYN="N">Collateral Circulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003326" MajorTopicYN="N">Coronary Circulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006400" MajorTopicYN="N">Hematocrit</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006454" MajorTopicYN="N">Hemoglobins</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019157" MajorTopicYN="Y">Ischemic Preconditioning, Myocardial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>3</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>4</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>2</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>5</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16705468</ArticleId><ArticleId IdType="doi">10.1007/s00395-006-0599-y</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16705224</PMID><DateCompleted><Year>2006</Year><Month>07</Month><Day>17</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>133</Issue><PubDate><Year>2006</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal><ArticleTitle>[Heart arrhythmias and congestive heart failure].</ArticleTitle><Pagination><StartPage>41</StartPage><EndPage>44</EndPage><MedlinePgn>41-4</MedlinePgn></Pagination><Abstract>Along with the successful pharmacotherapic achievements in patients with congestive heart failure survival rate in this category of patients still remains unfavourable. Many antiarrhythmic drugs that cause proarrhythmic effect in patients with congestive heart failure, are characterized by narrow therapeutic window of action and their metabolism is usually changed. Patients with ventricular arrhythmias and disturbances of left ventricular function belong to group with elevated risk of sudden death and complex ventricular impairments are predictors of lethal outcome. Use of ACE inhibitors, angiotensin II receptor inhibitors, beta-blockers (in order to control ventricular rhythm during tachycardia) in combination with antiarrythmic drugs increases effectiveness and safety of therapy, lowers degree of congestive heart failure development and improves prognosis of diseases of that kind. Utilization of nonarrhythmic drugs during treatment of arrhythmias including atrial fibrillation, is novel approach in the treatment with antiarhythmic drugs. |
9,619 | Focal pharmacological modulation of atrioventricular nodal conduction via implantable catheter: a novel therapy for atrial fibrillation? | Pharmacological ventricular rate control is an acceptable atrial fibrillation (AF) therapy limited by systemic toxicity. We postulate that focal catheter-based drug delivery into the atrioventricular nodal (AVN) region may effectively control ventricular rate during AF without systemic toxicity. This study evaluated the effects of focally administered acetylcholine on AVN conduction and refractoriness during sinus rhythm and AF.</AbstractText>Canines (n=7) were anesthetized and instrumented to assess cardiac electrophysiology and blood pressure. A custom drug delivery catheter was implanted in the AVN region. Incremental doses of acetylcholine starting at 10 microg/min were infused until complete AV block was achieved. Acetylcholine induced dose-dependent AV block. AF induction and electrophysiology measurements were performed during baseline and acetylcholine-induced first-degree and third-degree AV block. During AF, infusion of acetylcholine decreased ventricular rates from 182+/-32 to 77+/-28 and 28+/-8 bpm (first-degree and third-degree AV block, respectively; P<0.05). At the first-degree AV block dose, AVN effective refractory period increased from 186+/-37 to 282+/-33 ms, and Wenckebach cycle length increased from 271+/-29 to 378+/-58 ms (P<0.05). The first-degree AV block dose prolonged AV and AH intervals by 26% and 23% (P<0.05), whereas AA intervals and blood pressure remained unchanged, demonstrating a local effect. All effects were reversed 20 minutes after infusion was stopped.</AbstractText>Focal acetylcholine delivery into the AVN increased AVN refractoriness and significantly decreased ventricular rate response during induced AF in a dose-related, reversible manner without systemic side effects. This may represent a novel therapy for AF whereby ventricular rate is controlled with the use of an implantable drug delivery system.</AbstractText> |
9,620 | Transvenous pacing leads and systemic thromboemboli in patients with intracardiac shunts: a multicenter study. | The risk of systemic thromboemboli associated with transvenous leads in the presence of an intracardiac shunt is currently unknown.</AbstractText>To define this risk, we conducted a multicenter, retrospective cohort study of 202 patients with intracardiac shunts: Sixty-four had transvenous leads (group 1), 56 had epicardial leads (group 2), and 82 had right-to-left shunts but no pacemaker or implantable cardioverter defibrillator leads (group 3). Patient-years were accrued until the occurrence of systemic thromboemboli or study termination. Censoring occurred in the event of complete shunt closure, death, or loss to follow-up. Mean ages for groups 1, 2, and 3 were 33.9+/-18.0, 22.2+/-12.6, and 22.9+/-15.0 years, respectively. Respective oxygen saturations were 91.2+/-9.1%, 88.1+/-8.1%, and 79.7+/-6.7%. During respective median follow-ups of 7.3, 9.3, and 17.0 years, 24 patients had at least 1 systemic thromboembolus: 10 (15.6%), 5 (8.9%), and 9 (11.0%) in groups 1, 2, and 3, respectively. Univariate risk factors were older age (hazard ratio [HR], 1.05; P=0.0001), ongoing phlebotomy (HR, 3.1; P=0.0415), and an transvenous lead (HR, 2.4; P=0.0421). In multivariate, stepwise regression analyses, transvenous leads remained an independent predictor of systemic thromboemboli (HR, 2.6; P=0.0265). In patients with transvenous leads, independent risk factors were older age (HR, 1.05; P=0.0080), atrial fibrillation or flutter (HR, 6.7; P=0.0214), and ongoing phlebotomy (HR, 14.4; P=0.0349). Having had aspirin or warfarin prescribed was not protective. Epicardial leads were, however, associated with higher atrial (P=0.0407) and ventricular (P=0.0270) thresholds and shorter generator longevity (HR, 1.9; P=0.0176).</AbstractText>Transvenous leads incur a >2-fold increased risk of systemic thromboemboli in patients with intracardiac shunts.</AbstractText> |
9,621 | [Conventional surgery for congestive heart failure]. | Congestive heart failure is a major public health problem in western countries. Although substantial efforts have been made in the last decades in the prevention, diagnosis and treatment of cardiovascular disease, the incidence of end-stage dilated cardiomyopathy is still increasing. Heart transplantation represents the most effective therapy in this setting, but due to shortage of donors, it remains a realistic option just for a very small number of patients. Therefore, conventional surgical treatment for end-stage heart disease has gained increasing attention in recent years and a variety of surgical interventions have been improved or optimized to manage the multifactorial pathophysiology of the heart failure picture. The aim of this review is to report our experience with more than 500 patients with advanced dilated cardiomyopathy, treated with conventional surgical procedures such as myocardial revascularization, left ventricular restoration, mitral valve repair and surgical ablation of atrial fibrillation. Indications, results, controversial issues and future perspectives will be discussed. |
9,622 | [Recurrent cardiac arrest due to electro-mechanical dissociation in a patient with variant angina -- a case report]. | We present a case of a 44-year-old male with recurrent episodes of cardiac arrest in the course of Prinzmetal's angina. Episodes of variant angina can be life threatening due to episodes of advanced atrioventricular block, asystole, ventricular tachycardia or ventricular fibrillation. It has been suggested to implant an ICD in all patients with variant angina after cardiac arrest. This patient received an ICD, however, he died suddenly 6 months later. The possible mechanism of cardiac arrest was an electromechanical dissociation. |
9,623 | Tachyarrhythmias in percutaneous coronary interventions. | Accompanying the clear benefits, there are certain risks of tachyarrhythmias in percutaneous coronary interventions (PCI), including serious ventricular arrhythmias and atrial fibrillation (AF). Ventricular arrhythmias may result from excess catheter manipulation, intracoronary dye injection, new ischemic events, or reperfusion. In patients with heart failure such kind of arrhythmias can occur more frequently. Atrial dysfunction, sino-atrial and nodal ischemia, congestive heart failure, sympathetic stimulation, iatrogenic factors are the possible causes of AF especially in patients undergoing primary PCI. Atrial fibrillation, on the other hand, can cause clinical squeal in the setting of a rapid ventricular response or if the loss of atrial systole results in hypotension, as in a patient with mitral stenosis or diastolic ventricular dysfunction. Majority of the ventricular arrhythmias and AF tend to revert spontaneously. However, the special treatment must be given, when necessary. |
9,624 | Cellular basis for trigger and maintenance of ventricular fibrillation in the Brugada syndrome model: high-resolution optical mapping study. | We examined how repolarization and depolarization abnormalities contribute to the development of extrasystoles and subsequent ventricular fibrillation (VF) in a model of the Brugada syndrome.</AbstractText>Repolarization and depolarization abnormalities have been considered to be mechanisms of the coved-type ST-segment elevation (Brugada-electrocardiogram [ECG]) and development of VF in the Brugada syndrome.</AbstractText>We used high-resolution (256 x 256) optical mapping techniques to study arterially perfused canine right ventricular wedges (n = 20) in baseline and in the Brugada-ECG produced by administration of terfenadine (5 micromol/l), pinacidil (2 micromol/l), and pilsicainide (5 micromol/l). We recorded spontaneous episodes of phase 2 re-entrant (P2R)-extrasystoles and subsequent self-terminating polymorphic ventricular tachycardia (PVT) or VF under the Brugada-ECG condition and analyzed the epicardial conduction velocity and action potential duration (APD) restitutions in each condition.</AbstractText>Forty-one episodes of spontaneous P2R-extrasystoles in the Brugada-ECG were successfully mapped in 9 of 10 preparations, and 33 of them were originated from the maximum gradient of repolarization (GR(max): 176 +/- 54 ms/mm) area in the epicardium, leading to PVT (n = 12) or VF (n = 5). The epicardial GR(max) was not different between PVT and VF. Wave-break during the first P2R-extrasystole produced multiple wavelets in all VF cases, whereas no wave-break or wave-break followed by wave collision and termination occurred in PVT cases. Moreover, conduction velocity restitution was shifted lower and APD restitution was more variable in VF cases than in PVT cases.</AbstractText>Steep repolarization gradient in the epicardium but not endocardium develops P2R-extrasystoles in the Brugada-ECG condition, which might degenerate into VF by further depolarization and repolarization abnormalities.</AbstractText> |
9,625 | Atrial fibrillation and risk of clinical events in chronic heart failure with and without left ventricular systolic dysfunction: results from the Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) program. | We assessed the risk of adverse cardiovascular (CV) outcomes associated with atrial fibrillation (AF) in the Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) program, which enrolled patients with chronic heart failure (CHF) and a broad range of ejection fractions (EFs).</AbstractText>Atrial fibrillation is associated with an increased risk of adverse CV outcomes in patients with CHF and reduced EF. The risk of AF in patients with CHF and preserved left ventricular ejection fraction (PEF) is unknown.</AbstractText>A total of 7,599 patients with symptomatic CHF were randomized to candesartan or placebo. Patients were divided by baseline EF (< or =40% or >40%) in low or preserved EF groups. Major outcomes were cardiovascular death or hospitalization for worsening heart failure, and all-cause mortality. Median follow-up was 37.7 months.</AbstractText>A total of 670 (17%) patients in the low EF group and 478 (19%) in the PEF group had AF at baseline. Atrial fibrillation predicted a high risk of cardiovascular morbidity and mortality regardless of baseline EF. Patients with AF and low EF had the highest absolute risk for adverse CV outcomes. However, AF was associated with greater relative increased risk of the major outcomes in patients with PEF than in patients with low EF: hazard ratio 1.72 (95% confidence interval [CI] 1.45 to 2.06) versus 1.29 (95% CI 1.14 to 1.46), respectively. The same was true for the risk of all-cause mortality. Candesartan was associated with similar treatment effects regardless of baseline rhythm.</AbstractText>Atrial fibrillation is associated with an increased risk of CV outcomes in patients with CHF and either reduced EF or PEF. Candesartan improved outcomes similarly regardless of baseline rhythm.</AbstractText> |
9,626 | Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. | The aim of our study was to evaluate the feasibility, the safety, and hemodynamic improvements induced by permanent para-Hisian pacing in patients with chronic atrial fibrillation and narrow QRS who underwent atrioventricular (AV) node ablation.</AbstractText>Right ventricular apical pacing, inducing asynchronous ventricular contraction, may impair cardiac function; permanent para-Hisian pacing could preserve interventricular synchrony and improve left ventricular function.</AbstractText>After AV node ablation, 16 patients were implanted with a dual-chamber pacemaker connected to a screw-in lead positioned in close proximity to the His bundle and to a right ventricular apical lead. Clinical and echocardiographic data were collected at baseline and after two randomized six-month periods (with para-Hisian and conventional pacing).</AbstractText>During para-Hisian pacing, the interventricular electromechanical delay improved as well (34 +/- 18 ms) as during right apical pacing (47 +/- 19 ms), p < 0.05. Para-Hisian pacing allowed an improvement in New York Heart Association functional class (1.75 +/- 0.4 vs. 2.33 +/- 0.6 at baseline and 2.5 +/- 0.4 during apical pacing, p < 0.05 for both), in quality-of-life score (16.2 +/- 8.7 vs. 32.5 +/- 15.0 at baseline, p < 0.05), and in the 6-min walk test (431 +/- 73 m vs. 378 +/- 60 m at baseline and 360 +/- 71 m during apical pacing, p < 0.5 for both). Mitral and tricuspid regurgitation improved during para-Hisian pacing (1.22 +/- 0.8 and 1.46 +/- 0.5 index, respectively, vs. 1.68 +/- 0.6 [p < 0.05] and 1.62 +/- 0.7 [p = NS] index at baseline, respectively), with a slight worsening during apical pacing (1.93 +/- 1 and 1.93 +/- 0.7 index, respectively, p < 0.05 for both).</AbstractText>Permanent para-Hisian pacing is feasible and safe. Compared with conventional right apical pacing, it allows an improvement in functional and hemodynamic parameters over long-term follow-up.</AbstractText> |
9,627 | Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: the Homburg Biventricular Pacing Evaluation (HOBIPACE). | The Homburg Biventricular Pacing Evaluation (HOBIPACE) is the first randomized controlled study that compares the biventricular (BV) pacing approach with conventional right ventricular (RV) pacing in patients with left ventricular (LV) dysfunction and a standard indication for antibradycardia pacing in the ventricle.</AbstractText>In patients with LV dysfunction and atrioventricular block, conventional RV pacing may yield a detrimental effect on LV function.</AbstractText>Thirty patients with standard indication for permanent ventricular pacing and LV dysfunction defined by an LV end-diastolic diameter > or =60 mm and an ejection fraction < or =40% were included. Using a prospective, randomized crossover design, three months of RV pacing were compared with three months of BV pacing with regard to LV function, N-terminal pro-B-type natriuretic peptide (NT-proBNP) serum concentration, exercise capacity, and quality of life.</AbstractText>When compared with RV pacing, BV stimulation reduced LV end-diastolic (-9.0%, p = 0.022) and end-systolic volumes (-16.9%, p < 0.001), NT-proBNP level (-31.0%, p < 0.002), and the Minnesota Living with Heart Failure score (-18.9%, p = 0.01). Left ventricular ejection fraction (+22.1%), peak oxygen consumption (+12.0%), oxygen uptake at the ventilatory threshold (+12.5%), and peak circulatory power (+21.0%) were higher (p < 0.0002) with BV pacing. The benefit of BV over RV pacing was similar for patients with (n = 9) and without (n = 21) atrial fibrillation. Right ventricular function was not affected by BV pacing.</AbstractText>In patients with LV dysfunction who need permanent ventricular pacing support, BV stimulation is superior to conventional RV pacing with regard to LV function, quality of life, and maximal as well as submaximal exercise capacity.</AbstractText> |
