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14,700 | A rare cause of atrial fibrillation: mad honey intoxication. | Mad honey intoxication occurs after ingestion of honey containing grayanotoxin.</AbstractText>We report the case of a 36-year-old man who ingested mad honey and developed atrial fibrillation.</AbstractText>Mad honey intoxication is often characterized by symptoms such as hypotension, bradycardia, and syncope. Patients may also experience gastrointestinal, neurologic, and cardiovascular symptoms due to intoxication. Cardiac rhythm abnormalities, including sinus bradycardia, atrioventricular blocks, and nodal rhythms, also may be observed. To our knowledge, this is the first case report of a 36-year old man developing atrial fibrillation with a slow ventricular response after mad honey ingestion.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,701 | Risk factors and in-hospital mortality in Chinese patients undergoing coronary artery bypass grafting: analysis of a large multi-institutional Chinese database. | This study was undertaken to delineate outcomes and to assess risk factors for in-hospital mortality among Chinese patients undergoing coronary artery bypass grafting.</AbstractText>From 2007 to 2008, a total of 9838 consecutive adult patients undergoing coronary artery bypass grafting were enrolled in the Chinese Coronary Artery Bypass Grafting Registry, which included 43 centers from 17 province-level regions in China. This registry collected information on 67 preoperative factors and 30 operative factors believed to influence in-hospital mortality. The relationship between risk factors and in-hospital mortality was evaluated by univariate and logistic regression analyses.</AbstractText>Overall in-hospital mortality was 2.5%. Eleven risk factors were found to be significant predictors for outcome: age (continuous), body mass index (continuous), left ventricular ejection fraction (continuous), preoperative New York Heart Association functional class III or IV, chronic renal failure, extracardiac arteriopathy, chronic obstructive pulmonary disease, preoperative atrial fibrillation or flutter (within 2 weeks), preoperative critical state, other than elective surgery, and combined valve procedure. Calibration with the Hosmer-Lemeshow test was satisfactory (P=.35), and the discrimination power was good (area under the receiver operating characteristic curve, 0.81; 95% confidence interval, 0.79-0.84).</AbstractText>The risk profiles and in-hospital mortality of Chinese patients undergoing coronary artery bypass grafting were determined from data in the most up-to-date multi-institutional database. Eleven variables were demonstrated to be independent risk factors for in-hospital death after coronary artery bypass grafting.</AbstractText>Copyright © 2012 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.</CopyrightInformation> |
14,702 | Patients with atrial fibrillation in a primary care setting: Val-FAAP study. | To assess the clinical characteristics of patients with atrial fibrillation in the primary care setting.</AbstractText>This was a 2-phase, cross-sectional, multicenter study: phase A assessed the proportion of atrial fibrillation patients assisted in primary care over 5 days; phase B analyzed atrial fibrillation patients' clinical characteristics and management.</AbstractText>In phase A, 119 526 subjects (age 52.9 [15.2] years; 40.9% male) received primary care in participating centers; 6.1% had atrial fibrillation. This proportion increased with age, hypertension, and male sex. In phase B, we analyzed 3287 atrial fibrillation patients (age 71.9 [10.1] years; 52.3% male). Risk factors were hypertension (92.6%), hypercholesterolemia (70.6%), related cardiovascular disease, heart failure (21.3%), and ischemic heart disease (20.9%). Permanent atrial fibrillation was the most frequent type of atrial fibrillation (45.3%). Age and cardiac and renal diseases were related to permanent atrial fibrillation development. Although more than two-thirds of patients had a CHADS(2) score ≥2, about one-third of them were not taking anticoagulants; by contrast, 46.8% of patients with CHADS(2)=0 were taking oral anticoagulants.</AbstractText>In primary care, 6.1% of patients had atrial fibrillation. Patients with atrial fibrillation had high comorbidity. Anticoagulant treatment is far from optimal for atrial fibrillation patients in primary care.</AbstractText>Copyright © 2011 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.</CopyrightInformation> |
14,703 | [Non compaction cardiomyopathy: a series of 15 cases]. | Non compaction cardiomyopathy is a rare disorder caused by the arrest of myocardial compaction during embryogenesis, leading to a non compacted endocardial layer with marked hypertrabeculation and deep recesses.</AbstractText>To report the clinical and echocardiographic characteristics of a series of 15 adult patients with non-compaction cardiomyopathy.</AbstractText>We included a total of 15 patients aged 52 ± 17 years (40% males) diagnosed at our echocardiography laboratory between January 2001 and July 2010.</AbstractText>The form of presentation was heart failure in 53% of subjects, syncope in 20%o, ventricular arrhythmias in 13%o and stroke in 7%>. Left ventricular end-diastolic diameter was 66 ± 11 mm and estimated ejection fraction was 27 ± 10%>. Apical and/or mid-ventricular segments of the left ventricle were involved in all the cases. Pulmonary hypertension was present in 40%o. The average follow-up was 19 months and no patient died during this period. Sixty seven percent of the patients had manifestations of heart failure, 27%o presented sustained ventricular arrhythmias and 20%> had atrial fibrillation or flutter, whereas 13%o had cerebral embolic events. An automated internal cardioverter defibrillator was implanted in 47%o of patients.</AbstractText>Non-compaction cardiomyopathy is associated with high cardiovascular morbidity. The diagnosis is made in advanced stages of the disease, with significant dilation and ventricular dysfunction.</AbstractText> |
14,704 | The changes of brain water diffusion and blood flow on diffusion-weighted and perfusion-weighted imaging in a canine model of cardiac arrest. | To study the changes of brain water diffusion and cerebral haemodynamics of cortical areas using magnetic resonance imaging (MRI) in canine models of cardiac arrest (CA) and restoration of spontaneous circulation (ROSC). The secondary study objective was to evaluate whether MRI can be used to observe haemodynamic disorders in brain microcirculation.</AbstractText>CA was induced in six beagle dogs using electrical stimulation followed by resuscitation to spontaneous circulation 3 min later. The dogs were scanned using MRI for echo planar, diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) with injection of Gd-diethylene triamine pentaacetic acid (DTPA) prior to induction of CA and 3 days after ROSC. The arterial blood pressure, unilateral common carotid artery flow and intracranial microcirculation were recorded.</AbstractText>All dogs successfully underwent electric-induced ventricular fibrillation which lasted 3 min and were resuscitated to maintain blood pressure stability. Serial MRI scans found that cerebral blood flow (RCBF) decreased in day 1 after ROSC and returned to baseline on day 3. Apparent diffusion coefficient (ADC), however, decreased on day 1 and remained lower than baseline on day 3, with 765.8±82.5×10(-6) mm(2) s(-1) on day 1 and 770.4±59.4×10(-6) mm(2) s(-1) on day 3 comparing to 855.8±43.4×10(-6) mm(2) s(-1) on baseline.</AbstractText>These data provide the evidence that early MRI can be used to observe acute haemodynamic disorders in brain microcirculation in a canine model of cardiac arrest.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,705 | Mechanical stretch of atrial myocyte monolayer decreases sarcoplasmic reticulum calcium adenosine triphosphatase expression and increases susceptibility to repolarization alternans. | The purpose of this study was to investigate the effect of stretch (the major risk factor for atrial fibrillation [AF]) on spatial and temporal alternations of action potential duration (APD-ALT) and calcium transient in cultured atrial myocyte monolayer.</AbstractText>How rapid firings or premature beats trigger AF is not completely understood. Discordant repolarization alternans, characterized by simultaneous prolongation and shortening of APD in different myocardial regions, is central to the genesis of ventricular fibrillation. We hypothesized that repolarization alternans also is central to the initiation of multiple re-entry circuits and AF.</AbstractText>Confluent HL-1 atrial myocyte monolayer with spontaneous depolarization was cultured in silicone membrane and subjected to mechanical stretch. Rapid field pacing was used to induce alternans. A high-resolution dual optical mapping system was used to record action potentials and calcium transients.</AbstractText>High-rate pacing induced APD-ALT and calcium transient in atrial myocyte monolayer. Mechanical stretch significantly decreased the thresholds for APD-ALT and calcium transient. Mechanical stretch decreased the expression of sarcoplasmic reticulum adenosine triphosphatase 2, and thus slower calcium reuptake kinetics, which was responsible for the susceptibility to alternans. Mechanical stretch did not alter the APD restitution kinetics. Mechanical stretch also enhanced spatially discordant alternans. Overexpression of sarcoplasmic reticulum adenosine triphosphatase 2 reversed all the effects of stretch on susceptibility to alternans. In intact atrium, mechanical stretch also enhanced discordant alternans.</AbstractText>Mechanical stretch increased the susceptibility to alternans in atrial myocytes, which may explain the susceptibility to AF in conditions of atrial stretch, such as mitral valvular heart disease, heart failure, and hypertension.</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,706 | Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. | We reviewed available evidence for cardiovascular effects of n-3 polyunsaturated fatty acid (PUFA) consumption, focusing on long chain (seafood) n-3 PUFA, including their principal dietary sources, effects on physiological risk factors, potential molecular pathways and bioactive metabolites, effects on specific clinical endpoints, and existing dietary guidelines. Major dietary sources include fatty fish and other seafood. n-3 PUFA consumption lowers plasma triglycerides, resting heart rate, and blood pressure and might also improve myocardial filling and efficiency, lower inflammation, and improve vascular function. Experimental studies demonstrate direct anti-arrhythmic effects, which have been challenging to document in humans. n-3 PUFA affect a myriad of molecular pathways, including alteration of physical and chemical properties of cellular membranes, direct interaction with and modulation of membrane channels and proteins, regulation of gene expression via nuclear receptors and transcription factors, changes in eicosanoid profiles, and conversion of n-3 PUFA to bioactive metabolites. In prospective observational studies and adequately powered randomized clinical trials, benefits of n-3 PUFA seem most consistent for coronary heart disease mortality and sudden cardiac death. Potential effects on other cardiovascular outcomes are less-well-established, including conflicting evidence from observational studies and/or randomized trials for effects on nonfatal myocardial infarction, ischemic stroke, atrial fibrillation, recurrent ventricular arrhythmias, and heart failure. Research gaps include the relative importance of different physiological and molecular mechanisms, precise dose-responses of physiological and clinical effects, whether fish oil provides all the benefits of fish consumption, and clinical effects of plant-derived n-3 PUFA. Overall, current data provide strong concordant evidence that n-3 PUFA are bioactive compounds that reduce risk of cardiac death. National and international guidelines have converged on consistent recommendations for the general population to consume at least 250 mg/day of long-chain n-3 PUFA or at least 2 servings/week of oily fish. |