9,628 | Modelling the health benefits and economic implications of implanting dual-chamber vs. single-chamber ventricular pacemakers in the UK. | To estimate the consequences of managing bradycardia due to sinoatrial node disease or atrioventricular block with dual-chamber vs. single-chamber ventricular pacemakers.</AbstractText>A discrete-event simulation was conducted to predict outcomes over 5 years. Patients could develop post-operative complications, clinically relevant pacemaker syndrome leading to replacement of single-chamber with dual-chamber, atrial fibrillation (AF; which if chronic might require anticoagulants) or stroke. Survival, quality-adjusted life years (QALYs), complications, and associated direct medical costs were estimated (2003 British Pounds pounds sterling). Identical patients were simulated after receiving a single-chamber device or a more expensive dual-chamber pacemaker. Probabilities of conditions were obtained from clinical trials. Benefits were discounted at 1.5% and costs at 6%. Post-operative complications increased from 6.4% with single-chamber to 7.7% with dual-chamber but AF decreased (22 vs. 18%) as did clinically relevant pacemaker symptoms (16.8 vs. 0%). Approximately 4300 pounds sterling were accrued per patient over 5 years. Additional health benefits with dual-chamber are achieved at a mean net cost of 43 pounds sterling per patient, leading to 0.09 QALY with a cost-effectiveness ratio of 477 pounds sterling/QALY.</AbstractText>Implanting the costlier device increases the cost of the initial operation; however, this is expected to be offset by a reduction in costs associated with re-operations and AF.</AbstractText> |
9,629 | Indices of electrical and contractile remodeling during atrial fibrillation in man. | Atrial electrical and contractile remodeling have been demonstrated to coincide during atrial fibrillation (AF) in experimental studies. We explored whether electrical and contractile remodeling correlate in man and explored its clinical implications.</AbstractText>Forty-nine patients with persistent AF were studied. Electrical remodeling was assessed noninvasively using spectral analysis to estimate the average fibrillatory rate (AFR). Atrial contractility was assessed by transesophageal echocardiography (TEE) measurement of left atrial appendage outflow velocity (LAAOV).</AbstractText>The AFR was 403+/-43 fibrillations per minute (fpm) and the LAAOV was 0.27+/-0.14 m/s. A significant correlation was found between AFR and LAAOV (r=-0.47, P=0.001). In patients with a LAAOV>or=0.25 m/s, the AFR was 387+/-48 fpm compared to 419+/-31 fpm among patients with LAAOV<0.25 m/s (P<0.01).</AbstractText>This study demonstrates that indices of electrical and contractile remodeling are strongly correlated in persistent AF in man. The interindividual overlap, however, is too large to allow predictions of LAAOV based on fibrillatory frequency alone.</AbstractText> |
9,630 | Automatic implantable cardioverter-defibrillators in Chagas' heart disease patients with malignant ventricular arrhythmias.<Pagination><StartPage>467</StartPage><EndPage>470</EndPage><MedlinePgn>467-70</MedlinePgn></Pagination><Abstract><AbstractText>A total of 46 consecutive Chagas' disease patients had an automatic cardioverter defibrillator implanted at our institution from October 1998 to January 2004. A retrospective longitudinal study was carried out to identity type of life-threatening ventricular arrhythmias as well as type of therapy delivered. Of these, 41 (91%) had been recovered from cardiac arrest. Five (15%) of 33 patients in whom echocardiography was done had no left ventricular function. Antiarrhythmic therapy was delivered to 37 (80%) patients during postimplant follow-up. Thirty-one of 37 (84%) patients received both shock and antitachycardia pacing, five (13%) only antitachycardia pacing, and one (3%) patient only shock. Median time to first shock was 16 days, varying from 1 to 576 days. Ventricular fibrillation was the cause of first shock in 12 patients (32%), ventricular tachycardia in 11 (29%), and ventricular tachycardia not responding to antitachycardia pacing degenerating into ventricular fibrillation in nine (24%). Five patients with ventricular tachycardia were treated with antitachycardia pacing. Probability of freedom from device discharged was 47% at 90 days, 34% at 180 days, and 9% at 360 days in the postimplant follow-up. Thus, patients with chronic Chagas' heart disease recovered from cardiac arrest have a peculiar arrhythmogenic profile characterized by a high frequency of ventricular fibrillation and no left ventricular systolic dysfunction and a short period of time for first shock.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cardinalli-Neto</LastName><ForeName>Augusto</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology and Cardiovascular Surgery, Hospital de Base, Sâo José do Rio Preto Medical School, São José do Rio Preto city, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Greco</LastName><ForeName>Osvaldo T</ForeName><Initials>OT</Initials></Author><Author ValidYN="Y"><LastName>Bestetti</LastName><ForeName>Reinaldo B</ForeName><Initials>RB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pacing Clin Electrophysiol</MedlineTA><NlmUniqueID>7803944</NlmUniqueID><ISSNLinking>0147-8389</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002598" MajorTopicYN="N">Chagas Cardiomyopathy</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017147" MajorTopicYN="N">Defibrillators, Implantable</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="Y">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018572" MajorTopicYN="N">Disease-Free Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>10</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>5</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16689840</ArticleId><ArticleId IdType="doi">10.1111/j.1540-8159.2006.00377.x</ArticleId><ArticleId IdType="pii">PACE377</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16689089</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>1-2</Issue><PubDate><Year>2006</Year><Season>Jan-Sep</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal>[Indices of excitation in different heart region: age-related pecularities and sensitivity (according to magnetocardiography data]. | A total of 46 consecutive Chagas' disease patients had an automatic cardioverter defibrillator implanted at our institution from October 1998 to January 2004. A retrospective longitudinal study was carried out to identity type of life-threatening ventricular arrhythmias as well as type of therapy delivered. Of these, 41 (91%) had been recovered from cardiac arrest. Five (15%) of 33 patients in whom echocardiography was done had no left ventricular function. Antiarrhythmic therapy was delivered to 37 (80%) patients during postimplant follow-up. Thirty-one of 37 (84%) patients received both shock and antitachycardia pacing, five (13%) only antitachycardia pacing, and one (3%) patient only shock. Median time to first shock was 16 days, varying from 1 to 576 days. Ventricular fibrillation was the cause of first shock in 12 patients (32%), ventricular tachycardia in 11 (29%), and ventricular tachycardia not responding to antitachycardia pacing degenerating into ventricular fibrillation in nine (24%). Five patients with ventricular tachycardia were treated with antitachycardia pacing. Probability of freedom from device discharged was 47% at 90 days, 34% at 180 days, and 9% at 360 days in the postimplant follow-up. Thus, patients with chronic Chagas' heart disease recovered from cardiac arrest have a peculiar arrhythmogenic profile characterized by a high frequency of ventricular fibrillation and no left ventricular systolic dysfunction and a short period of time for first shock.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cardinalli-Neto</LastName><ForeName>Augusto</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology and Cardiovascular Surgery, Hospital de Base, Sâo José do Rio Preto Medical School, São José do Rio Preto city, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Greco</LastName><ForeName>Osvaldo T</ForeName><Initials>OT</Initials></Author><Author ValidYN="Y"><LastName>Bestetti</LastName><ForeName>Reinaldo B</ForeName><Initials>RB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pacing Clin Electrophysiol</MedlineTA><NlmUniqueID>7803944</NlmUniqueID><ISSNLinking>0147-8389</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002598" MajorTopicYN="N">Chagas Cardiomyopathy</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017147" MajorTopicYN="N">Defibrillators, Implantable</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="Y">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018572" MajorTopicYN="N">Disease-Free Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>10</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>5</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16689840</ArticleId><ArticleId IdType="doi">10.1111/j.1540-8159.2006.00377.x</ArticleId><ArticleId IdType="pii">PACE377</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16689089</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>1-2</Issue><PubDate><Year>2006</Year><Season>Jan-Sep</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal><ArticleTitle>[Indices of excitation in different heart region: age-related pecularities and sensitivity (according to magnetocardiography data].</ArticleTitle><Pagination><StartPage>27</StartPage><EndPage>31</EndPage><MedlinePgn>27-31</MedlinePgn></Pagination><Abstract>Some deterioration of the homogeneity of atrium and ventricular excitement has been noticed by the authors in practically healthy elderly subjects. Patients with ischemic heart disease had significant differencies in above mentioned indices than healthy subjects, with all this the degree of non-homogeneity of atria was greater in patients with atrial fibrillation. A new criterium (delta RT) was proposed to reveal subjects with low possibility of the development of ischemic heart disease. |
9,631 | Clinical practicality and predictive value of transoesophageal echocardiography in early cardioversion of atrial fibrillation. | The objective of this study is to evaluate the feasibility of transoesophageal echocardiography (TOE)-guided cardioversion (CV) of atrial fibrillation (AF) in daily clinical practice.</AbstractText>Transthoracic echocardiography and TOE were performed in 346 consecutive patients with AF lasting longer than 48 h or of unknown duration. If no intracavitary thrombus was found, CV was performed within 24 h of the TOE examination. Anticoagulation with subcutaneous low-molecular-weight heparin and warfarin was always started before CV. Warfarin was continued for at least 1 month after CV. The predictive value of several echocardiographic parameters including peak left atrial appendage emptying velocity (PLAAEV), left ventricular ejection fraction, left atrial diameter, and spontaneous echo contrast for the initial and long-term success of CV were evaluated. Transoesophageal echocardiography revealed no thrombus or other contraindications to CV in 274/346 (79%) patients. Early CV restored normal sinus rhythm or pacemaker rhythm in 90% (246/274) of the patients. One patient (0.3%) had a stroke within 30 days after CV. Peak left atrial appendage emptying velocity was significantly lower in patients with contraindications to early CV (P<0.001). However, neither PLAAEV nor any other echocardiographic parameter predicted the initial success of CV and the maintenance of sinus rhythm during long-term follow-up.</AbstractText>Early TOE-guided CV with short-term anticoagulation is a safe and clinically effective alternative in treatment of AF lasting longer than 48 h or of unknown duration. The initial and long-term success of CV cannot be reliably predicted by echocardiographic parameters.</AbstractText> |
9,632 | Documented exercise-induced cardiac arrest in a paediatric patient with hypertrophic cardiomyopathy. | A paediatric patient with hypertrophic cardiomyopathy (HCM) presented cardiac arrest due to ventricular fibrillation. Ventricular arrhythmias were not induced in an electrophysiological study, but an implantable cardioverter defibrillator (ICD) was implanted. Nine months later, the child experienced a recurrence of cardiac arrest during exercise, which was successfully treated with a defibrillator shock from the device. Analysis of the stored electrograms demonstrated ventricular fibrillation of abrupt onset following sinus tachycardia. The risk factors and the potential mechanism leading to recurrent cardiac arrest in this case are discussed. This report supports implantation of an ICD as a life-saving therapeutic approach not only for adults but also for children with HCM at high risk. |
9,633 | Pro-arrhythmic effects of amiodarone and concomitant rate-control medication. | Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Although pro-arrhythmic effects of amiodarone therapy are rare, the aim of the present study was to identify clinical constellations which may lead to amiodarone-associated pro-arrhythmia.</AbstractText>Sixty-three consecutive patients (pts) (49 males; 64+/-10.3 years; 35 with coronary heart disease, 17 with lone AF) were retrospectively included in this study. All received an oral (92.1%) or i.v. (7.9%) loading dose of amiodarone for the treatment of AF. Cardiac diseases, concomitant medical treatment, and incidence of pro-arrhythmic effects were analysed. Three pts (4.8% of the total population) developed a clinical relevant, polymorphic ventricular tachyarrhythmia, 3-48 h after initiation of amiodarone loading. Coronary heart disease was present in all of these pts, and in two of them left ventricular ejection fraction was severely reduced. The mean QTc in these pts was only slightly prolonged; mean heart rate was significantly decreased compared with the total study population (61.0+/-7.5 vs. 74.5+/-24.1 bpm; P < or = 0.05). In all pts with pro-arrhythmia, amiodarone (two pts i.v., one patient oral) was initiated during concomitant beta-blocker/digitalis therapy. Twenty-five per cent of the patients receiving this 'triple' therapy developed ventricular arrhythmia.</AbstractText>The present study implies that initiation of amiodarone therapy in pts with structural heart disease and AF that are concomitantly treated with beta-blockers and digitalis may have an increased risk of amiodarone-associated pro-arrhythmia.</AbstractText> |
9,634 | The role of late I and antiarrhythmic drugs in EAD formation and termination in Purkinje fibers. | Multiple components of cardiac Na current play a role in determining electrical excitation in the heart. Recently, the role of nonequilibrium components in controlling cardiac action potential plateau duration, and their importance in regulating the occurrence of afterdepolarizations and arrhythmias have garnered more attention. In particular, late Na current (late I(Na)) has been shown to be important in LQT2 and LQT3 arrhythmias. Class III agents like dofetilide, clofilium, and sotalol, which can all cause a drug-induced form of LQT2, significantly lengthen action potential duration at 50% and 90% repolarization in isolated rabbit Purkinje fibers, and can initiate the formation of early afterdepolarizations, and extra beats. These actions can lead to the development of a serious ventricular tachycardia, torsades de pointes, in animal models and patients. However, pretreatment with agents that block late I(Na), like lidocaine, mexiletine, and RSD1235, a novel mixed ion channel blocker for the rapid pharmacologic conversion of atrial fibrillation, significantly attenuates the prolonging effects of Class III agents or those induced by ATX-II, a specific toxin that delays Na channel inactivation and amplifies late I(Na) greatly, mimicking LQT3. The Na channel block caused by lidocaine and RSD1235 can be through the open or inactivated states of the channel, but both equivalently inhibit a late component of Na current (I(Na)), recorded at 22 degrees C using whole-cell patch clamp of Nav 1.5 expressed in HEK cells. These protective actions of lidocaine, mexiletine, and RSD1235 may result, at least in part, from their ability to inhibit late I(Na) during action potential repolarization, and inhibition of the inward currents contributing to EAD and arrhythmia formation. |
9,635 | Familial Wolff-Parkinson-White Syndrome: a disease of glycogen storage or ion channel dysfunction? | Wolff-Parkinson-White (WPW) syndrome is the most common cause of ventricular pre-excitation, a condition where, due to defects in the conduction pathway, all or part of the ventricle is excited earlier than would normally be expected, often leading to ventricular fibrillation and sudden cardiac death. It was recently discovered that many of the underlying mutations responsible for the familial form of WPW syndrome are located in the gene encoding for the regulatory gamma(2)-subunit (PRKAG2) of the AMP-activated protein kinase. The cellular mechanisms for the observed arrhythmias are currently being studied and may involve glycogen storage with associated hypertrophy as well as alterations in the properties of cardiac ion channels such as voltage-gated sodium channel. It is the aim of this review to discuss our current knowledge of the cellular disturbances underlying the induction of arrhythmias in patients with PRKAG2 mutations. |
9,636 | Cardiac arrest associated with febrile illness due to U.K. acquired Cyclospora cayetanensis. | This report describes a 43 yr old man diagnosed with U.K. acquired cyclospora cayetanensis infection resulting in fever and diarrhoea. In course of the febrile illness, he suffered an out of hospital cardiac arrest. Extensive cardiac investigation including a transthoracic echocardiogram, coronary angiogram, and cardiac electrophysiological studies failed to identify the cause. The possible links between cyclospora infection and cardiac arrest are explored. Fever has been reported as a precipitant for idiopathic ventricular fibrillation in patients with the Brugada syndrome but also rarely in individuals with normal hearts. Clinicians should be aware of a possible link between any febrile illness and potentially fatal ventricular dysrhythmia. |
9,637 | Anomalous LAD and CX artery arising separately from the proximal right coronary artery--a case report of single coronary artery with coronary artery disease. | Coronary artery anomaly has been reported at a rate of 0.6% to 1.3% in routine angiographic series. Moreover, single coronary artery is one of the rarest anomalies among coronary anomalies. Eventhough patients with coronary anomalies are usually asymptomatic, they may also be associated with myocardial ischemia, ventricular fibrillation, syncope, congestive heart failure, and sudden death. In this article, we report a case of single coronary artery anomaly with the left anterior descending (LAD) and left circumflex (LCx) coronary artery arising separately from the proximal right coronary artery. Since the presented case was associated with ischemic heart disease, coronary artery bypass grafting was carried out. He is currently well. |
9,638 | Comparison of the effects of VVI versus DDD pacing on cardiac baroreflex function. | Conventional baroreceptor-heart rate (HR) reflex sensitivity cannot be examined in chronotropically incompetent patients or in pacemaker recipients. However, cardiac baroreceptor reflex sensitivity (BRS)-stroke volume (SV), which is closely and linearly correlated with BRS-HR, may be an alternative in that population. The aim of this study was to compare the BRS-SV in pacemaker recipients with a fixed HR paced in VVI versus DDD modes in the supine and upright positions.</AbstractText>The pacing mode was set randomly to DDD or VVI with complete atrial and/or ventricular capture, then crossed over to the alternate mode in 9 recipients of dual-chamber pacemakers with atrioventricular (AV) block. Beat-to-beat mean blood pressure and SV were measured in the supine and upright positions, using a tilt table. The BRS-SV, expressed in %/mmHg, was the ratio of low-frequency (LF) power to total power (TP) of SV variability, measured by spectral analysis of spontaneous variations in mean blood pressure and SV.</AbstractText>BRS-SV was significantly lower in the VVI than in the DDD mode in the supine (37.2 +/- 26.7 vs 14.5 +/- 7.7%/mmHg) and upright (22.9 +/- 16.9 vs 10.6 +/- 6.6%/mmHg) positions (P < 0.05 for both comparisons).</AbstractText>VVI pacing is adverse from the standpoint of cardiac autonomic baroreflex function. A decreased BRS-SV may be one of the factors involved in the hemodynamic intolerance associated with VVI pacing.</AbstractText> |
9,639 | Results of the multicenter RENEWAL 3 AVT clinical study of cardiac resynchronization defibrillator therapy in patients with paroxysmal atrial fibrillation. | Atrial fibrillation impacts the clinical course of up to 50% of patients with advanced heart failure (HF) who are eligible for cardiac resynchronization therapy with a defibrillator (CRT-D). While RV-based defibrillators are available with advanced atrial diagnostics and therapies that provide rapid diagnosis and treatment of spontaneously occurring atrial tachycardia/fibrillation (AT/AF) episodes, there is no CRT-D device that combines atrial/ventricular and CRT therapies.</AbstractText>The purpose of the prospective multicenter RENEWAL 3 AVT study is to assess the performance of atrial diagnostics and therapies used in combination with a CRT-D device.</AbstractText>Enrolled patients were required to have indications for a CRT-D device and a documented episode of AT/AF within 12 months of enrollment. A total of 170 patients were enrolled over 9 months (85% male; mean age 72 +/- 10 years; NYHA classification: 88% III, 12% IV; left ventricular ejection fraction [LVEF] mean 23 +/- 6%; mean QRS duration 150 +/- 25 msec; 78% ischemic etiology). The documented atrial arrhythmia was AF in 77% of patients. A total of 60% of patients had the CRT-D device placed for primary prevention of sudden death and 40% of patients had a history of ventricular arrhythmia in addition to HF. The device operates in the biventricular (BiV) triggered mode for sensed ventricular events associated with AF.</AbstractText>A total of 159 patients (95%) had a successful CRT-D implant. Over a mean follow-up of 5.7 +/- 2.3 months, there were a total of 152 atrial shocks delivered in 108 patients for induced (93%) or spontaneous (7%) occurring episodes of AF. Spontaneously occurring AF was observed in 40 patients (25%). The rate of first shock conversion was 118/152 (78%, mean energy 11.6 +/- 5.9 J). Overall shock therapy conversion rate was 138/152 (91%). The number of shock conversions resulting in sinus rhythm maintained for at least 2 minutes postshock was 87% for induced episodes. Therapy was delivered for spontaneous ventricular tachycardia/fibrillation in nine patients (6%). There was no instance of ventricular proarrhythmia associated with atrial shock therapies, undersensing of ventricular arrhythmias, or interruption of CRT therapy associated with the combined device.</AbstractText>In CRT-D candidates with a history of AF, 25% experience recurrent AF within 6 months of implant. Atrial detection and ventricular detection, shock, and resynchronization therapies are not compromised by the addition of atrial therapies to a CRT-D device.</AbstractText> |
9,640 | Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome. | Our objective in this study was to evaluate Tpeak-Tend interval (Tp-e) and other electrocardiographic parameters as risk factors for recurrence of life-threatening cardiac events in patients with the Brugada syndrome (BS).</AbstractText>The Tp-e interval in the electrocardiogram (ECG) has been reported to predict life-threatening arrhythmias in the long QT syndrome.</AbstractText>Twenty-nine patients with the ECG pattern of BS and 29 healthy age- and gender-matched controls were studied. The follow-up period was 42.65 +/- 24.42 months (range 11 to 108 months).</AbstractText>Upon presentation, five patients had suffered aborted sudden death, five syncope, and two presyncope. Eleven patients with the ECG pattern of BS had a prolonged (>460 ms) QTc in V2 but usually not in inferior or left leads. No patient had abnormally prolonged QT dispersion. Programmed electrical stimulation induced ventricular tachycardia/fibrillation in 5 out of 26 patients. Inducibility did not predict recurrence of events. Cardioverter-defibrillators were implanted in 14 patients (all symptomatic and two asymptomatic). During follow-up, nine symptomatic patients experienced recurrences. Previous cardiac events and a QTc >460 ms in V2 were significant risk factors (p = 0.00002 and p = 0.03, respectively). Tp-e and Tp-e dispersion were significantly prolonged in patients with recurrences versus patients without events (104.4 and 35.6 ms vs. 87.4 and 23.2 ms; p = 0.006 and p = 0.03, respectively) or controls (90.7 and 17.9 ms; p = 0.02 and p = 0.001, respectively).</AbstractText>Our study demonstrates significant correlation between previous events, QTc >460 ms in V2, Tp-e, and Tp-e dispersion and occurrence of life-threatening arrhythmic events, suggesting that these parameters may be useful in risk stratification of patients with the Brugada syndrome.</AbstractText> |
9,641 | Preoperative C-reactive protein is predictive of long-term outcome after coronary artery bypass surgery. | Increased levels of C-reactive protein (CRP) are associated with the presence and severity of atherosclerosis, and with increased risk of coronary events as well as of cardiac events after coronary percutaneous intervention.</AbstractText>We have investigated whether preoperative CRP had an impact on the long-term outcome of 843 patients who underwent on-pump coronary artery bypass surgery (CABG).</AbstractText>Among operative survivors, patients with preoperative CRP < 1.0 mg/dL had significantly better 12-year overall survival rate (74.1% vs 63.0%, p = 0.004) and survival freedom from fatal cardiac event (86.7% vs 78.1%). Multivariate analysis including patients' age, extracardiac arteriopathy, urgent/emergent operation, recent myocardial infarction, congestive heart failure, left ventricular ejection fraction, atrial fibrillation, transient ischemic attack/stroke, number of distal anastomoses, diabetes, and preoperative CRP > or = 1.0 mg/dL or <1.0 mg/dL, showed that the latter was an independent predictor of late all-cause mortality (p = 0.017, RR 1.60, 95% CI 1.09-2.35). Its impact on overall survival was particularly evident in patients with left ventricular ejection fraction <50% (CRP < 1.0 mg/dL: 58.7% vs CRP > or = 1.0 mg/dL: 43.7%, p < 0.00001).</AbstractText>Increased preoperative levels of CRP are associated with significantly decreased overall survival after primary on-pump CABG.</AbstractText> |
9,642 | Inappropriate ICD discharge due to T-wave oversensing in a patient with the Brugada syndrome. | Accurate sensing is an essential requirement for appropriate functioning of implantable cardioverter-defibrillator (ICD). T-wave oversensing remains as an annoying problem in currently available ICD. The Brugada syndrome with its inherent dynamic variations in electrophysiologic phenomena may complicate ICD therapy. We report a patient with diagnosis of Brugada syndrome who presented with frequent inappropriate therapy due to intermittent T-wave oversensing. This problem could not be eliminated by device reprogramming and necessitated implantation of a new sense/pace lead. |
9,643 | Vulnerable window for conduction block in a one-dimensional cable of cardiac cells, 2: multiple extrasystoles. | Unidirectional conduction block of premature extrasystoles can lead to initiation of cardiac reentry, causing lethal arrhythmias including ventricular fibrillation. Multiple extrasystoles are often more effective at inducing unidirectional conduction block and reentry than a single extrasystole. Since the substrate for conduction block is spatial dispersion of refractoriness, in this study we investigate how the first extrasystole modulates this dispersion to influence the "vulnerable window" for conduction block by subsequent extrasystoles, particularly in relation to action potential duration restitution and conduction velocity restitution properties. Using a kinematic model to represent wavefront-waveback interactions and simulations with the Luo-Rudy model in a one-dimensional cable of cardiac cells, we show that in homogeneous tissue, a premature extrasystole can create a large dispersion of refractoriness leading to conduction block of a subsequent extrasystole. In heterogeneous tissue, however, a premature extrasystole can either reduce or enhance the dispersion of refractoriness depending on its propagation direction with respect to the previous beat. With multiple extrasystoles at random coupling intervals, vulnerability to conduction block is proportional to their number. In general, steep action potential duration restitution and broad conduction velocity restitution promote dispersion of refractoriness in response to multiple extrasystoles, and thus enhance vulnerability to conduction block. These restitution properties also promote spatially discordant alternans, a setting which is particularly prone to conduction block. The equivalent dispersion of refractoriness created dynamically in homogeneous tissue by spatially discordant alternans is more likely to cause conduction block than a comparable degree of preexisting dispersion in heterogeneous tissue. |
9,644 | Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs. | A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest.</AbstractText>After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15 min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure-right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)-intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman's Repeated Measures Analysis.</AbstractText>ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9+/-0.6 mmHg versus -3+/-0.3 mmHg, p<0.001), diastolic right atrial pressure (DRAP) (-0.1+/-0.2 mmHg versus 2.3+/-0.2 mmHg, p<0.001) and intracranial pressure (20.8+/-0.6 mmHg versus 23+/-0.5 mmHg, respectively, p=0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO(2)), (p<0.001). Common carotid artery blood flow was increased by an average of 70%, p<0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p=0.3.</AbstractText>ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15 min without any compromise in oxygenation.</AbstractText> |
9,645 | n-3 Fatty acids, cardiac arrhythmia and fatal coronary heart disease. | n-3 Polyunsaturated fatty acids (n-3 PUFA) are suggested to prevent cardiac death via inhibition of cardiac arrhythmia. In this review we discuss the results of human studies on intake of n-3 PUFAs and heart disease and, more specifically, on cardiac arrhythmia. Observational studies indicate that intake of fish is associated with a lower incidence of fatal coronary heart disease in several populations. These studies are fairly consistent, but people that have a high intake of fatty fish might have a healthier lifestyle in general, and such confounding is difficult to remove completely with statistical adjustments and corrections. Evidence from trials is less clear. In two open label trials in patients with a previous myocardial infarction intake of fish or fish oil prevented fatal coronary heart disease. In contrast, a trial in patients with angina suggested a higher risk of sudden cardiac death in patients taking fish oil. Furthermore, results of trials in patients with an implantable cardioverter defibrillator (ICD) that investigated effects of fish oil on arrhythmia in patients already suffering from ventricular tachycardia are not consistent. Also, studies on relationships between intake of n-3 PUFA from fish and less life-threatening forms of arrhythmia, such as atrial fibrillation and premature ventricular complexes (PVCs) are equivocal. Thus, after 35 years of research the question whether fish prevents heart disease remains unanswered, and an anti-arrhythmic effect of fish oil remains unproven although the idea is still viable and is being actively tested in further trials. |
9,646 | [Vagal effects on inducibility of atrial fibrillation at different sites of pulmonary veins after autonomic denervation]. | To investigate the vagal effects on the inducibility of atrial fibrillation (AF) at different sites of pulmonary vein after autonomic denervation.</AbstractText>The bilateral cervical vagal trunks of 10 male mongrel dogs were isolated and decentralized. The ansae subclaviae were exposed, ligated, and cut. Needle electrodes were inserted into the subcutaneous tissue of the 4 extremities to record the myocardiogram. Right ventricle electrode was introduced via femoral vein and an electrode with 4 poles was sutured with the right appendage (RAA), left appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), right superior pulmonary vein (RSPV), left inferior pulmonary vein (LIPV), and right inferior pulmonary vein (RIPV) respectively. Local burst stimulation (S1S1 = 80 ms, impulse duration = 0.5 ms) was performed on these sites to record the baseline AF inducibility. When sinus cardiac arrest for 2 s or complete atrio-ventricular block occurred programmed bilateral vagal nerves stimulation (VNS) was performed with the frequency of 12.5 Hz, impulse duration of 0.5 ms, and voltage of 5-8 V. Atropine 0.04 mg/kg was dripped intravenously. The changes of AV inducibility were observed.</AbstractText>In the baseline state, S1S1 programmed stimulation on all the sites evoked single or multiple atrial premature beats and short runs of atrial tachycardia, only a few sites induced AF. However, S1S1 programmed stimulation combined with VNS significantly increased the frequencies of induced AV at the sites of 4 PVs (P < 0.05, P < 0.01). When atropine was dripped the AV induction rates at all sites did not changed significantly (all P > 0.05).</AbstractText>Vagal nerve may play an important role in the initiation of AF originating from pulmonary veins.</AbstractText> |
9,647 | Cardiac dysrhythmias during donor care. | Organ procurement coordinators must treat various cardiac dysrhythmias (arrhythmias), including rhythm disturbances that may cause or follow a cardiac arrest, in about 15% to 50% of donors. Treatment decisions should be based on the particular dysrhythmia and its effect on donor blood pressure. Medications selected should be effective but short acting. In this article, data available in publications located through a PubMed search are reviewed and specific dysrhythmias that are likely to occur during donor care are described. Treatment recommendations are based on guidelines from the American Heart Association. |