14,707 | Beating heart surgery via right thoracotomy for reoperative mitral valve surgery: a safe and effective operative alternative. | Right thoracotomy using ventricular fibrillation with cooling has been used for redo mitral valve surgery. This approach avoids the complications of redo sternotomy, such as injury to prior grafts and hemorrhage. As a further refinement, we have used a beating heart technique to further minimize complications while simplifying the operation.</AbstractText>We reviewed the outcomes of 450 patients who underwent redo mitral valve surgery via a right thoracotomy from 1996 to 2011 at the University of Michigan. Of these, 134 patients underwent redo mitral valve surgery with ventricular fibrillation, and 316 patients underwent beating heart surgery. Although operative eras were consecutive, patients' age, risk factors, New York Heart Association, and preoperative left ventricular ejection fraction were not significantly different. Core temperature on cardiopulmonary bypass for beating heart surgery was 32°C versus 26°C for ventricular fibrillation.</AbstractText>Patients undergoing beating heart surgery had shorter periods of cardiopulmonary bypass: 81±9 minutes versus 113±36 minutes. Beating heart surgery required less blood products than ventricular fibrillation: 1.65±2 units versus 3.8±5 units packed red blood cells, 0.6±1.2 units versus 1.8±4 units fresh-frozen plasma, and 1.02±4 versus 7.5±17 platelet packs (all P<.01). Conversely, patients receiving ventricular fibrillation required longer postoperative ventilation: 34±101 hours versus 15.5±27 hours (P<.01). The 30-day mortality was similar for both (6.5% for beating heart and 7.4% for ventricular fibrillation), and postoperative length of stay was the same at 7 days. Stroke rate was 2.6% for patients undergoing beating heart surgery and 3% for patients receiving ventricular fibrillation. Significant operative complications were uncommon; there was no catastrophic hemorrhage, and only 2 patients receiving ventricular fibrillation and 2 patients undergoing beating heart surgery required reexploration.</AbstractText>As reoperative cardiac surgery continues to increase, techniques that safely facilitate operation while improving outcome should be adopted. As an operative alternative, redo right thoracotomy mitral valve surgery on the beating heart is associated with shorter bypass time, less transfusion requirements, shorter postoperative ventilation, and lower mortality. This safe and effective approach should be considered for this complex operation.</AbstractText>Copyright © 2012. Published by Mosby, Inc.</CopyrightInformation> |
14,708 | Investigation of the atrial electromechanical delay duration in Behcet patients by tissue Doppler echocardiography. | To investigate the atrial electromechanical delay (EMD) duration that is a non-invasive predictor of atrial fibrillation (AF) in patients with Behcet's disease (BD).</AbstractText>Thirty-eight Behcet's patients (24 females, 14 males; mean age: 43.6 ± 10.3 years) who were being followed in the dermatology or internal medicine department and 29 demographically matched controls (13 females, 16 males; mean: age 42.6 ± 11.1 years) were included in the study. The inclusion criteria were recurrent oral ulcerations and two of the following features: recurrent genital ulceration, eye lesions, skin lesions or positive pathergy skin test for Behcet's group. Using tissue Doppler imaging, atrial electromechanical coupling [time interval from the onset of P wave on surface electrocardiogram to the beginning of A wave interval with tissue Doppler echocardiography (PA)] were measured from the lateral mitral annulus (PA lateral), septal mitral annulus (PA septum), and right ventricular tricuspid annulus (PA tricuspid). The mean disease duration was 10.5 ± 7.7 years. The inter-atrial and intra-atrial EMD were significantly higher in the Behcet group than those in the controls (19.8 ± 8.2 vs. 13.1 ± 4.4 ms, P = 0.001; 11.5 ± 7.4 vs. 6.9 ± 3.7 ms, P = 0.02; respectively). The left atrial EMD was similar in both of the groups. However, the P(max) and PWD values were significantly higher in the BD group compared with those in the controls (120.5 ± 10.1 vs. 112.1 ± 5.9 ms, P < 0.0001; 44.9 ± 10.7 vs. 28.4 ± 5.9 ms, P < 0.0001; respectively).</AbstractText>Atrial electromechanical conduction times were increased in the BD patients compared with those in the controls. The tendency of BD patients to go into AF can be easily and non-invasively detected using tissue Doppler echocardiography. These findings may be indicators for subclinical cardiac involvement.</AbstractText> |
14,709 | Defibrillation 2: Using defibrillators in hospital. | Patients who have a cardiac arrest in hospital should, if it is indicated, be defibrillated as quickly as possible--ideally within three minutes. Most hospital wards and other clinical areas have access to defibrillators with both advisory (semi-automated) and manual modes. The former enables first responders, including nurses without ECG interpretation skills, to defibrillate the patient while awaiting the arrival of the cardiac arrest team who can then select and use the manual mode. Most hospital nurses will be trained in advisory defibrillation, while a few will be trained in manual defibrillation. This article provides an overview of defibrillation in hospital, and looks at both advisory and manual defibrillation. |
14,710 | Enhanced sensitivity to drug-induced QT interval lengthening in patients with heart failure due to left ventricular systolic dysfunction. | Patients with heart failure (HF) are at increased risk for drug-induced torsades de pointes (TdP) due to unknown mechanisms. Our objective was to determine if sensitivity to drug-induced QT interval lengthening is enhanced in patients with HF. In this multicenter, prospective study, 15 patients with atrial fibrillation or flutter requiring conversion to sinus rhythm were enrolled: 6 patients with New York Heart Association class II to III HF (mean ejection fraction [EF], 30% ± 9%), and 9 controls (mean EF, 53% ± 6%). Patients received ibutilide 1 mg intravenously. Blood samples and 12-lead electrocardiograms were obtained prior to and during 48 hours postinfusion. Serum ibutilide concentrations at 50% maximum effect on Fridericia-corrected QT (QT(F)) intervals (EC(50)) were determined, and areas under the effect (QT(F) interval vs time) curves (AUECs) were calculated. Ibutilide concentration-QT(F) relationships were best described by a sigmoidal E(max) model with a hypothetical effect compartment. Median [interquartile range] AUEC from 0 to 4 hours was larger in the HF group than in controls (1.86 [1.86-1.93] vs 1.82 [1.81-1.84] s·h; P = .04). Median EC(50) was lower in the HF group (0.48 [0.46-0.49] vs 1.85 [1.10-3.23] μg/L; P = .008). Sensitivity to drug-induced QT interval lengthening is enhanced in patients with systolic HF, which may contribute to the increased risk of drug-induced TdP. |
14,711 | A free-floating left atrial thrombus develops intermittent entrapment in the mid-ventricle during diastole. | Free-floating left atrial thrombi are rare. Here we report a case of a 75-year-old woman with atrial fibrillation who was admitted for treatment of acute myocardial infarction. A free-floating left atrial thrombus was found incidentally on echocardiography. Ten days after percutaneous coronary intervention, the patient had mild faintness with transient hypotension, and it was found that the left atrial thrombus had developed intermittent entrapment in the mid-ventricle during diastole, with abrupt rebound back to the left atrial cavity during systole. Urgent removal of the thrombus was performed successfully. Although the free-floating thrombus had appeared to be spherical, like a ball thrombus, on echocardiography, the excised thrombus was pedunculated. A cut section revealed a laminated thrombus with an onion-skin-like appearance. |
14,712 | The value of defibrillator far-field electrograms for ablation of idiopathic ventricular fibrillation. | We report a case of idiopathic ventricular fibrillation treated by catheter ablation of the monomorphic initiating premature beat. The initiating focus was identified using intacardiac defibrillator electrograms (EGMs). |
14,713 | An adult patient with isolated left ventricular noncompaction presented with atrial fibrillation and complete atrioventricular block. | Isolated left ventricular noncompaction (IVNC) is a rare congenital anomaly. The clinical manifestations include congestive heart failure, systemic thromboemboli, arrhythmias and sudden death. We report a case of IVNC in a male patient who presented with atrial fibrillation with complete heart block. |
14,714 | Catheter ablation for atrial fibrillation in patients with left ventricular systolic dysfunction. A systematic review and meta-analysis. | Atrial fibrillation (AF) and heart failure are often coexisting major public health burdens. Although several studies have reported partial restoration of systolic left ventricular (LV) function after catheter ablation for AF, the method is not widely applied in patients with LV dysfunction. We reviewed the results of AF ablation in patients with systolic LV dysfunction.</AbstractText>PubMed was searched for studies published after 2000 reporting original data on AF catheter ablation in adult patients with systolic LV dysfunction. Primary end point was the change of LV ejection fraction (LVEF) after catheter ablation; secondary endpoints were the changes of exercise capacity and quality of life after the procedure. We calculated mean difference (MD) of LVEF and 95% confidence interval (95% CI) using random-effects models. Heterogeneity was investigated by I(2) statistic, publication bias with Egger's test. The impact of covariates on LVEF improvement was evaluated with meta-regression analyses. Nine studies with a total of 354 patients with systolic LV dysfunction were analyzed. Study patients were mainly male with mean age 49 to 62 years, LVEF was moderately impaired and ranged in all but 1 study from 35% to 43%. LVEF improved after ablation with a MD of 11.1% (95% CI: 7.1-15.2, P < .001). Heterogeneity among analyzed studies was significant (I(2) = 92.9, P < .001). No potential publication bias was found. In meta-regression analyses, the proportion of patients with coronary artery disease was inversely related with LVEF improvement (P < .0001) whereas there was no association between the LVEF change and the proportion of patients with nonparoxysmal AF or the proportion of patients without AF recurrences during follow-up.</AbstractText>AF ablation in patients with systolic LV dysfunction results in significant improvement of LV function, but the extent of this improvement is heterogeneous. Patients with coronary artery disease seem to benefit less than patients with other underlying diseases. These results may be explained by patient selection.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,715 | A phased approach to cardiac arrest resuscitation involving ventricular fibrillation and pulseless ventricular tachycardia. | With the release of the 2010 American Heart Association (AHA) Guidelines for cardiopulmonary resuscitation and emergency cardiac care, evidence regarding management of out-of-hospital cardiac arrest suggests a more fundamental approach. To aid in understanding and learning, this article proposes a method that optimizes the timing and delivery of evidence-proven therapies with a 3-phase approach for out-of-hospital resuscitation from ventricular fibrillation and pulseless ventricular tachycardia. Although this model is not a new concept, it is largely based on the 2010 AHA Guidelines, enhancing the philosophy of the "CAB" concept (Chest compressions/Airway management/Breathing rescue). |