9,648 | Apical hypertrophic cardiomyopathy and arrhythmia in military pilots. | Apical hypertrophic cardiomyopathy (ApHCM), a subtype of hypertrophic cardiomyopathy, may be found incidentally in healthy young adults. Arrhythmias are poor prognostic signs, and are the most frequent cause of sudden cardiac death. We present two cases of military aviators with ApHCM. One was a high-performance jet weapon system operator, who had asymptomatic non-sustained ventricular tachycardia (NSVT) and subsequently a symptomatic episode of paroxysmal atrial fibrillation. The second was a helicopter pilot, who had asymptomatic NSVT. Both aviators continue their aviation duties without exposure to +Gz under a regime of regular thorough cardiac assessment. |
9,649 | Optical recording-guided pacing to create functional line of block during ventricular fibrillation. | Low-energy defibrillation is very desirable in cardiac rhythm management. We previously reported that ventricular fibrillation (VF) can be synchronized with a novel synchronized pacing technique (SyncP) using low-energy pacing pulses. This study sought to create a line of block during VF using SyncP. SyncP was performed in six isolated rabbit hearts during VF using optical recording to control the delivery of pacing pulses in real time. Four pacing electrodes with interelectrode distances of 5 mm were configured in a line along and across the myocardial fiber direction. The electrodes were controlled independently (independent mode) or fired together (simultaneous mode). Significant wavefront synchronization was observed along the electrode line as indicated by a decrease in variance. With the independent SyncP protocol, the decrease in the variance was 19.3 and 13.7% (P<0.001) for the along-, and across-fiber configurations, respectively. With the simultaneous SyncP protocol, the variance was reduced by 24.2 and 10.7% (P<0.001) in the along- and across-fiber configurations. The effect of synchronization dropped off with distance from the line of pacing. We conclude that SyncP can effectively create a line of functional block that isolates regions of VF propagation. Further optimization of this technique may prove useful for low-energy ventricular defibrillation. |
9,650 | Therapeutic hypothermia after cardiac arrest. | Patients who are successfully resuscitated following cardiac arrest often have a significant medical condition termed postresuscitation disease. This includes myocardial stunning, metabolic abnormalities and neurologic injury from global ischemia. There are no clinical signs or diagnostic tests for 24-72 h to distinguish patients who will and will not recover neurologic function.</AbstractText>Therapeutic hypothermia had been advocated for decades as a treatment to improve neurologic outcome after cardiac arrest. The early studies focused on moderate hypothermia, which was associated with complications and was not clearly beneficial. Over the past decade, studies have focused on mild hypothermia with target temperatures of 32-34 degrees C. Two recent multicentered, randomized, controlled trials have demonstrated improved neurologic outcome with mild therapeutic hypothermia applied to comatose survivors after cardiac arrest compared with a normothermic control group.</AbstractText>As a result of these studies the International Liaison Committee on Resuscitation recommends that 'Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32 degrees C to 34 degrees C for 12 to 24 hours when the initial rhythm was ventricular fibrillation'. Mild therapeutic hypothermia should also be considered for patients with in-hospital arrest and asystole and pulseless electrical activity who are comatose after return of spontaneous circulation.</AbstractText> |
9,651 | Incidence and significance of gasping or agonal respirations in cardiac arrest patients. | This review examines the clinical significance of agonal respirations associated with cardiac arrest.</AbstractText>Observational data indicate that agonal respirations are frequent (55% of witnessed cardiac arrests and probably higher) and that they are associated with successful resuscitation. They also are found more commonly in ventricular fibrillation compared with other rhythms. Agonal respirations pose the greatest challenge to bystanders at the scene and to emergency dispatchers. Bystanders are often lulled into thinking the person is still breathing thus identification of cardiac arrest may be missed by the dispatcher. In a study from King County, Washington, cardiopulmonary resuscitation instructions were not provided by emergency dispatchers in 20% of cardiac arrest cases because the caller reported signs of life - typically abnormal breathing.</AbstractText>Agonal respirations occur frequently in cardiac arrest. Emergency dispatchers and the general public must be more aware of their presence and significance.</AbstractText> |
9,652 | Haemodynamics of cardiac arrest and resuscitation. | This review will summarize the available data regarding the haemodynamic changes occurring following cardiac arrest in humans and animal models.</AbstractText>Following cardiac arrest due to ventricular fibrillation without cardiopulmonary resuscitation, blood flow exponentially falls but continues for approximately 5 min until the pressure gradient between the aorta and the right heart is completely dissipated. During cardiopulmonary resuscitation forward flow occurs into the aorta during the compression phase. Coronary blood flow is retrograde during the compression phase and antegrade during the decompression phase. Carotid blood flow takes over a minute to reach plateau levels following the initiation of chest compressions, and even brief interruptions of compressions result in a dramatic reduction in carotid blood flow which takes a minute or so to recover to plateau levels when compressions are reinstituted. Coronary perfusion pressure during the release phase of cardiopulmonary resuscitation has been shown to be a powerful predictor of the likelihood of recovery of spontaneous circulation following restoration of electrical activity.</AbstractText>Recent studies have provided important insights into the haemodynamics of cardiac arrest and of cardiopulmonary resuscitation which may inform more effective strategies for the management of cardiac arrest in the future.</AbstractText> |
9,653 | [Perioperative management of cardiac arrhythmia: part II]. | Cardiac arrhythmias are an important cause of complications throughout the perioperative period. Although our understanding of arrhythmias has increased considerably in recent years, they remain a source of concern for anesthesiologists. Our objective was to review steps to take when diagnosing arrhythmia. Although treatment is still largely influenced by therapies used in nonsurgical patients, we will review the approaches that are most applicable to practice situations in which anesthesiologists must manage patients with arrhythmias or at high risk of developing them. |
9,654 | What are the etiology and epidemiology of out-of-hospital pediatric cardiopulmonary arrest in Ontario, Canada? | Pediatric cardiopulmonary arrest (CPA) outside of the hospital has a very high mortality rate.</AbstractText>To evaluate the etiology and initial compromise of pediatric CPA cases in hopes of developing strategies to improve out-of-hospital resuscitation.</AbstractText>The Ontario Prehospital Advanced Life Support (OPALS) study was a large multicenter initiative to evaluate the impact of emergency medical services (EMS) programs on 17 communities with 40,000 critically ill and injured patients who were older than 11 years. As part of this study, the authors conducted a retrospective observational cohort study that included all children younger than 18 years of age with out-of-hospital CPA, during an 11-year period from 1991-2002. CPA was defined as patient being pulseless, apneic, and requiring chest compressions. Data were collected from ambulance call reports and centralized dispatch data and were reviewed by two independent investigators.</AbstractText>There were 503 children with CPA in the sample. Mean age was 5.6 years (range, 0-17 yr); 58.4% of patients were male, and 37.8% were younger than 1 year of age. Cardiopulmonary resuscitation (CPR) first was started by a bystander in 32.4% of cases, whereas 66.0% were unwitnessed arrests. Initial rhythms were asystole 77.2% of the time, pulseless electrical activity 16.4% of the time, and ventricular fibrillation or ventricular tachycardia 4% of the time. Annual incidence was 9.1/100,000 children. CPA was witnessed in 34.0% of cases; 80.7% of these were bystander-witnessed, and 18.1% were EMS-witnessed. Primary pathogenic cause of arrest was medical in 61.2% of cases, trauma in 37.2% of cases, and indeterminate in 1.6% of cases. Initial underlying physiologic compromise of witnessed arrests was judged to be respiratory in 39.8% of cases, sudden collapse (presumed electrical) in 16.4% of cases, progressive shock in 1.2% of cases, and indeterminate in 42.6% of cases. Presumed etiology was trauma, 37.6%; sudden infant death syndrome (SIDS), 20.3%; and respiratory disease, 11.6%, most commonly. Survival to hospital discharge was 2.0%.</AbstractText>This is one of the largest population-based, prospective cohorts of pediatric CPA reported to date, and it reveals that most pediatric arrests are unwitnessed and receive no bystander CPR. Those that are witnessed most often are caused by respiratory arrests or trauma. Trauma, SIDS, and respiratory disease are the most common etiologies overall. These data are vital to planning large resuscitation trials looking at specific interventions (i.e., increasing bystander CPR) and highlight the need for better strategies for prevention and early recognition.</AbstractText> |
9,655 | Outcome of watchful waiting in asymptomatic severe mitral regurgitation. | The management of asymptomatic severe mitral regurgitation remains controversial. The aim of this study was to evaluate the outcome of a watchful waiting strategy in which patients are referred to surgery when symptoms occur or when asymptomatic patients develop left ventricular (LV) enlargement, LV dysfunction, pulmonary hypertension, or recurrent atrial fibrillation.</AbstractText>A total of 132 consecutive asymptomatic patients (age 55+/-15 years, 49 female) with severe degenerative mitral regurgitation (flail leaflet or valve prolapse) were prospectively followed up for 62+/-26 months. Patients underwent serial clinical and echocardiographic examinations and were referred for surgery when the criteria mentioned above were fulfilled. Overall survival was not statistically different from expected survival either in the total group or in the subgroup of patients with flail leaflet. Eight deaths were observed. Thirty-eight patients developed criteria for surgery (symptoms, 24; LV criteria, 9; pulmonary hypertension or atrial fibrillation, 5). Survival free of any indication for surgery was 92+/-2% at 2 years, 78+/-4% at 4 years, 65+/-5% at 6 years, and 55+/-6% at 8 years. Patients with flail leaflet tended to develop criteria for surgery slightly but not significantly earlier. There was no operative mortality. Postoperative outcome was good with regard to survival, symptomatic status, and postoperative LV function.</AbstractText>Asymptomatic patients with severe degenerative mitral regurgitation can be safely followed up until either symptoms occur or currently recommended cutoff values for LV size, LV function, or pulmonary hypertension are reached. This management strategy is associated with good perioperative and postoperative outcome but requires careful follow-up.</AbstractText> |
9,656 | 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: pediatric basic life support. | This publication presents the 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of the pediatric patient and the 2005 American Academy of Pediatrics/AHA guidelines for CPR and ECC of the neonate. The guidelines are based on the evidence evaluation from the 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations, hosted by the American Heart Association in Dallas, Texas, January 23-30, 2005. The "2005 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care" contain recommendations designed to improve survival from sudden cardiac arrest and acute life-threatening cardiopulmonary problems. The evidence evaluation process that was the basis for these guidelines was accomplished in collaboration with the International Liaison Committee on Resuscitation (ILCOR). The ILCOR process is described in more detail in the "International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations." The recommendations in the "2005 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care" confirm the safety and effectiveness of many approaches, acknowledge that other approaches may not be optimal, and recommend new treatments that have undergone evidence evaluation. These new recommendations do not imply that care involving the use of earlier guidelines is unsafe. In addition, it is important to note that these guidelines will not apply to all rescuers and all victims in all situations. The leader of a resuscitation attempt may need to adapt application of the guidelines to unique circumstances. The following are the major pediatric advanced life support changes in the 2005 guidelines: There is further caution about the use of endotracheal tubes. Laryngeal mask airways are acceptable when used by experienced providers. Cuffed endotracheal tubes may be used in infants (except newborns) and children in in-hospital settings provided that cuff inflation pressure is kept <20 cm H2O. Confirmation of tube placement requires clinical assessment and assessment of exhaled carbon dioxide (CO2); esophageal detector devices may be considered for use in children weighing >20 kg who have a perfusing rhythm. Correct placement must be verified when the tube is inserted, during transport, and whenever the patient is moved. During CPR with an advanced airway in place, rescuers will no longer perform "cycles" of CPR. Instead, the rescuer performing chest compressions will perform them continuously at a rate of 100/minute without pauses for ventilation. The rescuer providing ventilation will deliver 8 to 10 breaths per minute (1 breath approximately every 6-8 seconds). Timing of 1 shock, CPR, and drug administration during pulseless arrest has changed and now is identical to that for advanced cardiac life support. Routine use of high-dose epinephrine is not recommended. Lidocaine is de-emphasized, but it can be used for treatment of ventricular fibrillation/pulseless ventricular tachycardia if amiodarone is not available. Induced hypothermia (32-34 degrees C for 12-24 hours) may be considered if the child remains comatose after resuscitation. Indications for the use of inodilators are mentioned in the postresuscitation section. Termination of resuscitative efforts is discussed. It is noted that intact survival has been reported following prolonged resuscitation and absence of spontaneous circulation despite 2 doses of epinephrine. The following are the major neonatal resuscitation changes in the 2005 guidelines: Supplementary oxygen is recommended whenever positive-pressure ventilation is indicated for resuscitation; free-flow oxygen should be administered to infants who are breathing but have central cyanosis. Although the standard approach to resuscitation is to use 100% oxygen, it is reasonable to begin resuscitation with an oxygen concentration of less than 100% or to start with no supplementary oxygen (ie, start with room air). If the clinician begins resuscitation with room air, it is recommended that supplementary oxygen be available to use if there is no appreciable improvement within 90 seconds after birth. In situations where supplementary oxygen is not readily available, positive-pressure ventilation should be administered with room air. Current recommendations no longer advise routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born to mothers with meconium staining of amniotic fluid. Endotracheal suctioning for infants who are not vigorous should be performed immediately after birth. A self-inflating bag, a flow-inflating bag, or a T-piece (a valved mechanical device designed to regulate pressure and limit flow) can be used to ventilate a newborn. An increase in heart rate is the primary sign of improved ventilation during resuscitation. Exhaled CO2 detection is the recommended primary technique to confirm correct endotracheal tube placement when a prompt increase in heart rate does not occur after intubation. The recommended intravenous (IV) epinephrine dose is 0.01 to 0.03 mg/kg per dose. Higher IV doses are not recommended, and IV administration is the preferred route. Although access is being obtained, administration of a higher dose (up to 0.1 mg/kg) through the endotracheal tube may be considered. It is possible to identify conditions associated with high mortality and poor outcome in which withholding resuscitative efforts may be considered reasonable, particularly when there has been the opportunity for parental agreement. The following guidelines must be interpreted according to current regional outcomes: When gestation, birth weight, or congenital anomalies are associated with almost certain early death and when unacceptably high morbidity is likely among the rare survivors, resuscitation is not indicated. Examples are provided in the guidelines. In conditions associated with a high rate of survival and acceptable morbidity, resuscitation is nearly always indicated. In conditions associated with uncertain prognosis in which survival is borderline, the morbidity rate is relatively high, and the anticipated burden to the child is high, parental desires concerning initiation of resuscitation should be supported. Infants without signs of life (no heartbeat and no respiratory effort) after 10 minutes of resuscitation show either a high mortality rate or severe neurodevelopmental disability. After 10 minutes of continuous and adequate resuscitative efforts, discontinuation of resuscitation may be justified if there are no signs of life. |
9,657 | T-wave oversensing by an implantable cardioverter defibrillator after successful ablation of idiopathic ventricular fibrillation. | Focal ablation of trigger premature ventricular complexes (PVCs) from the Purkinje system helped to suppress idiopathic ventricular fibrillation (VF) in an athlete who had suffered from frequent appropriate shock therapies. However, only a few days after successful ablation T-wave oversensing occurred during exercise and resulted in repetitive distressing defibrillator shocks. Despite lack of any changes on the surface ECG, the endocardially recorded electrogram revealed an unfavorable ratio of R-to-T-wave amplitude predisposing to double counting with accelerated heart rates. This case illustrates that T-wave oversensing may complicate the clinical course after successful ablation of malignant Purkinje ectopy. |
9,658 | Reduction of RV pacing by continuous optimization of the AV interval. | In patients requiring permanent pacing, preservation of intrinsic ventricular activation is preferred whenever possible. The Search AV+ (SAV+) algorithm in Medtronic EnPulsetrade mark dual-chamber pacemakers can increase atrioventricular (AV) intervals to 320 ms in patients with intact or intermittent AV conduction. This prospective, multicenter study compared the percentage of ventricular pacing with and without AV interval extension.</AbstractText>Among 197 patients enrolled in the study, the percentage of ventricular-paced beats was evaluated via device diagnostics at the 1-month follow-up. Patient cohorts were defined by clinician assessment of conduction via a 1:1 AV conduction test at the 2-week follow-up. The observed percentage of ventricular pacing with SAV + ON and the predicted percentage of ventricular pacing with SAV + OFF were determined from the SAV + histogram data for the period between the 2-week and 1-month follow-up visits.</AbstractText>Of 197 patients, 110 (55.8%) had intact 1:1 AV conduction, of which 109 had 1-month data. SAV + remained ON in 99/109 patients; 10 patients had intrinsic A-V conduction intervals beyond SAV + nominal and therefore SAV + disabled. The mean percentage of ventricular pacing in the 109 patients was SAV+ ON = 23.1% (median 3.7%) versus SAV + OFF = 97.2% (median 99.7%). In 87 patients without 1:1 AV conduction, SAV + was programmed OFF in 6, automatically disabled in 52, and remained ON in 29. In 8 of these patients, 80-100% reduction in ventricular pacing was observed with SAV + ON.</AbstractText>The Search AV+ algorithm in the EnPulse pacemaker effectively promotes intrinsic ventricular activation and substantially reduces unnecessary ventricular pacing.</AbstractText> |
9,659 | Medium-term efficacy of segmental ostial pulmonary vein isolation for the treatment of permanent and persistent atrial fibrillation. | Previous studies suggest that segmental ostial isolation of the pulmonary veins for the treatment of patients with persistent and permanent atrial fibrillation is associated with a high rate of recurrence. Recurrence of atrial fibrillation is usually associated with electrical reconnection of the pulmonary veins to the left atrium.</AbstractText>We examined the efficacy of isolating all four pulmonary veins using an open irrigated tip ablation catheter and multiple procedures, to overcome the problem of electrical reconnection in the veins. Fifty-one patients (59 +/- 10 years, 48 male) with drug resistant and highly symptomatic persistent or permanent atrial fibrillation had their pulmonary veins electrically isolated using mapping guided segmental radiofrequency ablation. Atrial fibrillation had been present for 7.6 +/- 7.3 years, and patients had failed treatment with 2.2 +/- 1.6 antiarrhythmic medications. Thirty-nine percent had structural heart disease.</AbstractText>After a mean of 1.7 +/- 0.9 procedures per patient, 23 patients (45%) were in sinus rhythm (without cardioversion) after 16.9 +/- 9.1 months. Antiarrhythmic medications were required in four of those in sinus rhythm (17%). Recurrences were usually early (median 7 days). Neither age, duration of atrial fibrillation, type of atrial fibrillation, underlying heart disease, left atrial size, left ventricular wall thickness nor the number of failed antiarrhythmic drugs predicted outcomes.</AbstractText>Persistent and permanent atrial fibrillation can be successfully treated using segmental isolation. However, recurrence is common even when all four veins are isolated using an open irrigated tip catheter, and multiple procedures are performed. Alternative techniques are required in this population.</AbstractText> |
9,660 | Blanked atrial flutter in patients with cardiac resynchronization therapy: clinical significance and implications for device programming. | Atrial arrhythmias are frequently observed in patients with heart failure and may be a primary cause for decompensation during cardiac resynchronization therapy (CRT). The accurate detection of organized atrial tachyarrhythmias poses a challenge to the function of mode-switching biventricular pacemakers/defibrillators.</AbstractText>The purpose of the study was to determine retrospectively the incidence of blanked atrial flutter and mode switch failure (2:1 lock-in), and to look for factors predisposing to this problem. A total number of 65 patients with CRT devices has been followed regularly over 18 +/- 12 months. Five patients were excluded because of chronic atrial fibrillation and reprogramming to VVIR mode.</AbstractText>Seven out of 60 patients (12%) were diagnosed with blanked atrial flutter at unscheduled device interrogation. Sustained biventricular pacing at a median rate of 125/min-mimicking sinus tachycardia-resulted in rapid deterioration of heart failure and hospitalization. Mode switch failure occurred due to coincidence of every second flutter wave with atrial blanking. The group with 2:1 lock-in was programmed to longer atrial blanking times (143 +/- 34 ms vs 105 +/- 32 ms; P = 0.026) and AV intervals (126 +/- 8 ms vs 107 +/- 29; P = 0.001) than the group without lock-in. Other clinical characteristics examined did not differ between the two groups apart from a previous history of atrial fibrillation (P = 0.032).</AbstractText>Blanked atrial flutter with rapid ventricular pacing is a clinically important problem in heart failure patients treated with CRT devices. Efforts should be made to avoid this complication by atrial lead implantation without ventricular farfield oversensing, by programming short PVAB and AV intervals, and by implementation of dedicated device algorithms.</AbstractText> |
9,661 | "Torsade de pointes" in patients with structural heart disease and atrial fibrillation treated with amiodarone, beta-blockers, and digitalis. | Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Yet, though rare, proarrhythmic effects remain a clinical problem. We present three cases of amiodarone-associated "Torsade de pointes" tachycardia (Tdp) in patients treated concomitantly with heart rate controlling medication for AF. Amiodarone loading therapy was started for the treatment of tachyarrhythmic AF in all the three patients. All presented with a history of coronary heart disease, resulting in a severely reduced left ventricular ejection fraction in two patients. One received oral amiodarone loading, in the others, amiodarone was administered intravenously because of hemodynamically relevant AF episodes. Amiodarone therapy was combined with a heart rate controlling medication including a beta-blocking agent and digitalis in all the cases. All the subjects suffered from clinically relevant Tdp in the early run after initiation of amiodarone loading (max. 48 hours). The mean QTc in all patients before induction of Tdp was prolonged. The present case reports imply that amiodarone in combination with beta-blocker/digitalis therapy may be associated with an elevated proarrhythmic risk in selected patients with structural heart disease and AF. |
9,662 | Efficacy and safety of ibutilide for the conversion of monomorphic atrial tachycardia. | Ibutilide is a class III antiarrhythmic drug, frequently used for conversion of atrial fibrillation and flutter. We studied the efficacy of ibutilide for acute conversion of monomorphic atrial tachycardia (monoAT) in a prospective, open label study in the intensive care unit of a cardiological clinic.</AbstractText>We examined 49 episodes of monoAT in 38 patients (19 men/19 women). Thirty-three patients (87%) suffered from structural heart disease. Twenty-three episodes occurred while on antiarrhythmic therapy with class I or III drugs. Patients with prolonged QT interval (except for patients with pretreatment with class III drugs), hypokalemia, left ventricular failure, and recent myocardial infarction were excluded. All patients received one or two doses of 1 mg ibutilide fumarate under continuous rhythm monitoring.</AbstractText>Conversion to sinus rhythm occurred in 19 episodes (38.8%), in 6 episodes (12.2%) after the first dose. Conversion rate was significantly higher in patients with a short history of symptoms (66.6% vs 28.6%; P < 0.05), of documented arrhythmia (0.13 (0/5.7) vs 2.6 (0.38/23.5) months, median (interquartile range); P < 0.03), higher atrial rate (272 +/- 49 vs 207 +/- 36 beats/min (means +/- SD); P < 0.004), or without preexisting antiarrhythmic therapy (53.8% vs 21.7%; P < 0.02). No differences in conversion rates were found regarding gender, age, body mass index, left ventricular function, left atrial diameter, or underlying disease. In three episodes torsade de pointes occurred after ibutilide (6.1%), requiring defibrillation in two cases (4.1%).</AbstractText>Ibutilide can be used for conversion of monoAT with a similar efficacy as for atrial fibrillation, but with a considerably lower efficacy compared to typical atrial flutter.</AbstractText> |
9,663 | Assessment of markers of thrombin generation in patients with acute myocardial infarction complicated by ventricular fibrillation. | In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated.</AbstractText>We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias. Levels of thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2 (F1 + 2), fibrinopeptide A (FPA), plasmin-antiplasmin complexes (PAP), protein C, antithrombin, activated partial thromboplastin time (aPTT), thromboplastin time, D-Dimer, fibrinogen, and high-sensitivity C-reactive protein (hs-CRP) were measured in plasma samples of all patients. Blood collection was obtained sequentially in two separate settings. Patients were studied at a median of 351 days after the acute coronary event.</AbstractText>Higher levels of TAT complexes (13.4 +/- 22.2 vs. 3.03 +/- 4.3 microg/l; p = 0.02), FPA (79.7 +/- 132.3 vs. 24.04 +/- 41.3 ng/ml; p = 0.04), and F1+2 (1.89 +/- 1.3 vs. 1.16 +/- 0.5 nmol/l; p = 0.01) were observed in patients with VF compared with patients without ventricular tachyarrhythmias during the acute phase of MI. D-Dimer levels displayed a trend without reaching statistical significance (0.69 +/- 0.48 vs. 0.48 +/- 0.24 mg/l; p = 0.06). No differences were found in hs-CRP (3.25 +/- 4.5 vs. 4.4 +/- 8.8 mg/l; p = 0.5) and fibrinogen (2.8 +/- 0.9 vs. 2.7 +/- 0.9 g/l; p = 0.6) measurements. Repeat assessment of markers of coagulation activation at a median of 847 days revealed a highly significant decrease in patients with VF.</AbstractText>Markers of thrombin generation are transiently increased in patients with VF during the acute phase of MI. These findings have implications for risk assessment and genetic screening of patients prone to VF during acute myocardial ischemia.</AbstractText> |
9,664 | [Mild hypothermia for neuroprotection after cardiac arrest]. | The favorable effect of hypothermia on brain damage resulting from cardiac arrest was first demonstrated in animal studies. Subsequent small-scale human studies have also shown positive effects. In 2002, two large randomized studies investigating the use of controlled mild hypothermia after resuscitation were published in the New England Journal of Medicine. The results convincingly showed a positive effect on survival and neurologic outcome. Based on the currently available data, the International Liaison Committee on Resuscitation (ILCOR) strongly recommends that unconscious adult patients who are resuscitated after ventricular fibrillation be cooled to temperatures between 32 and 34 degrees C for 12-24 h. |
9,665 | T wave alternans in an in vitro canine tissue model of Brugada syndrome. | Macroscopic T wave alternans (TWA) associated with increased occurrence of ventricular arrhythmias has been reported in patients with Brugada syndrome. However, the mechanisms in this syndrome are still unclear. We evaluated the hypothesis that TWA in Brugada syndrome was caused by the dynamic instability and heterogeneity of action potentials (APs) in the right ventricle. Using an optical mapping system, we mapped APs on the epicardium or transmural surfaces of 28 isolated and arterially perfused canine right ventricular preparations having drug-induced Brugada syndrome (in micromol/l: 2.5-15 pinacidil, 5.0 terfenadine, and 5.0-13 pilsicainide). Bradycardia at cycle length (CL) of 2,632 +/- 496 ms (n = 19) induced alternating deep and shallow T waves in the transmural electrocardiogram. Compared with the shallow T waves, deep T waves were associated with epicardial APs having longer durations and larger domes. Adjacent regions having APs with alternating domes, with constant domes, and without domes coexisted simultaneously in the epicardium and caused TWA. In contrast to the alternating epicardial APs, midmyocardial and endocardial APs did not change during TWA. Alternans could be terminated by rapid (CL: 529 +/- 168 ms, n = 7) or very slow (CL: 3,000 ms, n = 7) pacing. The heterogeneic APs during TWA augmented the dispersion of repolarization both within the epicardium and from the epicardium to the endocardium and caused phase 2 reentry. In this drug-induced model of Brugada syndrome, heterogeneic AP contours and dynamic alternans in the dome of right ventricular epicardial, but not midmyocardial or endocardial, APs caused TWA and heightened arrhythmogenicity in part by increasing the dispersion of repolarization. |
9,666 | Characterization of the relationship between preshock state and virtual electrode polarization-induced propagated graded responses resulting in arrhythmia induction. | Studies have demonstrated that failed defibrillation shocks often are followed by an electrically quiescent period (isoelectric window); however, the underlying mechanisms remain incompletely understood. We recently suggested a new mechanism termed "virtual electrode polarization-induced propagated graded responses" (VEPiPGRs) that might play a role in the origin of the global postshock activation following the isoelectric window.</AbstractText>The purpose of this study to elucidate the circumstances under which VEPiPGR activations originate for shocks given to paced right ventricular preparations. Specifically, we examined the dependence of VEPiPGRs on coupling interval (CI) and shock polarity and whether VEPiPGRs emerge preferentially on the epicardium or the endocardium.</AbstractText>Simultaneous endocardial and epicardial activity in isolated right ventricular preparations (n = 4) was imaged optically following shocks of strength +/-5A. All VEPiPGRs were analyzed, and the time T from shock end to activation onset was recorded (isoelectric window is the smallest T among activations that propagated globally).</AbstractText>VEPiPGR activations occurred for CIs in the range from 80 to 150 ms. Average duration of T was 64.5 +/- 18.15 ms, with T decreasing as CI increased (Tmax = 82 ms, Tmin = 46 ms, linear-fit slope = -0.675). The average earliest CI at which cathodal (+5A) shocks resulted in VEPiPGRs was 87 ms compared with 116 ms for anodal (-5A) shocks. All VEPiPGR activations emerged first on the epicardium in a focal pattern, and all induced ventricular fibrillation.</AbstractText>The global activation that terminates the isoelectric window could result from VEPiPGRs that find an exit pathway. VEPiPGRs originate at the sites of maximum action potential abbreviation by the shock, always on the epicardium for the preparation used here.</AbstractText> |