14,716 | Right ventricular dysfunction is a predictor of non-response and clinical outcome following cardiac resynchronization therapy. | Cardiac resynchronization therapy (CRT) is an established treatment in advanced heart failure (HF). However, an important subset does not derive a significant benefit. Despite an established predictive role in HF, the significance of right ventricular (RV) dysfunction in predicting clinical benefit from CRT remains unclear. We investigated the role of RV function, assessed by cardiovascular magnetic resonance (CMR), in predicting response to and major adverse clinical events in HF patients undergoing CRT.</AbstractText>Sixty consecutive patients were evaluated with CMR prior to CRT implantation in a tertiary cardiac centre. The primary end-point was a composite of death from any cause or unplanned hospitalization for a major cardiovascular event. The secondary end-point was response to therapy, defined as improvement in left ventricular ejection fraction ≥ 5% on echocardiography at one year.</AbstractText>Eighteen patients (30%) met the primary end-point over a median follow-up period of 26 months, and 27 out of 56 patients (48%) were considered responders to CRT. On time-to-event analysis, only atrial fibrillation (HR 2.6, 95% CI 1.02-6.84, p = 0.047) and RV dysfunction, either by a reduced right ventricular ejection fraction-RVEF (HR 0.96, 95% CI 0.94-0.99, p = 0.006) or tricuspid annular plane systolic excursion-TAPSE (HR 0.88, 95% CI, 0.80-0.96, p = 0.006), were significant predictors of adverse events. On logistic regression analysis, preserved RVEF (OR 1.05, 95% CI 1.01-1.09, p = 0.01) and myocardial scar burden (OR 0.90, 95% CI 0.83-0.96, p = 0.004) were the sole independent predictors of response to CRT. Patients with marked RV dysfunction (RVEF < 30%) had a particularly low response rate (18.2%) to CRT.</AbstractText>Right ventricular function is an important predictor of both response to CRT and long-term clinical outcome. Routine assessment of the right ventricle should be considered in the evaluation of patients for CRT.</AbstractText> |
14,717 | Long-term follow-up of prophylactic implantable cardioverter-defibrillator-only therapy: comparison of ischemic and nonischemic heart disease. | The benefits of primary prophylactic implantable cardioverter-defibrillators (ICDs) are actually debated, as some drawbacks become more apparent and as the natural history of cardiac disease seems to improve. Therefore, contemporary follow-up data of non-trial populations treated according to current guidelines remain necessary. The aim of this study was to evaluate mortality and the occurrence of ICD interventions in patients with coronary artery disease (CAD) and dilated cardiomyopathy (DCM) who received in the recent era a primary prophylactic ICD without resynchronization therapy.</AbstractText>Survival and event-free rates from appropriate ICD therapy are different between ischemic and nonischemic ICD patients.</AbstractText>Prospective cohort study of 427 consecutive primary prevention ICD patients with ischemic or nonischemic heart disease, excluding patients with resynchronization.</AbstractText>Ischemic heart disease was present in 290 patients (68%), nonischemic heart disease in 137 patients (32%). During a median follow-up of 31 months (interquartile range [IQR] 15-45 months), 30 patients (7%) died. Mortality was not different in both disease categories. The incidence of appropriate ICD interventions was similar in CAD and DCM (23% vs 21%). Appropriate ICD intervention occurred more frequently in patients with atrial fibrillation (29% vs 19%). Inappropriate ICD intervention occurred in 11% of patients.</AbstractText>The clinical course of ischemic and nonischemic heart disease patients treated with a primary prophylactic ICD is similar with respect to mortality and to appropriate and inappropriate ICD interventions, in spite of a younger age at baseline of the DCM patients.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,718 | Cardiac fibrillation risk of TASER X-26 dart mode application. | In view of reported fatalities there are still controversial discussions on whether electronic stun law enforcement weapons can cause cardiac fibrillation. Experimental data are contradictory. Simplified theoretical estimations led to a negligible low risk of 8.10(-7). With a detailed numerical-anatomical model of an adult man (NORMAN) cardiac exposure to Taser X26 high-tension pulses was quantitatively assessed and the fibrillation risk estimated by accounting for its dependence on excited volume based on 3D cardiac exposure patterns. For distance mode and worst case dart hits it could be demonstrated that cardiac exposure can reach the 30% fibrillation risk level. Risk reduces considerably if direct current flow across the heart is prevented. The overall fibrillation risk of Taser application is further reduced by the limited probability of critical hits. However, in agreement with experimental findings it is demonstrated that cardiac fibrillation risk of Taser X26 dart mode application is small, however, not negligible. |
14,719 | Analysis of J waves during myocardial ischaemia. | The aim of this study was to investigate the relationship between J-wave dynamics and arrhythmias during myocardial ischaemia in patients with vasospastic angina (VSA).</AbstractText>Sixty-seven consecutive patients diagnosed with VSA by a provocation test for coronary spasm were grouped according to whether they had a J wave in the baseline electrocardiograms or not (VSA-JW group, n = 14; VSA-non-JW group: n = 53). We retrospectively studied the associations between J-wave and ST-segment dynamics and induced ventricular fibrillations (VFs) during coronary spasm.  In the VSA-JW group, 7 of the 14 patients showed changes in J-wave morphology and/or gains in J-wave voltage, followed by VF in 4 patients. Compared with patients without VF, the four patients with VF showed similar maximal voltage in the baseline J waves but a higher voltage during induced coronary spasms (0.57 ± 0.49 vs. 0.30 ± 0.11 mV; P = 0.011). In three patients with VF, J waves progressively increased and were accompanied by the characteristic coved-type or lambda-shaped ST-segment elevations. In the VSA-non-JW group, only four patients showed new appearances of J waves during coronary spasms and another patient without a distinct J wave developed VF. Ventricular fibrillations were induced more frequently in the VSA-JW group than in the VSA-non-JW group [4/14 (29%) vs. 1/53 (2%); P = 0.012].</AbstractText>J-wave augmentations were caused by myocardial ischaemia during coronary spasms. The presence and augmentation of J waves, especially prominent J waves with the characteristic ST-elevation patterns, were associated with VF.</AbstractText> |
14,720 | Role of cardiac troponin in the diagnosis of acute myocardial infarction in comatose patients resuscitated from out-of-hospital cardiac arrest. | Troponin is a major diagnostic criterion of acute myocardial infarction (AMI) but in out-of-hospital cardiac arrest (OHCA) patients, its diagnostic value may be altered by cardiopulmonary resuscitation.</AbstractText>Single-centre study assessing the diagnostic characteristics of troponin for AMI diagnosis in consecutive patients resuscitated from OHCA between 2002 and 2008 with coronary angiogram (CA) performed on admission. Patients with obvious non-cardiac cause of OHCA, unsustained or absent return of spontaneous circulation were excluded. AMI was defined on CA by the presence of acute occlusion or critical stenosis with intracoronary fresh thrombus easily crossed by an angioplasty wire. Troponin concentration was recorded once on admission and once 6-12h after the OHCA.</AbstractText>A total of 163 patients aged 56 (median) years (interquartile range (IQR) 48-65) was included, all comatose. Most prevalent initial OHCA rhythms were ventricular fibrillation (49%) and asystole (41%). AMI was diagnosed on coronary angiogram in 37% of the patients. Median troponin concentration on admission was 1.7 (0.3-10)ngml(-1) and sensitivity for AMI diagnosis was 72% and specificity 75% for a 2.5ngml(-1) cut-off. A combined criterion comprising ST elevation and troponin >2.5ngml(-1) had a sensitivity of 93% and specificity of 64%. Six to twelve hours after the OHCA, median troponin concentration was 7.6ngml(-1) (1.4-47.5), sensitivity was 84% and specificity 84% for a 14.5ngml(-1) cut-off.</AbstractText>Troponin I has a good diagnostic value for AMI diagnosis in OHCA patients. In combination with ST elevation, troponin I on admission achieves a very high sensitivity.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,721 | [Spanish catheter ablation registry. 10th official report of the Spanish Society of Cardiology Working Group on Electrophysiology and Arrhythmias (2010)]. | The findings of the 2010 Spanish Catheter Ablation Registry are presented.</AbstractText>Data were collected in two ways: retrospectively using a standardized questionnaire, and prospectively from a central database. Each participating center selected its own preferred method of data collection.</AbstractText>Fifty-seven Spanish centers voluntarily contributed data to the survey. A total of 8762 ablation procedures was analyzed, averaging 154 (97) per center. The 3 main conditions treated were atrioventricular nodal reentrant tachycardia (n=2321; 27%), typical atrial flutter (n=1839; 22%), and accessory pathways (n=1738; 20%). Atrial fibrillation was the fourth most common condition treated (n=1309; 15%), and reflects mild growth. The overall success rate was 94%, major complications occurred in 1.7%, and the overall mortality rate was 0.06%.</AbstractText>Data from the 2010 registry show that the number of ablations carried out continued to increase and exceeded 8700 ablations for the second time. In addition, they show, in general, a higher success rate and a lower number of complications. Again, cavotricuspid isthmus ablation for typical atrial flutter was the second most common condition treated. The number of catheter ablations carried out for ventricular arrhythmias in Spain is growing compared to the previous year.</AbstractText>Copyright © 2011 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.</CopyrightInformation> |
14,722 | Additional predictive value of serum potassium to Thrombolysis In Myocardial Infarction risk score for early malignant ventricular arrhythmias in patients with acute myocardial infarction. | The aim of this study was to evaluate the additional predictive value of serum potassium (SK) to Thrombolysis In Myocardial Infarction (TIMI) risk score for malignant ventricular arrhythmias (MVA) in patients within 24 hours of acute myocardial infarction (AMI).</AbstractText>This was a 6-year retrospective study. The receiver operating characteristic curve was used to evaluate the predictive value of SK and TIMI risk score for MVA attack. In addition, SK-modified TIMI risk score was created by incorporating SK information into the usual score; the accuracy of new score was compared with that of the usual TIMI risk score by comparing the area under the receiver operating characteristic curves (AUC).</AbstractText>Among the 468 patients enrolled, the incidence of MVA 24 hours after AMI was 9.4%, and it was higher in the hypokalemia group compared with that of the normokalemic group (27.3% vs 7.5%, P < .001; odds ratio, 4.594; 95% confidence interval [CI], 2.159-9.774). A significant predictive value of SK was indicated by AUC of 0.787 (95% CI, 0.747-0.823, P < .01). Serum potassium remained a predictor of MVA after being adjusted by the variables in TIMI risk score. The AUC of TIMI risk score in relation to MVA was 0.586 (95% CI, 0.54-0.631; P = .0676). The incorporation of SK into TIMI risk score improved its predictive value for MVA attack (AUC = 0.66; 95% CI, 0.568-0.753; P < .001), with significant difference between AUC of the new score and that of the original risk score (Z = 2.474, P = .013).</AbstractText>Serum potassium on admission to the emergency department may be used as a valuable predictor and could add predictive information to some extent to TIMI risk score for MVA attack during 24-hour post-AMI.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,723 | Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: role of pulmonary veins. | We aimed to characterize electrophysiological properties of pulmonary veins (PVs) in patients with Wolff-Parkinson-White (WPW) syndrome and atrial fibrillation (AF), and to compare them to those in patients with WPW without AF.</AbstractText>A total of 31 patients (mean age 40 ± 15 years, 23 males) with WPW were recruited: 16 patients with (AF group) and 15 without (controls) a history of AF. The basic electrophysiological (EPS) and echocardiographic data were not different between the 2 groups. Effective refractory periods (ERPs) of PVs were significantly shorter in the AF group compared to controls: left superior (LS) PV ERP 185±29 versus 230 ± 24 ms, P = 0.001; left inferior PV ERP 198 ± 25 versus 219 ± 26 ms, P = 0.04; right superior (RS) PV ERP 207 ± 25 versus 236 ± 19 ms, P = 0.001; right inferior PV ERP 208 ± 30 versus 240 ± 19 ms, P = 0.003. Maximal veno-atrial conduction delay (i.e., the maximal prolongation of interval from stimulus delivered at PV ostia to proximal coronary sinus after extrastimulus compared to the basic drive cycle) was longer in the AF group when pacing from LSPV (69.3 ± 37.9 vs 32.6 ± 16.1 ms, P = 0.01) and RSPV (74.1 ± 25.9 vs 50.2 ± 26.5 ms, P = 0.04). During EPS, AF was induced more often in the AF group (n = 7) compared to controls (n = 1; P = 0.04). Follow-up revealed that AF recurred in 3 patients in the AF group and none of the controls.</AbstractText>Patients with WPW syndrome and AF have shorter ERPs of PVs and greater maximal veno-atrial conduction delay compared to patients with WPW without AF. These findings suggest a potential role of PVs in the development of AF in patients with WPW.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,724 | Pacemaker and implantable cardioverter-defibrillator use in a US myotonic dystrophy type 1 population. | We assessed implant rates, indications, characteristics, and outcomes in patients with the neuromuscular disease, myotonic dystrophy type 1 (DM1) receiving a pacemaker or an implantable cardioverter-defibrillator (ICD).</AbstractText>Device use was evaluated in a prospective, multicenter registry of 406 genetically confirmed adult patients followed for 9.5 ± 3.2 years. Forty-six (11.3%) had or received a pacemaker and 21 (5.2%) received an ICD. Devices were primarily implanted for asymptomatic conduction abnormalities and left ventricular (LV) systolic dysfunction. However, 7 (15.2%) pacemakers were implanted for third-degree atrioventricular block and 6 (28.6%) ICDs were implanted for ventricular tachyarrhythmias (ventricular tachycardia [VT] or fibrillation [VF]). Patients receiving devices were older and more frequently had heart failure, LV systolic dysfunction, atrial tachyarrhythmias, and ECG conduction abnormalities compared to nondevice patients. Five (10.9%) pacemaker patients underwent upgrade to an ICD, 3 for LV systolic dysfunction, 1 for VT/VF, and 1 for progressive conduction disease. Seventeen (27.4%) of the 62 patients with devices were pacemaker-dependent at last follow-up. Three (14.3%) ICD patients had appropriate therapies. Twenty-four (52.2%) pacemaker patients died including 13 of respiratory failure and 7 of sudden death. Seven (33.3%) ICD patients died including 2 of respiratory failure and 3 of sudden death. The patients with ICDs and sudden death all had LV systolic dysfunction and 1 death was documented due to inappropriate therapies.</AbstractText> DM1 patients commonly receive antiarrhythmia devices. The risk of VT/VF and sudden death suggests that ICDs rather than pacemakers should be considered for these patients.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,725 | Head-to-head comparison of arrhythmia discrimination performance of subcutaneous and transvenous ICD arrhythmia detection algorithms: the START study. | The development of a totally subcutaneous implantable defibrillator (S-ICD) system requires a new approach for arrhythmia detection. To evaluate arrhythmia discrimination of one such system, the Subcutaneous versus Transvenous Arrhythmia Recognition Testing (START) study was designed as a prospective, multicenter trial comparing simulated sensing performances of the S-ICD system with single- (SC-TV) and dual-chamber transvenous (DC-TV) implantable cardioverter-defibrillator (ICD) systems.</AbstractText>At ICD implantation, induced ventricular and atrial arrhythmias were recorded simultaneously in transvenous (right ventricular [RV] → superior vena cava [SVC]+ Coil) and cutaneous electrode configurations. Recorded signals of ventricular (n = 46) and atrial arrhythmias (n = 50) with ventricular rates >170 bpm from 64 patients were used to compare detection performance of the S-ICD system with TV-ICD systems from 3 manufacturers. Appropriate detection of ventricular tachyarrhythmias was assessed with devices programmed in single-zone (rate ≥ 170 bpm) and dual-zone configurations (ventricular fibrillation ≥ 240 bpm; ventricular tachycardia ≥ 170 bpm). S-ICD specificity performance for supraventricular arrhythmias was compared to single- and dual-chamber devices in a dual-zone configuration.</AbstractText>Appropriate detection of ventricular tachyarrhythmias for subcutaneous and TV devices in single- and dual-zone configurations was 100% and >99%, respectively. Specificity for supraventricular arrhythmias was significantly better for the S-ICD system compared to 2 of 3 TV systems, as well as the composite of TV devices (98.0%[S-ICD] vs 76.7%[SC-TV range: 64.0-92.0%] vs 68.0%[DC-TV range: 32.7-89.8%; P < 0.001]).</AbstractText>Appropriate ventricular arrhythmia detection is excellent for all ICD systems evaluated; however, specificity of supraventricular arrhythmia discrimination by the S-ICD system is better than discrimination by 2 of 3 TV systems.</AbstractText>© 2012 Wiley Periodicals, Inc.</CopyrightInformation> |
14,726 | Spontaneous atrial fibrillation initiated by tyramine in canine atria with increased sympathetic nerve sprouting. | Chronic left ventricular myocardial infarction (LVMI) promotes atrial and pulmonary veins (PV) sympathetic nerve sprouting.</AbstractText>To test the hypothesis that sympathetic stimulation with tyramine initiates atrial fibrillation (AF) by early after depolarization (EAD)-mediated triggered activity at the left atrial PV (LAPV) junction.</AbstractText>LVMI was created in 6 dogs and 6 dogs served as controls. Six to 8 weeks later the activation pattern of the isolated LAPV was optically mapped using dual voltage and intracellular Ca(+2) (Ca(i) (2+) )-sensitive epifluorescent dyes before and after tyramine (5 μM) perfusion.</AbstractText>Tyramine initiated spontaneous AF in 5 of 6 atria but none in the control group (P < 0.01). The AF was initiated by late phase 3 EAD-mediated triggered activity that arose from the LAPV junction causing functional conduction block in LA, reentry, and AF. The AF was subsequently maintained by mixed reentrant and focal mechanisms. The EADs arose during the late phase 3, when the Ca(i) (2+) level was 64 ± 12% of the peak systolic Ca(i) (2+) transient amplitude, a property caused by tyramine's simultaneous shortening of the action potential duration and lengthening of the Ca(i) (2+) transient duration in the LVMI group but not in the control. Tyrosine hydroxylase and growth associated protein 43 positive nerve sprouts were significantly increased in the sinus node, LAA, and the LSPV in the LVMI group compared to control (P < 0.01).</AbstractText>Increased atrial sympathetic nerve sprouts after LVMI makes the LAPV junction susceptible to late phase 3 EAD-mediated triggered and AF during sympathetic stimulation with tyramine.</AbstractText>© 2012 Wiley Periodicals, Inc.</CopyrightInformation> |
14,727 | Ionic and cellular mechanisms underlying the development of acquired Brugada syndrome in patients treated with antidepressants. | Tricyclic antidepressants are known to induce cardiac arrhythmias at therapeutic or supratherapeutic doses. The tricyclic antidepressant, amitriptyline, is reported to induce ST segment elevation in the right precordial electrocardiogram (ECG) leads, thus unmasking Brugada syndrome (BrS). The mechanism by which antidepressants induce the BrS phenotype and associated sudden death is not well established.</AbstractText>Action potentials (AP) were simultaneously recorded from epicardial and endocardial sites of isolated coronary-perfused canine right ventricular wedge preparations, together with a transmural pseudo-ECG. Amitriptyline alone (0.2 μM-1 mM) failed to induce a BrS phenotype. NS5806 (8 μM), a transient outward potassium channel current (I(to) ) agonist, was used to produce an outward shift of current mimicking a genetic predisposition to BrS. In the presence of NS5806, a therapeutic concentration of amitriptyline (0.2 μM) accentuated the epicardial AP notch leading to ST-segment elevation of the ECG. All-or-none repolarization at some epicardial sites but not others gave rise to phase-2-reentry and polymorphic ventricular tachycardia (VT) in 6 of 9 preparations. Isoproterenol (100 nM) or quinidine (10 μM) reversed the effects of amitriptyline aborting phase 2 reentry and VT (4/4). Using voltage-clamp techniques applied to isolated canine ventricular myocytes, 0.2 μM amitriptyline was shown to produce use-dependent inhibition of sodium channel current (I(Na) ), without significantly affecting I(to) (n = 5).</AbstractText>Our data suggest that amitriptyline-induced inhibition of I(Na) unmasks the Brugada ECG phenotype and facilitates development of an arrhythmogenic substrate only in the setting of a genetic predisposition by creating repolarization heterogeneities that give rise to phase 2 reentry and VT.</AbstractText>© 2012 Wiley Periodicals, Inc.</CopyrightInformation> |
14,728 | Impact of adenosine-provoked acute dormant pulmonary vein conduction on recurrence of atrial fibrillation. | Adenosine can be associated with acute recovery of conduction to the pulmonary veins (PVs) immediately after isolation. The objective of this study was to evaluate whether the response to adenosine predicts atrial fibrillation (AF) recurrence after a single ablation procedure in patients with paroxysmal AF.</AbstractText>A total of 109 consecutive patients (61 ± 10 years; 91 males) with drug-refractory paroxysmal AF who underwent AF ablation were analyzed. After PV antrum isolation (PVAI), dormant PV conduction was evaluated by an administration of adenosine in all patients. No acute reconnections were provoked by the adenosine in 70 (64.2%) patients (Group-1), but they were provoked in at least one side of the ipsilateral PVs in 39 (35.8%) patients (Group-2). All adenosine-provoked dormant conductions were successfully eliminated by additional ablation applications. By 12 months after the initial procedure, 72 (66.1%) patients were free of AF recurrences without any antiarrhythmic drugs. A Cox regression multivariate analysis of the variables including the adenosine-provoked reconductions, age, gender, duration of AF, presence of hypertension or structural heart disease, left atrial size, left ventricular ejection fraction, and body mass index demonstrated that adenosine-provoked reconductions were an independent predictor of AF recurrence after a single ablation procedure (hazard ratio: 1.387; 95% confidence interval: 1.018-1.889, P = 0.038). At the repeat session for recurrent AF, conduction recovery was observed similarly in both groups (P = 0.27).</AbstractText>Even after the elimination of any adenosine-provoked dormant PV conduction, the appearance of acute adenosine-provoked reconduction after the PVAI was an independent predictor of AF recurrence after a single AF ablation procedure.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,729 | Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation. | This study aimed to determine whether (a) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); (b) with the duration of VF, the degree of the imbalance would be greater; and (c) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function.</AbstractText>Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 (P < .001), and with the duration of VF, the level of TIMP-1 declined (P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups (P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups (P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions (r = -0.83 and r = -0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction (r = 0.85; P < .01).</AbstractText>There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,730 | Investigation of mechanism of drug-induced cardiac injury and torsades de pointes in cynomolgus monkeys. | Drug candidates must be thoroughly investigated for their potential cardiac side effects. During the course of routine toxicological assessment, the compound RO5657, a CCR5 antagonist, was discovered to have the rare liability of inducing torsades de pointes (polymorphic ventricular arrhythmia) in normal, healthy animals. Studies were conducted to determine the molecular mechanism of this arrhythmia.</AbstractText>Toxicological effects of repeat dosing were assessed in naïve monkeys. Cardiovascular effects were determined in conscious telemetry-implanted monkeys (repeat dosing) and anaesthetized instrumented dogs (single doses). Mechanistic studies were performed in guinea-pig isolated hearts and in cells recombinantly expressing human cardiac channels.</AbstractText>In cynomolgus monkeys, RO5657 caused a low incidence of myocardial degeneration and a greater incidence of ECG abnormalities including prolonged QT/QTc intervals, QRS complex widening and supraventricular tachycardia. In telemetry-implanted monkeys, RO5657 induced arrhythmias, including torsades de pointes and in one instance, degeneration to fatal ventricular fibrillation. RO5657 also depressed both heart rate (HR) and blood pressure (BP), with no histological evidence of myocardial degeneration. In the anaesthetized dog and guinea-pig isolated heart studies, RO5657 induced similar cardiovascular effects. RO5657 also inhibited Kv11.1 and sodium channel currents.</AbstractText>The molecular mechanism of RO5657 is hypothesized to be due to inhibition of cardiac sodium and Kv11.1 potassium channels. These results indicate that RO5657 is arrhythymogenic due to decreased haemodynamic function (HR/BP), decreased conduction and inhibition of multiple cardiac channels, which precede and are probably the causative factors in the observed myocardial degeneration.</AbstractText>© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.</CopyrightInformation> |