9,667 | Benefit of millisecond waveform durations for patients with high defibrillation thresholds. | Patients with a high defibrillation threshold (DFT) present an atypical but vexing problem with regard to implantable cardioverter-defibrillator (ICD) therapy. Their implant procedures are lengthy and involve more risk of complications. These patients often sustain a reduced safety margin that may compromise their survival.</AbstractText>The purpose of this study was to evaluate the use of fixed millisecond duration model-optimized biphasic waveforms compared with conventional tilt-based waveforms in patients having a high DFT.</AbstractText>We compared a 65%/65% tilt biphasic waveform to a millisecond duration biphasic waveform based on the biphasic burping theory using a 90-microF shock capacitor.</AbstractText>Fifty-four patients were evaluated. Mean DFT with tilt was reduced from 11.0 +/- 5.5 J to 8.8 +/- 4.1 J, for a mean reduction of 20% (P < .0001). For the 13 patients with tilt-based DFTs > or = 15 J, DFT was reduced from 18.7 +/- 4.1 J to 13.4 +/- 3.5 J, for a mean DFT reduction of 28% (P = .009). The population peak DFT was reduced from 29.0 J to 17.5 J, for a 41% reduction (P = .03).</AbstractText>Use of simple millisecond biphasic waveforms instead of conventional tilt-based waveforms can lead to substantial reductions in DFT, especially in patients with high DFT.</AbstractText> |
9,668 | [Comparative study on characteristics of congestive heart failure patients with preserved versus abnormal left ventricular systolic function and evaluation effects of therapy]. | To compare clinical characteristics and effects of therapy for hospitalized patients with congestive heart failure (CHF) and different left ventricular ejection fraction (LVEF) during hospitalization.</AbstractText>The medical records of 1 074 unselected consecutive patients with CHF who were admitted to Queen Mary Hospital from January, 2001 to January, 2002 were retrospectively reviewed. Three hundred and ninety-nine patients were categorized as having either normal left ventricular systolic function or systolic dysfunction based on the results of echocardiography. Clinical features with a slightly modified version of the Framingham criteria, laboratory results and drug therapies at discharge were compared.</AbstractText>Among patients, the majority were women, 95.5% were > or =65 years and 50.6% > or =80 years of age. Classification of the severity of heart failure showed that 70.2% were New York Heart Association (NYHA) III and IV. Only 399 patients had borderline LVEF at the time of hospitalization, of these patients 191 (47.9%) had preserved systolic function (LVEF > or =0.50), and 208 (52.1%) with LVEF<0.50. Patients with LVEF > or =0.50, who tended to be elderly and more often female, exhibited a lower incidence of coronary artery disease and diabetes than patients with LVEF<0.50 (all P<0.05). Patients with preserved systolic function had a significantly higher prevalence of auricular fibrillation (P<0.05), accounting for up to 84 patients (44.0%) with it, and number of hospitalization for CHF increased. Among patients with systolic dysfunction, 22.6% were discharged on a therapeutic regimen of digoxin, 63.0% on an angiotensin-converting enzyme inhibitor (ACEI), and 12.0% on a beta-blocker, 13.9% on a calcium channel blocker. These accounted for 62.3%, 35.1%, 9.4% and 18.3% in patients with preserved systolic function, respectively. There was a higher incidence of use of digoxin (P<0.05).</AbstractText>In hospitalized patients with heart failure, the clinical signs and symptoms of chronic heart failure are similar to those of patients with CHF, LVEF is a powerful prognostic predictor to distinguish CHF patients with normal systolic function from those with systolic dysfunction. Criteria for use of ACEI and beta-blocker are still not clear cut. It is important to differentiate CHF patients with LVEF<0.50 from that with LVEF> or =0.50 in order to achieve a better therapeutic result in the treatment of CHF.</AbstractText> |
9,669 | Cardiac ischemia and uncoupling: gap junctions in ischemia and infarction. | Acute cardiac ischemia is often associated with ventricular arrhythmia and fibrillation. Due to the loss of ATP, the depolarization of the fibers, and the intracellular Na(+) and Ca(2+) overload with concomitant acidification as well as the accumulation of lysophosphoglyceride and arachidonic acid metabolites, propagation of action potentials will be impaired by two factors: (a) reduced sodium channel availability and (b) gap junction uncoupling. While gap junction uncoupling leads to predominant transverse uncoupling, reduced I (Na) availability results in impaired longitudinal conduction. Complete gap junction uncoupling would initiate arrhythmia, while intermediate uncoupling has been shown to enhance the safety factor (SF) of propagation, limiting the current loss to non-depolarized areas. In contrast, a reduction in I(Na) availability reduces SF, and partial gap junction uncoupling might enable effective but slow conduction which, on the other hand, could form the basis for some kind of reentrant arrhythmia, paving the way for new anti-arrhythmic approaches in gap junction coupling. In the chronic phase, remodeling processes also involve gap junctions and lead to highly heterogeneous non-uniform tissue which may serve as an arrhythmogenic trigger. |
9,670 | Role of connexins in atrial fibrillation. | Atrial fibrillation (AF) is the most common arrhythmia in humans. AF is accompanied by a remodeling process which changes the electrophysiology of the cells and the gap junctional communication within the tissue. Gap junctions, forming communicating channels between neighboring cells, and their specific geometric arrangement seem to contribute to the initiation of AF within the pulmonary veins as well as to the stabilization of AF providing a heterogeneous biophysical network of cells enabling multiple wavelets. These tissue changes are accompanied by fibrosis and changes in the expression levels of Cx43 and Cx40, probably depending on the underlying diseases or the animal model used. New studies point to a modulating role of angiotensin II in this process and a possible therapeutic role for ACE inhibitors or AT(1) antagonists. |
9,671 | [The design of the external defibrillator using the truncated exponential biphasic waveform]. | The external defibrillator is an emergency instrument used very widely in clinics. It plays an important role in rescuing ventricle fibrillation (VF) patients. We have designed an external defibrillator using the truncated exponential biphasic waveform. The system consists of three parts: the ECG collection module, the control module and the defibrillator module. They are introduced respectively, listing the main problems and the methods to solve them. Some experiments have been done and the corresponding results are given. |
9,672 | Syncope secondary to transient atrioventricular block in a German shepherd dog with dilated cardiomyopathy and atrial fibrillation. | This case report describes transient atrioventricular block as the etiology for syncopal events in a 6-year-old male German shepherd dog with atrial fibrillation and dilated cardiomyopathy. The arrhythmia diagnosis was obtained via Holter monitoring. Medical treatment with a sustained-release preparation of theophylline, as an additive to the standard congestive heart failure treatment (benazepril, furosemide and pimobendan) may have contributed to temporary remission of the syncopal events. However, the congestive heart failure progressed and the dog was euthanized. Veterinarians should be aware of the possibility of transient atrioventricular block causing syncope in dogs with DCM and AF and should be careful in empirically lowering the ventricular response rate if these dogs present with syncopal episodes. |
9,673 | Survival in dogs with dilated cardiomyopathy and congestive heart failure treated with digoxin, furosemide and propranolol: A retrospective study of 62 dogs. | To retrospectively evaluate survival and potential adverse effects in dogs with congestive heart failure (CHF) attributable to dilated cardiomyopathy (DCM) treated with propranolol, furosemide and digoxin.</AbstractText>The use of beta-blocking agents has been shown to improve survival in human patients with CHF, including patients with DCM.</AbstractText><AbstractText Label="ANIMALS, MATERIALS AND METHODS" NlmCategory="METHODS">Sixty-two dogs with DCM and CHF NYHA class IV were included in the study. All dogs were initially treated with digoxin (mean dose 0.009mg/kg per day) and furosemide (mean dose 3.6mg/kg per day). Propranolol (mean dose 2.4mg/kg per day) was added after signs of CHF had been resolved, approximately one week after initial presentation. Survival analysis was based on the Kaplan-Meier method.</AbstractText>Pulmonary edema was found at initial presentation in 60 dogs, and pleural effusion in 2 dogs. Thirty-one dogs (50%) presented with atrial fibrillation, and ventricular premature complexes were found in 9 dogs. Survival time ranged from 8 to 1335 days (median, 126 days). Nine dogs were censored in the analysis, 8 because euthanasia was performed for reasons unrelated to cardiac disease, and 1 dog was lost on follow-up. Fifty-two dogs were euthanized, 9 dogs died suddenly. Survival rate at 1 year was 34%, and 20% at 2 years.</AbstractText>The present study shows that the median survival time in dogs treated with digoxin, furosemide and propranolol was 126 days, with a survival rate at 1 year of 34%. This treatment regiment was well tolerated.</AbstractText> |
9,674 | The Wolff-Parkinson-White electrocardiogram pattern in athletes: how and when to evaluate the risk for dangerous arrhythmias. The opinion of the paediatric cardiologist. | Although diagnostic assessment and treatment have been described in detail in patients with symptomatic Wolff-Parkinson-White (WPW) syndrome, the management of asymptomatic subjects remains controversial. Usually they are assumed to have a benign prognosis, although they do very occasionally present with ventricular fibrillation (VF) as the first manifestation of the syndrome. Discovering a WPW pattern in a previously asymptomatic athlete on a routine electrocardiogram (ECG) identifies the necessity for more accurate screening tests. However, non-invasive methods (Holter monitoring, exercise treadmill testing) seem to be relatively incomplete for risk stratification, especially for athletes. Current guidelines do not always recommend a routine electrophysiological study (EPS) in patients with an asymptomatic WPW ECG pattern, especially in children younger than 12 years. Individuals who engage in high-risk occupations or those patients who have a pre-excitation pattern which precludes them from following their chosen career or activities may be exceptions. The presence of inducible reciprocating tachycardia during EPS, especially when it triggers atrial fibrillation with short RR interval, can represent a specific risk marker of dangerous arrhythmias. |
9,675 | Long QT syndrome and short QT syndrome: how to make correct diagnosis and what about eligibility for sports activity. | Cardiologists are involved in evaluating the eligibility of athletes to practise competitive sport and they should therefore be able to identify the electrocardiographic markers of long QT syndrome (LQTS) and short QT syndrome (SQTS). An overview of the clinical criteria to perform measurement of QT interval on 12-lead electrocardiogram is provided herein and several instances in which the diagnosis of either LQTS or SQTS may leave the clinician uncertain are discussed. A critical appraisal of current recommendations for eligibility to competitive sport is also provided as well as some of the authors' personal opinions on the practice of recreational activities in patients with abnormal repolarization. |
9,676 | Brugada-like electrocardiogram pattern: how to stratify the risk for sudden cardiac death. Is sports activity contraindicated? | Brugada syndrome is associated with a considerable risk of sudden death in young and otherwise healthy adults. The syndrome is estimated to be responsible for at least 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts. The diagnosis of Brugada syndrome is based on peculiar electrocardiogram (ECG) abnormalities classified by the European Society of Cardiology in three types: type 1 (coved-type) is the diagnostic pattern; type 2 (saddle-back type); and type 3 are considered significant if there is a conversion to a type 1, spontaneously or during administration of class I A/C anti-arrhythmic drugs (flecainide, etc.). There is a general agreement about the high risk of sudden death in patients with previous cardiac arrest, for whom an implantable defibrillator (ICD) is recommended. In contrast, controversy exists on the correct clinical behaviour in individuals without a history of previous cardiac arrest. To stratify the risk in patients with type 1 pattern, three major factors have been suggested: typical ECG pattern in the basal state; a history of syncope; and inducible ventricular tachycardia/ventricular fibrillation during electrophysiological study (EPS). However, the indication and usefulness of an EPS is debatable. In patients with a type 2 or 3 pattern a pharmacological test is indicated in the presence of symptoms or of a familial history. With regard to sports eligibility, patients with a history of cardiac arrest should have an ICD and they can practise (low intensity) sport only after the implant of the device. Patients without documented cardiac arrest but at high risk (basal type 1 ECG pattern, syncope and/or positive EPS) should also have an ICD and they can practise (low intensity) sport only after the implant of the device. In patients at low risk (type 1 ECG pattern in the absence of symptoms, without family history and negative EPS) the behaviour regarding sport eligibility is not a matter of debate. In cases with type 2 or 3 pattern, in the absence of familial history and symptoms, a permissive behaviour should be assumed. |
9,677 | Medical and surgical treatment of chronic mitral regurgitation. | Chronic severe mitral regurgitation is a progressive disease that can lead to left ventricular dysfunction. New information on the natural history of the disease, along with advances in surgical techniques, has changed the roles of medical and surgical therapies. There is no well-defined role for medical therapy in chronic mitral regurgitation. The goal of the treating physician is therefore to identify the optimal timing for surgical intervention. The timing of surgical intervention depends primarily on two factors: (i) clinical symptoms and (ii) the left ventricular response to volume overload. However, the aetiology of mitral regurgitation, the likelihood of surgical repair, the occurrence of atrial fibrillation and the presence of pulmonary hypertension, together with the haemodynamic response to exercise, are important factors in the optimal surgical timing. New concepts in the understanding of the natural history of the disease coupled with success of mitral repair have recently resulted in a widespread evolution towards earlier surgery. |
9,678 | Effects of radial left ventricular dyssynchrony on cardiac performance using quantitative tissue Doppler radial strain imaging. | Our objective was to test the hypothesis that novel angle-corrected radial strain imaging can quantify left ventricular dyssynchrony associated with contractile impairment and improved with biventricular pacing. Eight open-chest dogs were studied by novel angle-corrected color-coded radial strain imaging and high-fidelity pressure-conductance catheters recording pressure-volume loops. Heart rate was controlled by right atrial pacing and all timing intervals were corrected by R-R interval (corrected interval = measured interval/(R-R interval)(1/2)). Left bundle branch block, simulated by right ventricular free wall pacing, resulted in marked radial dyssynchrony, which we defined as maximal time difference between peak segmental strain, from 39 +/- 17 to 354 +/- 49 milliseconds and stroke work decreased from 157 +/- 40 to 60 +/- 37 mJ, (P < .005 vs baseline). Depression of contractility by high-dose esmolol (end-systolic pressure-volume relationship from 5.7 +/- 2.4 to 3.6 +/- 1.0 mm Hg/mL) was associated with augmented dyssynchrony to 388 +/- 53 milliseconds (P < .05 vs baseline right ventricular pacing). Biventricular pacing improved dyssynchrony to 55 +/- 19 milliseconds and stroke work to 143 +/- 33 mJ (P < .05 vs right ventricular pacing). Changes in radial dyssynchrony correlated significantly with 6-site average regional strain (r = -0.93 +/- 0.05 individually, r = 0.80 overall) and stroke work (r = -0.88 +/- 0.12 individually, r = -0.82 overall). Angle-corrected radial strain imaging has clinical potential to quantify mechanical dyssynchrony and effects of biventricular pacing. |