14,731 | Electrocardiographic characteristics and SCN5A mutations in idiopathic ventricular fibrillation associated with early repolarization. | Recently, we and others reported that early repolarization (J wave) is associated with idiopathic ventricular fibrillation. However, its clinical and genetic characteristics are unclear.</AbstractText>This study included 50 patients (44 men; age, 45 ± 17 years) with idiopathic ventricular fibrillation associated with early repolarization, and 250 age- and sex-matched healthy controls. All of the patients had experienced arrhythmia events, and 8 (16%) had a family history of sudden death. Ventricular fibrillation was inducible by programmed electric stimulation in 15 of 29 patients (52%). The heart rate was slower and the PR interval and QRS duration were longer in patients with idiopathic ventricular fibrillation than in controls. We identified nonsynonymous variants in SCN5A (resulting in A226D, L846R, and R367H) in 3 unrelated patients. These variants occur at residues that are highly conserved across mammals. His-ventricular interval was prolonged in all of the patients carrying an SCN5A mutation. Sodium channel blocker challenge resulted in an augmentation of early repolarization or development of ventricular fibrillation in all of 3 patients, but none was diagnosed with Brugada syndrome. In heterologous expression studies, all of the mutant channels failed to generate any currents. Immunostaining revealed a trafficking defect in A226D channels and normal trafficking in R367H and L846R channels.</AbstractText>We found reductions in heart rate and cardiac conduction and loss-of-function mutations in SCN5A in patients with idiopathic ventricular fibrillation associated with early repolarization. These findings support the hypothesis that decreased sodium current enhances ventricular fibrillation susceptibility.</AbstractText> |
14,732 | Activation of epidermal growth factor receptor mediates reperfusion arrhythmias in anaesthetized rats. | Epidermal growth factor receptor (EGFR) plays a critical role in the development and function of the heart. Previous studies have demonstrated that EGFR is involved in regulating electrical excitability of the heart. The present study was designed to investigate whether EGFR activation would mediate cardiac arrhythmias induced by reperfusion in anaesthetized rats.</AbstractText>Reperfusion arrhythmias were induced by 10 min ligation of the left anterior descending coronary artery, followed by a 30 min reperfusion in anaesthetized rats. The incidence and severity of cardiac arrhythmias were significantly reduced by pre-treatment with the EGFR kinase inhibitor AG556. The phosphorylation level of myocardial EGFR was increased during ischaemia and at early reperfusion. Intramyocardial transfection of EGFR siRNA reduced EGFR mRNA and protein, and decreased the incidence of ventricular fibrillation induced by reperfusion. Interestingly, tyrosine phosphorylation levels of cardiac Na(+) channels (I(Na)) and L-type Ca(2+) channels (I(Ca,L)) were significantly increased at time points corresponding to the alteration of EGFR phosphorylation levels during reperfusion. AG556 pre-treatment countered the increased tyrosine phosphorylation level of Na(+) and L-type Ca(2+) channels induced by reperfusion. Patch-clamp studies proved that AG556 could inhibit I(Na) and I(Ca,L) in rat ventricular myocytes. No significant alteration was observed in tyrosine phosphorylation levels of cardiac Kv4.2 and Kir2.1 channels during reperfusion.</AbstractText>These results demonstrate for the first time that EGFR plays an important role in the genesis of arrhythmias induced by reperfusion, which is likely mediated at least in part by enhancing tyrosine phosphorylation of cardiac Na(+) and L-type Ca(2+) channels.</AbstractText> |
14,733 | Fever-induced QTc prolongation and ventricular fibrillation in a healthy young man. | Long QT syndrome is associated with lethal tachyarrhythmia that can lead to syncope, seizure, and sudden death. Congenital long QT syndrome is a genetic disorder, characterized by delayed cardiac repolarization and prolongation of the QT interval on the electrocardiogram (ECG). Type 2 congenital long QT is linked to mutations in the human ether a go-go-related gene (HERG). There are environmental triggers of adverse cardiac events such as emotional and acoustic stimuli, but fever can also be a potential trigger of life-threatening arrhythmias in long QT syndrome type 2 patients. Herein, we report a healthy young man who experienced fever-induced polymorphic ventricular tachycardia and QT interval prolongation. |
14,734 | [Fatal succinylcholine-induced hyperkalemia in an intensive care unit]. | Succinylcholine-induced hyperkalemia is reported, but is still used in rapid sequence induction. In our case a 44 year-old man with septic shock was mechanically ventilated for 13 days, extubated but because of respiratory insufficiency reintubated. During induction an increase in p-potassium (4.2-11.7 mmol/l) caused ventricular fibrillation. Immobilization/infection cause an up-regulation and change in acetylcholine receptors is probably the reason for the extensive hyperkalemia and death. Caution in using succinylcholine is recommended and using rocuronium as an alternative is discussed. |
14,735 | [Commotio cordis]. | Blunt, non-penetrating trauma of the chest (commotio cordis) can cause sudden death in individuals without known cardiac disease. Sudden death in commotio cordis is due to ventricular fibrillation. The timing of the blow must be during the electric vulnerable period of the ECG cyclus, 10-40 milliseconds before the peak of the T-wave. The risk of arrhythmia increases progressively, until a velocity of 64 km/h, and at higher velocities the risk of ventricular fibrillation begins to diminish. The location of the impact must be directly over the cardiac silhouette. |
14,736 | Shaping a new Ca²⁺ conductance to suppress early afterdepolarizations in cardiac myocytes. | Sudden cardiac death (SCD) due to ventricular fibrillation (VF) is a major world-wide health problem. A common trigger of VF involves abnormal repolarization of the cardiac action potential causing early afterdepolarizations (EADs). Here we used a hybrid biological-computational approach to investigate the dependence of EADs on the biophysical properties of the L-type Ca(2+) current (I(Ca,L)) and to explore how modifications of these properties could be designed to suppress EADs. EADs were induced in isolated rabbit ventricular myocytes by exposure to 600 μmol l(-1) H(2)O(2) (oxidative stress) or lowering the external [K(+)] from 5.4 to 2.0-2.7 mmol l(-1) (hypokalaemia). The role of I(Ca,L) in EAD formation was directly assessed using the dynamic clamp technique: the paced myocyte's V(m) was input to a myocyte model with tunable biophysical parameters, which computed a virtual I(Ca,L), which was injected into the myocyte in real time. This virtual current replaced the endogenous I(Ca,L), which was suppressed with nifedipine. Injecting a current with the biophysical properties of the native I(Ca,L) restored EAD occurrence in myocytes challenged by H(2)O(2) or hypokalaemia. A mere 5 mV depolarizing shift in the voltage dependence of activation or a hyperpolarizing shift in the steady-state inactivation curve completely abolished EADs in myocytes while maintaining a normal Ca(i) transient. We propose that modifying the biophysical properties of I(Ca,L) has potential as a powerful therapeutic strategy for suppressing EADs and EAD-mediated arrhythmias. |
14,737 | Electromechanical wave imaging for arrhythmias. | Electromechanical wave imaging (EWI) is a novel ultrasound-based imaging modality for mapping of the electromechanical wave (EW), i.e. the transient deformations occurring in immediate response to the electrical activation. The correlation between the EW and the electrical activation has been established in prior studies. However, the methods used previously to map the EW required the reconstruction of images over multiple cardiac cycles, precluding the application of EWI for non-periodic arrhythmias such as fibrillation. In this study, new imaging sequences are developed and applied based on flash- and wide-beam emissions to image the entire heart at very high frame rates (2000 fps) during free breathing in a single heartbeat. The methods are first validated by imaging the heart of an open-chest canine while simultaneously mapping the electrical activation using a 64-electrode basket catheter. Feasibility is then assessed by imaging the atria and ventricles of closed-chest, conscious canines during sinus rhythm and during right-ventricular pacing following atrio-ventricular dissociation, i.e., during a non-periodic rhythm. The EW was validated against electrode measurements in the open-chest case, and followed the expected electrical propagation pattern in the closed-chest setting. These results indicate that EWI can be used for the characterization of non-periodic arrhythmias in conditions similar to the clinical setting, in a single heartbeat, and during free breathing. |
14,738 | Ionic mechanisms underlying cardiac toxicity of the organochloride solvent trichloromethane. | Trichloromethane (chloroform) is widely used for industrial chemical synthesis and also as an organic solvent in laboratories or ingredient of pesticides. Sudden death resulted from cardiac arrhythmias has been reported in clinic with acute trichloromethane intoxication. The present study was designed to investigate ionic mechanisms underlying arrhythmogenic effect (cardiac toxicity) of trichloromethane in isolated rat hearts and ventricular myocytes and HEK 293 cells stably expressing human Nav1.5, HCN2, or hERG channel using conventional electrophysiological approaches. It was found that trichloromethane (5mM) induced bradycardia and atrial-ventricular conduction blockade or ventricular fibrillation, and inhibited cardiac contractile function in isolated rat hearts. It shortened action potential duration (APD) in isolated rat ventricular myocytes, and increased the threshold current for triggering action potential, but had no effect on the inward rectifier K(+) current I(K1). However, trichloromethane significantly inhibited the L-type calcium current I(Ca.L) and the transient outward potassium current I(to) in a concentration-dependent manner (IC(50)s: 1.01 and 2.4mM, respectively). In HEK 293 cells stably expressing cardiac ion channel genes, trichloromethane reduced hNav1.5, HCN2, and hERG currents with IC(50)s of 8.2, 3.3, and 4.0mM, respectively. These results demonstrate for the first time that trichloromethane can induce bradycardia or ventricular fibrillation, and the arrhythmogenic effect of trichloromethane is related to the inhibition of multiple ionic currents including I(Ca.L), I(to), I(Na), HCN2, and hERG channels. |
14,739 | Sex-Based Differences in Cardiac Arrhythmias, ICD Utilisation and Cardiac Resynchronisation Therapy. | Many important differences in the presentation and clinical course of cardiac arrhythmias are present between men and women that should be accounted for in clinical practice. In this paper, we review published data on gender differences in cardiac excitable properties, supraventricular tachycardias, ventricular tachycardias, sudden cardiac death, and the utilisation of implantable defibrillators and cardiac resynchronisation therapy. Women have a higher heart rate at rest, and a longer QT interval than men. They further have a narrower QRS complex and lower QRS voltages on the 12-lead ECG with more often non-specific repolarisation abnormalities at rest. Supraventricular tachycardias, such as AV nodal reentrant tachycardia, are twice as frequent in women compared with men. Atrial fibrillation, however, has a 1.5-fold higher prevalence in men. The triggers for idiopathic right ventricular outflow tract tachycardia (VT) initiation are gender specific, i.e. hormonal changes play an important role in the occurrence of these VTs in women. There are clear-cut gender differences in acquired and congenital LQTS. Brugada syndrome affects men more commonly and severely than women. Sudden cardiac death is less prevalent in women at all ages and occurs 10 years later in women than in men. This may be related to the later onset of clinically manifest coronary heart disease in women. Among patients who receive ICDs and CRT devices, women appear to be under-represented, while they may benefit even more from these novel therapies. |
14,740 | Kounis syndrome is likely culprit of coronary vasospasm induced by capecitabine. | Capecitabine administration has been associated with various allergic reactions including acneiform skin rash, linchenoid photosensitive eruption, exudative non healing scalp, skin reactions, pyogenic granuloma, subacute cutaneous systemic lupus erythematosus, exudative hyponychia dermatitis, and hand-foot syndrome. A patient who developed ventricular fibrillation following capecitabine-induced coronary vasospasm and necessitating cardioverter-defibrillator implantation was published recently in. |
14,741 | Impact of heart rate and rhythm on radiation exposure in prospectively ECG triggered computed tomography. | To evaluate the influence of different heart rates and arrhythmias on scanner performance, image acquisition and applied radiation exposure in prospectively ECG triggered computed tomography (pCT).</AbstractText>An ECG simulator (EKG Phantom 320, Müller & Sebastiani Elektronik GmbH, Munich, Germany) was used to generate different heart rhythms and arrhythmias: sinus rhythm (SR) at 45, 60, 75, 90 and 120/min, supraventricular arrhythmias (e.g. sinus arrhythmia, atrial fibrillation) and ventricular arrhythmias (e.g. ventricular extrasystoles), pacemaker-ECGs, ST-changes and technical artifacts. The analysis of the image acquisition process was performed on a 64-row multidetector CT (Brilliance, Philips Medical Systems, Cleveland, USA). A prospectively triggered scan protocol as used for routine was applied (120 kV; 150 mAs; 0.4s rotation and exposure time per scan; image acquisition predominantly in end-diastole at 75% R-R-interval, in arrythmias with a mean heart rate above 80/min in systole at 45% of the R-R-interval; FOV 25 cm). The mean dose length product (DLP) and its percentage increase from baseline (SR at 60/min) were determined.</AbstractText>Radiation exposure can increase significantly when the heart rhythm deviates from sinus rhythm. ECG-changes leading to a significant DLP increase (p<0.05) were bifocal pacemaker (61%), pacemaker dysfunction (22%), SVES (20%), ventricular salvo (20%), and atrial fibrillation (14%). Significantly (p<0.05) prolonged scan time (>8 s) could be observed in bifocal pacemaker (12.8 s), pacemaker dysfunction (10.7 s), atrial fibrillation (10.3 s) and sinus arrhythmia (9.3 s).</AbstractText>In prospectively ECG triggered CT, heart rate and rhythm can provoke different types of scanner performance, which can significantly alter radiation exposure and scan time. These results might have an important implication for indication, informed consent and contrast agent injection protocols.</AbstractText>Crown Copyright © 2011. Published by Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,742 | Novel c.367_369del LMNA mutation manifesting as severe arrhythmias, dilated cardiomyopathy, and myopathy. | The 3-bp deletion in exon 2 of the Lamin A/C (LMNA) gene has not been described in association with dilated cardiomyopathy, which is characterized by progressive heart failure, atrioventricular (AV) block, tachyarrhythmias, and variable skeletal muscle involvement.</AbstractText>In a 43-year-old woman with a long-term history of palpitations and newly diagnosed AV blocks I and II, ventricular ectopic beats, inducible nonsustained ventricular tachycardias (VTs), cardiac arrest, and successful resuscitation, an implantable cardioverter defibrillator was successfully implanted. Her family history was positive for sudden cardiac death (her father and sister), dyspnea and heart failure (her grandmother and sister), palpitations (her brother), and elevated levels of creatine-kinase (CK) (her sister). Two cousins had died of nonspecific muscular dystrophy at ages 10 years and 11 years. Upon neurological investigations revealing sore neck muscles, reduced tendon reflexes, and detached, spot-like white matter lesions bilaterally, a neuromuscular disorder was suspected. The direct sequencing of all exons and flanking intronic regions of the LMNA gene detected the heterozygote 3-bp deletion (AAG) c.367_369del in exon 2 of the gene. This mutation resulted in the deletion of a lysine at position 123 (p.lys123del) in the lamin A/C protein.</AbstractText>The novel 3-bp deletion in exon 2 of the LMNA gene may phenotypically manifest as dilated cardiomyopathy, heart failure, severe tachyarrhythmias, and muscular dystrophy. Sudden cardiac death from ventricular fibrillation may be prevented in LMNA mutation carriers if the diagnosis is established early enough to implant a cardioverter defibrillator.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,743 | Cardiac resynchronization therapy to prevent life-threatening arrhythmias in patients with congestive heart failure. | Various clinical data demonstrate that cardiac resynchronization therapy (CRT) provides a favorable structural as well as electrical remodeling. The CArdiac Resynchronization-Heart Failure study, which tested the pure effect of CRT (using CRT devices without the capability of defibrillation) clearly showed a significant reduction in the total mortality by partly preventing sudden cardiac death. The antiarrhythmic effects of CRT are explained, at least in part, by ionic and genetic modulation of ventricular myocytes. It has been revealed in animal experiments to mimic disorganized ventricular contraction that CRT reverses down-regulation of certain K(+) channels and abnormal Ca(2+) homeostasis in the failing heart. However, CRT can be proarrhythmic in some particular cases especially in the early phase of this therapy. According to our study, proarrhythmic effects after CRT can be observed in approximately 10% of patients. The relatively high incidence of the proarrhythmic effects of CRT may promote a trend toward selecting CRT-D rather than CRT-P. |
14,744 | Electrical storm and calcium signaling: a review. | Electrical storm (ES), characterized by recurrent ventricular tachycardia/fibrillation, is a serious condition, adversely affecting prognosis in patients with implantable cardioverter/defibrillators. Electrical storm patients often die of progressive heart failure, but the underlying molecular basis is poorly understood. We have recently created an animal model of ES that features repetitive implantable cardioverter/defibrillator firing for recurrent ventricular fibrillation and found that ES events cause striking activation of Ca(2+)/calmodulin-dependent protein kinase II and prominent alteration of Ca(2+)-handling protein phosphorylation, possibly explaining mechanical dysfunction and arrhythmia promotion that characterize ES. Here, the pathophysiology and potential therapeutic strategies for ES, based on experimental and clinical studies by us and others, are described. |
14,745 | Basic and advanced paediatric cardiopulmonary resuscitation - guidelines of the Australian and New Zealand Resuscitation Councils 2010. | Guidelines for basic and advanced paediatric cardiopulmonary resuscitation (CPR) have been revised by Australian and New Zealand Resuscitation Councils. Changes encourage CPR out-of-hospital and aim to improve the quality of CPR in-hospital. Features of basic CPR include: omission of abdominal thrusts for foreign body airway obstruction; commencement with chest compression followed by ventilation in a ratio of 30:2 or compression-only CPR if the rescuer is unwilling/unable to give expired-air breathing when the victim is 'unresponsive and not breathing normally'. Use of automated external defibrillators is encouraged. Features of advanced CPR include: prevention of cardiac arrest by rapid response systems; restriction of pulse palpation to 10 s to diagnosis cardiac arrest; affirmation of 15:2 compression-ventilation ratio for children and for infants other than newly born; initial bag-mask ventilation before tracheal intubation; a single direct current shock of 4 J/kg for ventricular fibrillation (VF) and pulseless ventricular tachycardia followed by immediate resumption of CPR for 2 min without analysis of cardiac rhythm and avoidance of unnecessary interruption of continuous external cardiac compressions. Monitoring of exhaled carbon dioxide is recommended to detect non-tracheal intubation, assess quality of CPR, and to help match ventilation to reduced cardiac output. The intraosseous route is recommended if immediate intravenous access is impossible. Amiodarone is strongly favoured over lignocaine for refractory VF and adrenaline over atropine for severe bradycardia, asystole and pulseless electrical activity. Family presence at resuscitation is encouraged. Therapeutic hypothermia is acceptable after resuscitation to improve neurological outcome. Extracorporeal circulatory support for in-hospital cardiac arrest may be used in equipped centres. |
14,746 | Prolapsed double-canted bipolar left ventricular lead for pacing the left atrium via the coronary sinus: experience in 11 patients. | High thresholds and frequent lead dislodgement limit pacing the left atrium (LA) from the mid to distal coronary sinus (CS). The aim of this report is to describe a method for and the results of prolapsing a double-canted bipolar lead into the mid-to-distal CS to eliminate lead dislodgement and improve pacing thresholds.</AbstractText>After CS access the 9 Fr. anatomic sheath is withdrawn to the right atrium (RA) over an extra support wire. A double-canted bipolar lead is advanced into the RA until the proximal bend is outside the tip of the sheath. With the stylet withdrawn to the proximal bend, the sheath and lead are advanced over the wire back into the CS. The lead distal to the proximal bend is prolapsed beside the sheath as the tip of the sheath enters the CS. The lead was successfully prolapsed in 11 consecutive patients. In one patient, capture was >5 V in all locations. Of the 10 successful implants, the acute thresholds were: mean 1.53 V, median 1.35 V, range 0.4-4.0 V. Chronic thresholds were: mean 2 V, median 2 V range 0.4-4.0 V. There were no displaced leads or lead fractures through 6-10 months of follow-up.</AbstractText>Prolapse of a commercially available double-canted bipolar passive fixation lead eliminates lead dislodgment and improves thresholds providing a means for permanent pacing of the LA from the mid to distal CS and provides the design principles for a dedicated lead.</AbstractText> |