9,679 | Prevention of atrial fibrillation in patients with symptomatic chronic heart failure by candesartan in the Candesartan in Heart failure: assessment of Reduction in Mortality and morbidity (CHARM) program. | Atrial fibrillation (AF) is frequent in patients with chronic heart failure (CHF). Experimental and small patient studies have demonstrated that blocking the renin-angiotensin-aldosterone system may prevent AF. In the CHARM program, the effects of the angiotensin receptor blocker candesartan on cardiovascular mortality and morbidity were evaluated in a broad spectrum of patients with symptomatic CHF. CHARM provided the opportunity to prospectively determine the effect of candesartan on the incidence of new AF in this CHF population.</AbstractText>7601 patients with symptomatic CHF and reduced or preserved left ventricular systolic function were randomized to candesartan (target dose 32 mg once daily, mean dose 24 mg) or placebo in the 3 component trials of CHARM. The major outcomes were cardiovascular death or CHF hospitalization and all-cause mortality. The incidence of new AF was a prespecified secondary outcome. Median follow-up was 37.7 months. A conditional logistic regression model for stratified data was used.</AbstractText>6446 patients (84.8%) did not have AF on their baseline electrocardiogram. Of these, 392 (6.08%) developed AF during follow-up, 177 (5.55%) in the candesartan group and 215 (6.74%) in the placebo group (odds ratio 0.812, 95% CI 0.662-0.998, P = .048). After adjustment for baseline covariates, the odds ratio was 0.802 (95% CI 0.650-0.990, P = .039). There was no heterogeneity of the effects of candesartan in preventing AF between the 3 component trials (P = .57).</AbstractText>Treatment with the angiotensin receptor blocker candesartan reduced the incidence of AF in a large, broadly-based, population of patients with symptomatic CHF.</AbstractText> |
9,680 | Reentrant and nonreentrant forms of atrio-ventricular nodal tachycardia mimicking atrial fibrillation. | Atrial fibrillation (AF) manifests disorganized atrial activity and irregular R-R intervals on electrocardiogram (ECG). Variation in R-R intervals can also be seen with other supraventricular tachycardias that may mimic AF.</AbstractText>We report our observations on three patients who were referred to our center to undergo pulmonary vein (PV) isolation for erroneously diagnosed AF in the setting of dual atrio-ventricular (AV) nodal pathways manifesting as AV nodal reentrant tachycardia (AVNRT) and/or double response during sinus rhythm.</AbstractText>These three subjects (two females) were derived from a group of 456 consecutive patients undergoing AF ablation at our center over a 3-year period. All three patients had been symptomatic for over 2 years, having failed two or more antiarrhythmic medications. In each case AF was initially diagnosed on ECG and/or recordings from ambulatory monitoring. However, in all three cases the correct diagnosis was established during the invasive electrophysiologic study. In one patient during the stimulation protocol, two narrow complex tachycardias were serially induced (cycle lengths: 305 and 360 msecs; VA time: 60 and 240 msecs). The latter was confirmed to be atypical AVNRT and during this tachycardia, block in upper pathway was observed. In the other two patients, sinus rhythm with repetitive runs of double response and isolated junctional beats were observed in the absence of retrograde conduction. Successful slow pathway modification was performed in each subject and all three patients have remained arrhythmia free over a mean follow-up of 31 +/- 16 months off antiarrhythmic medications.</AbstractText>AF can be erroneously diagnosed in patients with dual AV nodal pathways manifesting double response and/or AVNRT. Incorporating a stimulation protocol as a part of the AF ablation procedure may help in diagnosing these rare clinical presentations that can be cured by slow pathway modification alone.</AbstractText> |
9,681 | Do intramural virtual electrodes facilitate successful defibrillation? Model-based analysis of experimental evidence. | Recent computer model and experimental studies have suggested that microscopic intramural collagenous planes may facilitate successful defibrillation through the generation of shock-induced virtual electrodes deep within the ventricular wall. Evidence supporting the existence of intramural virtual electrodes has been drawn from several recent studies, which map shock-induced membrane potential (Vm) over the cut transmural surface of dissected segments of porcine left ventricle (LV). The artificially created transmural boundary in these experiments is impermeable to intracellular current. It is not known how this constraint limits the interpretation of these experiments in terms of the shock response of the intact ventricle.</AbstractText>This study uses a realistic 3D computer model of LV myocardium to aid experimental interpretation. The model incorporates a microstructural description of intramural cleavage plane discontinuities measured by confocal microscopy of rat LV. Electrical shocks are applied across the model tissue, with and without introduced transmural boundaries. Shocks of varying strength (4-40 V/cm) are also applied to the model and the response analyzed. Results show that shock-induced Vm changes (deltaVm) on a transmural tissue boundary are significantly different to deltaVm of the intact ventricle, and the extent of difference depends on boundary orientation. However, the presence and qualitative behavior of intramural virtual electrodes is preserved irrespective of boundary placement. The model also confirms experimental observations that most rapid transmural activation occurs for shocks of strength 5-10 V/cm. Two distinct mechanisms suppress virtual electrode propagation, and hence slow tissue activation, outside of this optimal shock strength range.</AbstractText>This study supports the hypothesis that distributed microscopic intramural virtual electrodes contribute to rapid activation of the ventricular wall during defibrillation.</AbstractText> |
9,682 | Effects of sildenafil citrate on defibrillation efficacy. | Although fatal arrhythmia and sudden death have been reported in patients taking sildenafil citrate, its effect on defibrillation efficacy has not been investigated. The aim of this study was to test the hypothesis that sildenafil citrate increases the shock strength required to successfully defibrillate during ventricular fibrillation (VF).</AbstractText>A total of 26 pigs (20-25 kg) were randomly assigned into three groups. In each group, the defibrillation threshold (DFT) was determined at the beginning of the study using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic) was delivered after 10 seconds of VF. Group 1 (n = 10) received 50 mg and group 2 (n = 10) received 100 mg of sildenafil citrate intravenously at a rate of 2 mL/minute for 50 minutes. Group 3 (n = 6) received 100 mL of saline intravenously at the same rate as in group 1. The DFT was determined again after the drug (drug-DFT) and saline (saline-DFT) administration. For 100-mg sildenafil citrate infusion, the DFT (483 +/- 39 V, 18 +/- 3 J) was significantly (P < 0.003 and P < 0.01, respectively) higher than the control-DFT (407 +/- 123 V, 13 +/- 7 J). This sildenafil citrate infusion increased the DFT approximately 19% by voltage, and approximately 38% by total energy. After 50-mg sildenafil citrate infusion, the DFT (454 +/- 28 V, 15 +/- 2 J) was not different than the control DFT (449 +/- 28 V, 15 +/- 2 J). Saline infusion (391 +/- 18 V, 12 +/- 1 J) did not alter the control DFT (399 +/- 22 V, 12 +/- 1 J).</AbstractText>The 100-mg sildenafil citrate infusion, representing a supra-therapeutic plasma level, significantly increased the DFT. This finding indicates that VF occurring during supra-therapeutic sildenafil citrate treatment would require a stronger shock to successfully defibrillate.</AbstractText> |
9,683 | A randomized comparison of permanent septal versus apical right ventricular pacing: short-term results. | This study compared chronic right ventricular (RV) pacing at the septum versus apex.</AbstractText>Chronic RV apical pacing may be detrimental to ventricular function. This randomized, pilot study examined whether, compared with apical, permanent septal pacing preserves cardiac function.</AbstractText>Ablation of the atrioventricular junction for permanent AF, followed by implantation of a DDDR pacemaker connected to two ventricular leads was performed in 28 patients. One lead screwed into the septum and another placed at the apex were connected to the atrial and ventricular port, respectively. Septum or apex was paced by programming AAIR or VVIR modes, respectively. Patients were randomly assigned, 4 months later, to pacing at one site for 3 months, and crossed over to the other for 3 months. New York Heart Association class, QRS width and axis, left ventricular ejection fraction (LVEF), exercise duration, and peak oxygen uptake were measured. Results in patients with LVEF > 45% and < or = 45% were compared.</AbstractText>Septal pacing was associated with shorter QRS (145 +/- 4 msec vs 170 +/- 4 msec, P < 0.01) and normal axis (40 degrees +/- 10 degrees vs -71 +/- 4 degrees , P < 0.01). At 3 months, among patients with baseline LVEF < or = 45%, LVEF was 42 +/- 5% after septal pacing versus 37 +/- 4% after apical pacing (P < 0.001).</AbstractText>In contrast to RV apical pacing, chronic RV septal pacing preserved LVEF in patients with baseline LVEF < or = 45%.</AbstractText> |
9,684 | Catheter ablation of ventricular fibrillation storm in patients with infiltrative amyloidosis of the heart. | Recent studies have demonstrated that premature ventricular contractions (PVCs) originating from the Purkinje system are responsible for initiation of ventricular fibrillation (VF) in patients with and without structural heart disease. Ablation of the PVCs has been shown to be feasible. We report 2 patients with repetitive VF associated with cardiac amyloidosis. Each episode of ventricular arrhythmia was preceded by monomorphic PVC. The electrical storms were drug resistant. Electrophysiological testing was performed and the sites of earliest activation were localized within the left ventricle in the absence of significant scar tissue. After ablation, PVCs subsided and there were no further VF recurrences. |
9,685 | The effect of induction method on defibrillation threshold and ventricular fibrillation cycle length. | Since no clinical data are available on the comparison of the "shock on T-wave" and "high frequency burst" ventricular fibrillation (VF) induction modes during defibrillation threshold (DFT) testing, we aimed to compare these two methods during implantable cardioverter defibrillator implantation.</AbstractText>The DFT was determined with a step-down protocol using biphasic, anodal polarity (100%, 40%, 20% voltage control) shocks. Patients were randomized: VF was induced by 50 Hz burst in group B (n = 45) and T-wave shock in group T (n = 41). The DFT was defined as the lowest energy level that terminated VF; confirmed DFT (DFTc) was defined as the minimal energy level that consecutively terminated VF twice. Success rate of DFTc was calculated during an intraindividual test for the alternate induction method.</AbstractText>A total of 546 episodes of VF were induced: n = 278 (B) vs n = 268 (T). Incidence of VT during inductions was 9.9% (B) vs 2.7% (T), P < 0.05. Neither the DFT, 8.8 +/- 4.0 J (B) vs 9.7 +/- 4.2 J (T), nor the DFTc, 10.6 +/- 5.1 J (B) vs 10.8 +/- 4.2 J (T), proved to be significantly different. A significant correlation was found between VF cycle length (CL) and the concomitant DFT (r = 0.298, P < 0.05) in group T only. Subgroup analysis of patients under chronic class III antiarrhythmic treatment showed no increase of the DFT in either group and significantly lower incidence of VT induction in group T regardless of antiarrhythmic treatment.</AbstractText>The DFT and the VFCL proved to be independent of the VF induction method. The T-wave shock was more unlikely to induce VT during DFT testing. These results suggest that both methods are reliable in DFT determination, though T-wave shock application is a more reliable method for DFT testing.</AbstractText> |
9,686 | Procainamide: Test your drug IQ. | Learn how to safely give this treatment for ventricular arrhythmias. |
9,687 | Prognostic impact of prolonged ventricular repolarization in hypertension. | QT interval prolongation on the surface electrocardiogram (ECG) predicts cardiovascular complications in high-risk subjects, but its prognostic role in uncomplicated hypertension has been understudied.</AbstractText>For up to 13 years (average, 5.3 years), we followed up 2110 white patients with initially untreated essential hypertension (mean +/- SD age, 49 +/- 12 years; 55% men) without prevalent cardiovascular or renal disease who underwent 12-lead ECG before therapy. We excluded patients with ECG abnormalities including ischemia, necrosis, complete bundle branch block, atrial fibrillation, arrhythmias, and ventricular preexcitation.</AbstractText>Heart rate-corrected QT interval (QTc) showed a weak but significant direct association with systolic blood pressure (r = 0.07; P<.001), diastolic blood pressure (r = 0.11; P<.001), and Cornell voltage (r = 0.06; P = .006). During follow-up, 84 patients developed new-onset ischemic heart disease (0.75 event per 100 patient-years). After adjustment (Cox model) for the effects of age, sex, diabetes mellitus, serum cholesterol level, serum creatinine level, smoking, left ventricular hypertrophy, and 24-hour systolic blood pressure, patients with a prolonged QTc (>or=450 milliseconds in women and >or=440 milliseconds in men) had a nearly 2-fold increase in risks of coronary events (hazard ratio, 1.95; 95% confidence interval, 1.12-3.42; P = .02) and cardiovascular death (hazard ratio, 2.05; 95% confidence interval, 1.03-4.37; P = .04). Coronary heart disease risk was independently higher by 33% (95% confidence interval, +7% to +66%; P = .01) for each 32-millisecond increase in QTc.</AbstractText>Prolonged ventricular repolarization is a risk factor for ischemic heart disease and cardiovascular mortality in subjects with uncomplicated hypertension. Its prognostic significance adds to that of several traditional cardiovascular risk factors, including left ventricular hypertrophy.</AbstractText> |
9,688 | Heart failure during cardiac pacing. | Right ventricular apical (RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA pacing with an increased risk of heart failure hospitalization (HFH) in clinical trials.</AbstractText>Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a 2010-patient, 6-year trial of dual-chamber (DDDR) versus ventricular (VVIR) pacing in sinus node dysfunction. A Cox model showed that New York Heart Association (NYHA) class at baseline and follow-up predicted HFH (hazard ratio [HR], 3.99; 95% confidence interval [CI], 2.74-5.79 for NYHA class III/IV and HR, 2.17; 95% CI, 1.54-3.04 for NYHA class II versus class I); other predictors were heart failure (HR, 2.30; 95% CI, 1.70-3.11), atrioventricular (AV) block (HR, 1.48; 95% CI, 1.11-1.97), and myocardial infarction (MI)(HR, 1.37; 95% CI, 1.00-1.86). Postimplantation predictors were VVIR cumulative percent ventricular pacing (Cum%VP) >80 (HR, 3.58; 95% CI, 1.72-7.45), DDDR Cum%VP >40 or VVIR Cum%VP < or =80 (HR, 1.81; 95% CI, 0.94-3.50) versus DDDR Cum%VP < or =40; whether QRS duration (QRSd) was paced or spontaneous (HR, 2.21; 95% CI, 1.39-3.54; spontaneous versus paced); and drugs for atrial fibrillation (HR, 1.60; 95% CI, 1.19-2.15). Low baseline ejection fraction (EF) and postimplantation RVA-paced or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF (HR, 1.18; 95% CI, 1.11-1.27; versus HR, 1.08; 95% CI, 1.01-1.15; for a 10-ms increase); at a QRSd of approximately 200 ms, normal- and low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was < or =80 or DDDR Cum%VP was >40 versus DDDR Cum%VP < or =40 and was additive with other risk factors.</AbstractText>Differences in HFH risk can be explained by interactions between substrate (atrial fibrillation, AV conduction, heart failure, MI, EF) and pacing promoters (ventricular desynchronization-paced QRSd and Cum%VP, and AV desynchronization-pacing mode). Management of RVA pacing is important for reducing the risk of HFH, particularly among patients with low EF and heart failure.</AbstractText> |
9,689 | Amiodarone-induced alveolar hemorrhage. | Amiodarone is increasingly prescribed for patients with ventricular and supraventricular tachyarrhythmias. Many adverse effects have been reported due to this drug and include injury to the liver, thyroid, cornea, skin, and neuromuscular system. Pulmonary toxicity is one of the more serious side effects of this anti-arrhythmic drug and is potentially fatal. Since the first case of amiodarone-induced pneumonitis was described in the early 1980s, amiodarone pneumonitis has been recognized as a distinctive and not uncommon form of drug-induced lung injury. On the other hand, amiodarone-induced pulmonary toxicity resulting in alveolar hemorrhage is rare. The authors report a patient with amiodarone-induced alveolar hemorrhage and review the literature. |