14,747 | Outcomes from out-of-hospital cardiac arrest in the Wellington region of New Zealand. Does use of the Fire Service make a difference? | Survival from community cardiac arrest in the Wellington region was analysed and compared with similar data reported nationally and internationally. In particular, the impact of a dual fire and ambulance service response was studied.</AbstractText>A retrospective comparative study was undertaken of out-of-hospital cardiac arrests in the Wellington region between 1 July 2007 and 31 December 2009. Data was collected from Wellington Free Ambulance and hospital records in accordance with the Utstein template. The New Zealand Fire Service provided details of firefighter attendance and timings. The primary outcome measure was survival to hospital discharge.</AbstractText>Overall survival to hospital discharge was 11% (37/339) whilst survival from initial ventricular fibrillation or tachycardia (VF/VT) was 21% (34/161). Initial VF/VT was more common in witnessed than unwitnessed arrests (57% v. 35%, p=0.001) and this mirrored survival in these groups (15% vs 6%, p=0.01). Survival to hospital discharge was also associated with younger age and shorter emergency service response time. Bystanders attempted CPR in 55% and the fire service in 50% but neither intervention influenced outcome. Although, when activated, the fire service arrived on average 1-2 minutes ahead of the ambulance, the dual response did not influence survival to hospital admission or discharge.</AbstractText>Survival from out-of-hospital cardiac arrest in Wellington is similar to that of other New Zealand cities and better than that reported from several large centres overseas. The combined fire and ambulance response was not shown to have any beneficial impact on survival over and above that achieved by the ambulance service alone. System changes are proposed to try and improve survival from community cardiac arrest in Wellington.</AbstractText> |
14,748 | Arrhythmia rate distribution and tachyarrhythmia therapy in an ICD population: results from the INTRINSIC RV trial. | Appropriate implantable cardioverter-defibrillator (ICD) therapy for ventricular tachycardia (VT) or ventricular fibrillation (VF) depends, in part, on the programming of tachycardia zones.</AbstractText>We assessed events treated with ICD shocks or antitachycardia pacing (ATP) in the Inhibition of Unnecessary RV Pacing with AV Search Hysteresis in ICDs (INTRINSIC RV) trial.</AbstractText>ATP and shock episodes from 1530 patients with dual-chamber ICDs were analyzed.</AbstractText>For episodes in which electrograms were stored and adjudicated, ATP was delivered for 763 episodes (182 patients), shock-only was delivered for 300 episodes (146 patients), and shock following ATP was delivered for 81 episodes (56 patients). ATP was delivered appropriately for 507 episodes (130 patients), with 93% success, and inappropriately for 256 episodes (89 patients). For ATP episodes, appropriate (VT: 170 ± 28 bpm) and inappropriate (not VT: 165 ± 21 bpm) rates did not differ (P = .16). When the initial therapy was shock, onset rates were higher for appropriate therapy than for inappropriate therapy (224 ± 46 bpm vs 187 ± 31 bpm; P <.001). Inappropriate ATP was more likely to be followed by a shock (odds ratio 2.49; 95% confidence interval 1.56-3.97; P <.001). Fifty-eight percent (225 of 381) of shocked episodes had rates <200 bpm. For episodes between 200 and 250 bpm, 20% (23 of 113) were polymorphic VT or VF, 59% were monomorphic VT, 19% were supraventricular, and <1% was artifact. For episodes >250 bpm, 37% were VF, 28% polymorphic VT, 23% monomorphic VT, 7% supraventricular, and 5% artifact.</AbstractText>In a general ICD population, ATP treated VT effectively or obviated the need for shock. Most ventricular arrhythmias <250 bpm were not VF. Proper zone programming may identify and treat VT without shock.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,749 | Anaesthetic management of a case of Wolff-Parkinson-White syndrome. | We report a case of fibroid uterus with Wolff-Parkinson-White (WPW) syndrome in a 48-year-old female, posted for elective hysterectomy. Patient gave history of short recurrent episodes of palpitation and electrocardiograph confirmed the diagnosis of WPW syndrome. The anaesthetic management of these patients is challenging as they are known to develop life threatening tachyarrhythmia like paroxysmal supra-ventricular tachycardia (PSVT) and atrial fibrillation (AF). Epidural anaesthesia is preferred compared to general anaesthesia to avoid polypharmacy, noxious stimuli of laryngoscopy and intubation. To deal with perioperative complications like PSVT and AF, anti-arrhythmic drugs like adenosine, beta blockers and defibrillator should be kept ready. Perioperative monitoring is essential as patients can develop complications. |
14,750 | Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction. | In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation.</AbstractText>Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches.</AbstractText>Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P < 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P < 0.05). SEVO was associated with a reduction in myocardial IL-1β protein concentrations (0.16 pg/μg total protein [0.14 to 0.17] vs 0.12 pg/μg total protein [0.11 to 0.14]; P < 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P < 0.05), increased hypoxia-inducible factor (HIF)-1α protein expression (P < 0.05) and increased activity of matrix metalloproteinase 9 (P < 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways.</AbstractText>SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1α expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.</AbstractText> |
14,751 | [Massive lamotrigine poisoning--case report]. | Lamotrigine is a phenyltriazine derivative used as antiepileptic drug with pharmacological profile similar to phenytoin. It is chemically unrelated to the other antiepileptic drugs and mechanism of anticonvulsant action is that lamotrigine inhibits sodium channels, resulting in neuronal membrane stabilization and block of excitatory neurotransmitter release. Mean therapeutical dose of lamotrigine is 200 - 400 mg/day. Overdose experience with lamotrigine is limited. In severe cases of poisonings there were serious effects such as: coma, respiratory depression, recurrent seizures and intraventricular conduction disturbances. We report massive suicidal poisoning with lamotirigine unknown dose. Clinical course was severe--we observed deep coma, respiratory depression, epileptical state, ventricular disrhytmias, atrio-venticular heart block, cardiovascular shock, rhabdomyolysis and hypokalemia. There was ventricular fibrillation in course of poisoning. The patient was successfully resuscitated and discharged on 18 hospital day. |
14,752 | [Severe digoxin poisoning a case study]. | Digitalis glycosides are among the oldest drugs used in cardiology. Nowadays, due to the limited indications for their use (advanced heart failure, usually concomitant with atrial fibrillation), cases of poisoning induced by this class of drugs are rarely observed. Digoxin produces a positive inotropic and bathmotropic effect on the heart, but has a negative chronotropic and dromotropic effect. Cardiac glycosides have a narrow therapeutic window, so digitalis treatment can easily lead to symptoms of overdose. In patients taking digoxin, the drug therapeutic level should be maintained at 1-2 ng/ml; the toxic effects occur at concentrations > 2.8 ng/ml and are mainly related to disturbances of cardiac function and of the circulatory system, as well as gastrointestinal symptoms and CNS disturbances. We present, a 45-years-old patient who was hospitalized following the ingestion with suicidal intent of 100 0.25 mg tablets of digoxin. In spite of rapidly applied gastric irrigation and administration of activated charcoal, the drug level in the patient's blood was estimated at 12.0 ng/ml. During her stay on the ward, typical symptoms of severe poisoning were observed: from gastric symptoms (severe nausea, vomiting) to numerous severe arrhythmias and conduction disturbances. Type I, II and III AV blocks were detected, as well as numerous ventricular and supraventricular extrasystoles. These conduction disorders required the use of temporary endocardial pacing. Due to the unavailability of specific antidotes (antidigitalis antibodies) and lack of efficient methods of extracorporeal elimination of the drug, symptomatic treatment comprising the correction of electrolyte disturbances and heart rate control remains the most effective. |
14,753 | [Electrocardiographic abnormalities in acute olanzapine poisonings]. | Olanzapine is an atypical antipsychotic used for many years in the treatment of schizophrenia and bipolar disorder. Poisonings with this medicine can results with cardiotoxic effects in the form of ECG abnormalities.</AbstractText>To evaluate the nature and incidence of electrocardiographic abnormalities in patients with acute olanzapine poisoning.</AbstractText>23 adult (mean age 38.4 +/- 15.5 years) patients with acute olanzapine poisoning, including 10 men (30.4 +/- 8.1 years) and 11 women (45.7 +/- 17.2 years), where 1 man and 1 woman were poisoned twice. The toxic serum level of olanzapine (above 100 ng/mL) was confirmed in each patient.</AbstractText>Evaluation of electrocardiograms performed in patients in the first day of hospitalization with automatic measurement of durations of PQ, QRS and QTc and the identification of arrhythmias and conduction disorders on the basis of visual analysis of the ECG waveforms. Statistical analysis of the results using the methods of descriptive statistics.</AbstractText>The mean durations of PQ, QRS and QTc in the study group were as follows: 135 +/- 23 ms, 91 +/- 12 ms, and 453 +/- 48 ms, respectively. The most common ECG abnormalities were prolonged QTc and supraventricular tachycardia (including sinus tachycardia) - each 22%; less common were ST-T changes (17%) and supraventricular premature complexes (9%), and only in individual cases (4%) ventricular premature complexes, bundle branch block, sinus bradycardia and atrial fibrillation were present.</AbstractText>In the course of acute olanzapine poisonings: (1) prolonged QTc interval is quite common, but rarely leads to torsade de pointes tachycardia; (2) fast supraventricular rhythms are also common, but rarely cause irregular tachyarrhythmias, eg. atrial fibrillation; (3) conduction disorders (atrioventricular blocks, bundle branch blocks) are not typical abnormalities; (4) the observed ECG abnormalities emphasize the need of continuous ECG monitoring in these patients.</AbstractText> |
14,754 | An atypical case of Brugada syndrome. | Polymorphic ventricular tachycardia and ventricular fibrillation are the most common arrhythmias in Brugada syndrome causing syncope or sudden death. Sustained monomorphic ventricular tachycardias are rare in this context. We report of a patient with syncopal episodes due to episodes of sustained ventricular tachycardia, where a Type-I Brugada pattern was revealed after pharmacological provocation with procainamide. |
14,755 | Determinants of a reduced heart rate variability in chronic atrial fibrillation. | We aimed to evaluate whether clinical factors, which influence heart rate variability (HRV) in the presence of undisturbed sinus rhythm, have any associations with HRV in patients with permanent atrial fibrillation (AF).</AbstractText>One hundred ninety-seven consecutive patients with permanent AF were included (122 males, 75 females, aged 64 ± 11 years, range 25-85). In each patient a 24-hour electrocardiographic recording was performed and an HRV fraction (HRVF)-the index based on scatter plot numerical processing-was calculated. Additionally, standard HRV measures were analyzed. Reduced HRVF was defined as its value lower than lower normal limit. Demographic and clinical factors were examined for their association with a reduced HRVF by means of a univariate and multivariate logistic regression analysis.</AbstractText>The reduced HRVF was associated with advanced age, clinical diagnosis of a previous MI or dilated cardiomyopathy, presence of diabetes, depressed left ventricular function, NYHA class > II, treatment regimen, use of digoxin, diuretics or antiarrhythmic agents, nonuse of beta-blockers, and increased heart rate. The independent determinants that sustained after multivariate analysis were: heart rate (per 10 bpm increase, odds ratio 2.77 [1.88-4.07]), age (per 5 years increase 1.43 [1.1-1.85]), depressed left ventricular EF (<30% vs higher 2.26 [1.19-4.31]), and presence of diabetes (3.45 [1.1-10.85]). The HRVF correlated moderately with standard HRV measures. This index showed also the strongest correlation with left ventricular ejection fraction.</AbstractText>We concluded that advanced age, left ventricular systolic dysfunction, increased heart rate, and presence of diabetes are cofactors of a reduced HRV in AF patients. Thus, the determinants of heart rate variability in the presence of atrial fibrillation are the same as those in sinus rhythm.</AbstractText>©2011, Wiley Periodicals, Inc.</CopyrightInformation> |