9,690 | ECG changes amongst patients with alcohol withdrawal seizures and delirium tremens. | Alcohol withdrawal seizures and delirium tremens (DT) are serious complications of alcohol dependence. The prevalence of arrhythmias and other electrocardiographic (ECG) changes occurring in these clinical situations is not well studied.</AbstractText>We performed a retrospective analysis of clinical data and ECG's from patients discharged between 1995 and 2005 with the diagnosis of DT (ICD-Code F10.4) or alcohol withdrawal seizures (F10.3). Measurement of the ECG intervals was done in lead II. The corrected QT interval (QTc) was obtained using Bazett's formula.</AbstractText>49 patients (38 males; 11 females) with a mean age of 48 years were included in the study. 23 patients with DT and 16 with convulsions were admitted to the hospitals. Ten patients developed DT while being hospitalised for other reasons. The QTc interval was prolonged (>440 ms and >460 ms in males and females, respectively) in 31 patients (63%). Five patients (10%) developed tachyarrhythmias (two torsade de pointes, one sustained ventricular tachycardia, two supraventricular tachycardia, one atrial fibrillation). All returned to sinus rhythm after appropriate treatment.</AbstractText>Tachyarrhythmias are common amongst patients with severe alcohol withdrawal syndromes. The majority of the patients had an acquired long QT syndrome which led to a torsade de pointes in two cases. No patient died in the hospital and all were discharged in sinus rhythm. Clinicians should possibly avoid QT prolonging drugs and carefully monitor the rhythm in patients with severe alcohol withdrawal syndromes.</AbstractText> |
9,691 | Effects of low-dose quinidine on ventricular tachyarrhythmias in patients with Brugada syndrome: low-dose quinidine therapy as an adjunctive treatment. | Quinidine is suggested as an effective agent to suppress ventricular fibrillation (VF) in the Brugada syndrome by inhibiting transient outward K(+) current (Ito) leading to the reduction and abbreviation of the disparity of repolarization in the right ventricular outflow region and ST segment elevation in the right precordial leads of electrocardiogram. We sought to assess the efficacy of low-dose (300-600 mg) quinidine sulfate on the prevention of ventricular fibrillation induction by programmed electrical stimulation (PES) and spontaneous ventricular fibrillation episodes during the subsequent follow-up period. Electrophysiologic study was performed in 14 patients with the Brugada syndrome (14 men, mean age 50 +/- 11 years, range 32-75) before and during the treatment with low-dose quinidine and evaluated the efficacy of the drug therapy. Ventricular fibrillation was induced in all the patients by programmed electrical stimulation at baseline. After oral quinidine administration (300 mg or 600 mg/d), programmed electrical stimulation was repeated. Ventricular fibrillation induction was prevented in 6 of 14 patients (44%). Serum quinidine concentration was higher in the patients with suppressed VF induction than those without (1.88 +/- 0.44 versus 1.31 +/- 0.43 microg/ml, respectively). After programmed electrical stimulation, 9 of 14 patients (64%), in whom four had implantable cardioverter defibrillator implantation, continued to receive quinidine. During a mean follow-up period of 31 months on quinidine, no side effects except one with diarrhea were observed (12.5%). There were no ventricular fibrillation recurrences in 3 of the 9 patients, who had frequent implantable cardioverter defibrillator discharges due to ventricular fibrillation attacks before treatment with quinidine. Low-dose quinidine has a potential as an adjunctive therapy for patients of the Brugada syndrome with frequent implantable cardioverter defibrillator discharges. |
9,692 | Lifetimes of epicardial rotors in panoramic optical maps of fibrillating swine ventricles. | During ventricular fibrillation (VF), electrical activation waves are fragmented, and the heart cannot contract in synchrony. It has been proposed that VF waves emanate from stable periodic sources (often called "mother rotors"). The objective of the present study was to determine if stable rotors are consistently present on the epicardial surface of hearts comparable in size to human hearts. Using new optical mapping technology, we imaged VF from nearly the entire ventricular surface of six isolated swine hearts. Using newly developed pattern analysis algorithms, we identified and tracked VF wave fronts and phase singularities (PS; the pivot point of a reentrant wave front). We introduce the notion of a compound rotor in which the rotor's central PS can change and describe an algorithm for automatically identifying such patterns. This prevents rotor lifetimes from being inappropriately abbreviated by wave front fragmentation and collision events near the PS. We found that stable epicardial rotors were not consistently present during VF: only 1 of 17 VF episodes contained a compound rotor that lasted for the entire mapped interval of 4 s. However, shorter-lived rotors were common; 12.2 (SD 3.3) compound rotors with lifetime >200 ms were visible on the epicardium at any given instant. We conclude that epicardial mother rotors do not drive VF in this experimental model; if mother rotors do exist, they are intramural or septal. This paucity of persistent rotors suggests that individual rotors will eventually terminate by themselves and therefore that the continual formation of new rotors is critical for VF maintenance. |
9,693 | Favorable long-term outcome of Maze surgery in patients with lone atrial fibrillation. | Rhythm control is indicated for patients suffering from symptomatic atrial fibrillation (AF), but remains difficult to establish. We investigated the long-term outcome of Cox maze III surgery in patients with symptomatic lone AF refractory to antiarrhythmic drug therapy.</AbstractText>Patients with a history of symptomatic paroxysmal or persistent AF refractory for at least two class I or III antiarrhythmic drugs and without structural heart disease or bradyarrhythmias were included. All patients underwent Cox maze III surgery. Complete success was defined as the absence of AF without antiarrhythmic drugs beyond 3 months after the procedure, and partial success as the absence of AF with antiarrhythmic drug use.</AbstractText>A total of 29 patients were included (27 male), with a mean age of 48 +/- 6 years. At the time of surgery, 11 patients (38%) had persistent AF. After a mean follow-up of 4.8 +/- 2.4 years, 79% of patients had complete success, and 2 patients (7%) were free of AF with antiarrhythmic drugs. At the end of follow-up, left ventricular fractional shortening was significantly improved (from 31% +/- 10% to 39% +/- 8%, p = 0.002), left atrial size was unchanged, exercise capacity was within normal ranges, and quality of life was comparable with that of healthy controls. Severe complications included reoperations for postoperative bleeding (n = 3), pericardial effusion (n = 1), and mediastinitis (n = 1). In 2 patients, a pacemaker was implanted postoperatively because of sinus node dysfunction.</AbstractText>Cox maze III surgery is a highly effective therapy for drug-refractory lone AF, and therefore remains an alternative to transvenous pulmonary vein ablation.</AbstractText> |
9,694 | Early and late outcome after off-pump coronary artery bypass graft surgery with coronary endarterectomy: a single-center 10-year experience. | We aimed to review the early and late results of off-pump coronary artery bypass graft surgery (OPCABG) with coronary endarterectomy in patients undergoing surgical revascularization at our institution.</AbstractText>Between 1995 and 2004, of 680 OPCABG patients in a single surgeon's practice (W.R.D.), 70 patients (10.29%) who underwent concomitant coronary endarterectomy were studied. The mean age was 63.6 +/- 9.29 years. Thirty-three patients (55%) were Canadian Cardiovascular Society class III or IV, and 24 patients (40%) were New York Heart Association class III or IV. Eighteen patients (35%) had impaired left ventricular function. The mean EuroSCORE of these patients was 5.9 +/- 1.8.</AbstractText>Fifty-seven patients (81%) underwent right coronary artery endarterectomy, and 12 patients (17%) underwent left anterior descending artery endarterectomy (8 left interior mammary arteries used as conduits). Four patients (5.7%) had two vessels endarterectomized. The mean number of grafts were 2.0 +/- 0.4. The 30-day mortality rate was 2.85% (n = 2). Three patients (4.3%) suffered from postoperative myocardial infarction, and 3 patients (4.3%) required postoperative intra-aortic balloon pump counterpulsation. Mean intensive therapy unit stay was 17.6 +/- 8.1 hours. Patients were extubated after a mean of 10.38 +/- 4.9 hours. The mean length of hospital stay was 6.1 +/- 2.0 days. Fourteen patients (20%) had postoperative atrial fibrillation, and only 1 patient (1.42%) had a transient stroke with complete recovery. There were no conversions to cardiopulmonary bypass. A mean of 0.86 +/- 0.17 units of blood were transfused postoperatively. There was one reopening for bleeding, and 1 patient had renal failure requiring hemofiltration. The median follow-up was 4.91 years, 90% of patients were angina free, and the actuarial survival at 10 years was 78.04% +/- 7.6%.</AbstractText>Off-pump coronary artery bypass graft survery with coronary endarterectomy is feasible and achieves surgical revascularization in patients with diffuse coronary artery disease.</AbstractText> |
9,695 | Inhibition of basic leucine zipper transcription is a major mediator of atrial dilatation. | Atrial fibrillation is the most prevalent clinically significant cardiac arrhythmia. Atrial dilatation, a predictor of atrial fibrillation, is thought to result from increased ventricular pressure. However, the underlying molecular mechanisms responsible for atrial dilatation are largely unknown. Here we sought to examine whether the expression of a basic leucine zipper inhibitor protein, JDP2, in the heart is sufficient for the generation of atrial dilatation.</AbstractText>A tetracycline-regulated transgene was used to express JDP2 specifically in the mouse heart. Mice hearts were dissected and subjected to Northern and Western analysis, or analyzed by ECG recording and echocardiography. Regulation of gene expression was studied using electromobility shift assays and luciferase gene reporter analysis.</AbstractText>Expression of JDP2 resulted in massive bi-atrial dilatation, defects in conduction, and a lethal phenotype. These effects were developmentally independent, acquired during adulthood, and were reversible upon abolishing of JDP2 expression. Connexin 40 and myosin light chain 2a expression were identified as potential target genes.</AbstractText>Expression of basic leucine zipper transcription inhibitors is sufficient to results in atrial dilatation. This dilatation is acquired postnatally and is reversible. Thus, basic leucine zipper transcription inhibitors may be a relevant therapeutic target for preventing atrial dilatation and atrial fibrillation.</AbstractText> |
9,696 | The relationship between stature and the prevalence of atrial fibrillation in patients with left ventricular dysfunction. | This study sought to determine the influence of stature on atrial fibrillation (AF) in high-risk patients with reduced left ventricular (LV) systolic function.</AbstractText>Left atrial (LA) enlargement is a potent risk factor for AF. Because LA size is strongly associated with stature, we hypothesized that height and body surface area (BSA) are risk factors for AF, independent of other known associations.</AbstractText>Data were obtained from ADVANCENT, a multicenter registry of patients with impaired LV function. Height and BSA were divided into quartiles by gender. Statistical analysis was done using the Cochran Mantel-Haenszel statistic, and multivariable logistic regressions were used to adjust for the effects of known confounders on the association between stature and AF.</AbstractText>A total of 25,268 patients were enrolled. The mean age was 66 years, and the cohort consisted mostly of white men (72%) and patients with ischemic cardiomyopathy (72%). The mean left ventricular ejection fraction was 31%. A history of AF was present in 7,027 patients (27.8%). The AF prevalence increased significantly between the lowest and highest quartiles for height (32% relative increase, p < 0.0001). In the multivariable analysis, the effect of height on AF risk persisted after adjusting for age, gender, race, left ventricular ejection fraction, heart failure class and etiology, hypertension, diabetes, and medication use (odds ratio 1.026/cm, 95% confidence interval [CI] 1.022 to 1.030). In the multivariable analysis, BSA was also an independent predictor of AF risk (odds ratio 4.221/m2, 95% CI 3.358 to 5.306).</AbstractText>In patients with LV dysfunction, increasing stature portends a higher risk of AF independent of other traditional risk factors for the arrhythmia. This association seems to account for the higher prevalence of AF in men and may be useful for identification of a high-risk population.</AbstractText> |
9,697 | Atrial near-field and ventricular far-field analysis by automated signal processing at rest and during exercise. | Sophisticated monitoring of atrial activity is a prerequisite for modern pacemaker therapy. Ideally, near-fields and ventricular far-fields ought to be distinguished by beat-to-beat template analysis of the atrial signal. A prerequisite is that atrial signals are stable under different conditions.</AbstractText>A Matlab routine was developed to analyze atrial electrograms of 23 patients at least 3 months after implantation of a dual chamber pacemaker under several conditions including at rest, bipolar at rest, in an upright position, during treadmill exercise, and postexercise. A near-field and far-field template was created and amplitudes, widths, and slew rates were measured. In bipolar configuration, near-field amplitude at rest was 3.04 +/- 0.94 mV (unipolar)/3.36 +/- 1.0 mV (bipolar) versus 3.18 +/- 1.0 mV (bipolar) at peak exercise. Far-field amplitude at rest was 1.66 +/- 1.18 (unipolar)/0.47 +/- 0.27 mV (bipolar) and 0.41 +/- 0.21 mV (bipolar) at peak exercise (n.s. for bipolar measurements). No overall significant changes were observed for near- and far-field widths and slew rates during exercise. Shorter tip-ring distances of the atrial bipole, lead position, and the presence of sinus node disease did not have any impact on overall near- and far-field signal characteristics. Intraindividual differences between rest and peak exercise were moderate (range: near-field +0.15 to -0.54 mV; range: far-field +0.05 to -0.18 mV).</AbstractText>Atrial near and far fields can be automatically classified and quantified by automated signal processing. Signals did not change during exercise or change of posture. This is a prerequisite for the implementation of beat-to-beat template analysis into pacemakers.</AbstractText> |
9,698 | Paradoxical effect of ajmaline in a patient with Brugada syndrome. | The typical Brugada ECG pattern consists of a prominent J-wave associated with ST-segment elevation localized in the right precordial leads V1-V3. In many patients, the ECG presents periods of transient normalization and the Brugada-phenotype can be unmasked by the administration of class-I antiarrhythmics. Reports have documented the heterogeneity of the Brugada syndrome ECG-phenotype characterized by unusual localization of the ECG abnormalities in the inferior leads. Case report A 51-year-old man, without detectable structural heart disease, was referred to us because of a history of syncope, dizziness, and palpitations. The ECG showed a J-wave and ST-segment elevation in the right precordial leads, suggesting Brugada syndrome. As other causes of the ECG abnormalities were excluded, the patient underwent an electrophysiological study that documented easy induction of ventricular fibrillation. During infusion of ajmaline, new prominent J-waves and ST-segment elevation appeared in the inferior leads, whereas the basal ECG abnormalities in the right precordial leads normalized. After infusion of isoprenaline, the ECG-pattern resumed the typical Brugada pattern. An implantable cardioverter-defibrillator was recommended.</AbstractText>In our patient, the double localization of the typical Brugada-pattern and the paradoxical effect of ajmaline on the ECG abnormalities confirmed the possibility of a phenotype heterogeneity in the Brugada syndrome.</AbstractText> |
9,699 | Detection of refrigerator-associated 60 Hz alternating current as ventricular fibrillation by an implantable defibrillator. | This report describes a patient with an implantable defibrillator who suffered an inappropriate defibrillation shock upon retrieving some food items from his inadequately earthed refrigerator. Noise typical of electrical interference can be observed in the stored electrogram of the episode. The patient was instructed to earth his home appliances, but he decided to avoid his refrigerator altogether, and has had no subsequent shocks. |
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