14,756 | Clarifying the arrhythmogenic substrate for Brugada syndrome. | The right ventricular outflow tract (RVOT) is considered the arrhythmogenic region that gives rise to Brugada syndrome. To obtain a better understanding of this substrate, we performed electroanatomic mapping of the right ventricle (RV) in patients with Brugada syndrome. The RV was mapped electroanatomically with the CARTO system in 11 patients with asymptomatic Brugada syndrome but in whom ventricular fibrillation was induced by programmed ventricular stimulation, and in 5 control patients. The low voltage zone area (< 1.5 mV) was larger (16.1% versus 7.8%, P < 0.01) and the bipolar electrogram duration was greater (81.6 ± 7.8 ms versus 53.4 ± 5.6 ms, P < 0.01) in the patients with Brugada syndrome versus the control patients; the bipolar electrogram duration was greater in the septal portion and free wall of the RVOT. Our data suggest that regional endocardial conduction slowing based on structural abnormalities exists at the RVOT in Brugada syndrome. |
14,757 | Detection of prior myocardial infarction patients prone to malignant ventricular arrhythmias using wavelet transform analysis. | Ventricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death remains responsible for significant mortality in patients with prior myocardial infarction (MI). The study population consisted of 50 normal controls and 50 patients with prior MI. The MI subjects were divided into 3 groups: VT/VF (-) group; 25 patients without ventricular tachyarrhythmia, VT group; 13 patients with sustained VT, and VF group; 12 patients with resuscitated VF. The parameters on the signal-averaged ECG and the frequency components recorded from the wavelet-transformed ECG were compared. The high-frequency components (HFC; 80-150 Hz) were developed in the MI group to a greater extent than those in the control group. Among the MI patients, the HFC were more developed in the VT and VF groups than in the VT/VF (-) group. In the VF group, the positive rate of LP was 50%. Meanwhile, when the peak power value at 150 Hz > 300 was defined as abnormal, the HFC was detected in 13 (100%) patients in the VT group and 12 (91.7%) in the VF group. The sensitivity of the abnormal HFC in identifying patients with VT/VF was higher than that of SAECG (96% versus 72%), although the specificity remained similar (68.5% versus 64.3%). Abnormal HFC recorded from the wavelet-transformed ECG may be a novel factor in detecting patients who are prone to VT/VF. |
14,758 | Getting to the heart of cardiac remodeling; how collagen subtypes may contribute to phenotype. | The objective of this study was to investigate the nature and biomechanical properties of collagen fibers within the human myocardium. Targeting cardiac interstitial abnormalities will likely become a major focus of future preventative strategies with regard to the management of cardiac dysfunction. Current knowledge regarding the component structures of myocardial collagen networks is limited, further delineation of which will require application of more innovative technologies. We applied a novel methodology involving combined confocal laser scanning and atomic force microscopy to investigate myocardial collagen within ex-vivo right atrial tissue from 10 patients undergoing elective coronary bypass surgery. Immuno-fluorescent co-staining revealed discrete collagen I and III fibers. During single fiber deformation, overall median values of stiffness recorded in collagen III were 37±16% lower than in collagen I [p<0.001]. On fiber retraction, collagen I exhibited greater degrees of elastic recoil [p<0.001; relative percentage increase in elastic recoil 7±3%] and less energy dissipation than collagen III [p<0.001; relative percentage increase in work recovered 7±2%]. In atrial biopsies taken from patients in permanent atrial fibrillation (n=5) versus sinus rhythm (n=5), stiffness of both collagen fiber subtypes was augmented (p<0.008). Myocardial fibrillar collagen fibers organize in a discrete manner and possess distinct biomechanical differences; specifically, collagen I fibers exhibit relatively higher stiffness, contrasting with higher susceptibility to plastic deformation and less energy efficiency on deformation with collagen III fibers. Augmented stiffness of both collagen fiber subtypes in tissue samples from patients with atrial fibrillation compared to those in sinus rhythm are consistent with recent published findings of increased collagen cross-linking in this setting. |
14,759 | Unusual complications of percutaneous epicardial access and epicardial mapping and ablation of cardiac arrhythmias. | Percutaneous epicardial access and mapping/ablation of cardiac arrhythmias are being increasingly performed. Although complications such as pericardial effusion are relatively common, other unusual complications may occur due to the complex anatomic architecture of the heart and surrounding tissues. In this report, we report a series of rare and unusual complications related to percutaneous epicardial procedures.</AbstractText>Between 2006 and 2011, 334 patients underwent attempts at percutaneous, subxiphoid access for epicardial mapping/ablation at 5 experienced centers. Seven selected complications are highlighted in this case series. Patient 1 had a 1-cm right ventricular pseudoaneurysm after several unsuccessful attempts at epicardial access. This was successfully managed conservatively. Patient 2 had intra-abdominal bleeding related to puncture of the left lobe of the liver during access that required surgical repair. Patient 3 had a subcapsular hepatic hematoma that was probably related to percutaneous access and was successfully managed conservatively. Patient 4 had severe pericardial bleeding followed by ventricular fibrillation, immediately after obtaining percutaneous epicardial access. A lacerated middle cardiac vein was repaired surgically. However, the patient ultimately died of complications. Patient 5 had a history of cardiothoracic surgery and developed a right ventricle-abdominal fistula after multiple attempts at percutaneous access. This was surgically repaired without major sequelae. Patient 6 had cardiac tamponade caused by a lacerated coronary sinus branch during epicardial catheter ablation and required surgical repair. Patient 7 had severe left coronary vasospasm and ventricular fibrillation during catheter manipulation in the pericardium. This complication was successfully managed with intracoronary nitrates.</AbstractText>Though generally safe, percutaneous epicardial access and mapping/ablation can result in uncommon complications. Awareness of these rare complications may facilitate early detection and successful management.</AbstractText> |
14,760 | Frequent early cardiac complications contribute to worse stroke outcome in atrial fibrillation. | Atrial fibrillation (AF) is associated with worse outcomes following ischemic stroke and more frequent cardiac complications in the general population. We aimed to establish whether early cardiac complications contribute to the poorer ischemic stroke outcomes in patients with AF, independent of baseline differences in age, stroke severity and cardiovascular risk factors. This might have important implications for acute stroke management in patients with AF.</AbstractText>We searched VISTA-Acute, an academic database containing standardized data for 28,131 patients from 30 randomized-controlled acute stroke trials and 1 stroke registry, for imaging-confirmed placebo-treated patients with complete documentation of baseline demographics, cardiovascular risk factors, presence or absence of AF, neurologic impairment [National Institutes of Health Stroke Scale (NIHSS)], cardiac complications and 3-month outcome (modified Rankin Scale). A total of 2,865 patients from 6 randomized-controlled trials met the selection criteria, of whom 819 had AF. Binary logistic regression modeling was used to determine the independent effect of AF on stroke outcome and serious cardiac adverse events (SCAE), a composite end point including acute coronary syndrome, symptomatic heart failure, cardiopulmonary arrest, ventricular tachycardia, ventricular fibrillation and cardiac mortality.</AbstractText>All patients were enrolled into the source trials within 24 h of stroke onset. At baseline, patients with AF were older (mean 75 vs. 67 years, p < 0.001) and had greater neurologic impairment (median NIHSS 15 vs. 13, p < 0.001). The median time to first cardiac adverse event was 3 days [median difference 0, 95% confidence interval (CI) 0-1, p = 0.06] for both patients with and without AF. SCAE occurred more frequently [14.2 vs. 6%, odds ratio (OR) = 2.58, 95% CI 1.97-3.37] in patients with AF, particularly cardiac mortality (4.9 vs. 2.6%, OR = 1.89, 95% CI 1.25-2.88), symptomatic heart failure (6.5 vs. 2.2%, OR = 3.01, 95% CI 2.01-4.50), and ventricular tachycardia and/or fibrillation (2.4 vs. 0.8%, OR = 3.18, 95% CI 1.64-6.16). At 3 months, AF was independently associated with SCAE (OR = 2.14, 95% CI 1.61-2.86) and early mortality (OR = 1.44, 95% CI 1.14-1.81) after adjusting for all baseline imbalances.</AbstractText>Early SCAE are common after stroke and are independently associated with the presence of AF. Given that many cardiac complications are potentially remediable, these results highlight the need for more rigorous surveillance for cardiac complications in acute ischemic stroke patients with AF.</AbstractText>Copyright © 2011 S. Karger AG, Basel.</CopyrightInformation> |
14,761 | Association among intracardiac T-wave alternans, ischemia, and spontaneous ventricular arrhythmias after coronary artery occlusion in a canine model. | T-wave alternans (TWA) has been investigated as a marker for susceptibility to lethal ventricular arrhythmia. In this article, we studied intracardiac TWA and ischemia as predictors of spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) in a canine model of coronary artery occlusion (CAO). Anesthetized, open-chest dogs were studied. Electrograms from intracardiac bipolar electrodes (IBEs) were assessed for TWA and spontaneous VT or VF. TWA was defined on IBE as T wave voltage change on every other complex. In each heart, we examined 62 electrograms measured in the risk zone and surrounding normal sites, filtered from 3 to 1300 Hz. Ischemia was measured as percent of all IBE recorded that had QRS voltage drop >45%. Mapping localized the three-dimensional origin of spontaneous VT or VF. The data from dogs with VF (n = 5), VT (n = 8), or controls (no VT or VF, n = 8) were analyzed before left CAO, at the 20th min after CAO and times immediately preceding VT and VF. We found a correlation between intracardiac TWA and ischemia. More importantly, increases in intracardiac TWA peaked immediately preceding spontaneous VF and VT and were significantly higher compared to controls at comparable times. At VT/VF origins and adjacent sites, the mean TWA magnitude and discordance of TWA distinguished between VT/VF and controls at comparable times but not between VT and VF or between reentry and focal mechanisms. TWA was more common than ischemia at VT/VF origins. In summary, changes in intracardiac TWA and ischemia correlate with impending spontaneous VT/VF in a clinically applicable canine model of CAO. |
14,762 | Atrial-selective sodium channel block strategy to suppress atrial fibrillation: ranolazine versus propafenone. | Ranolazine has been shown to produce atrial-selective depression of sodium channel-dependent parameters and suppress atrial fibrillation (AF) in a variety of experimental models. The present study contrasts the effects of ranolazine and those of a clinically used anti-AF class IC agent, propafenone. Electrophysiological and anti-AF effects of propafenone and ranolazine were compared at clinically relevant concentrations (i.e., 0.3-1.5 and 1-10 μM, respectively) in canine isolated coronary-perfused atrial and ventricular preparations. Transmembrane action potential and pseudo-ECG were recorded. Both ranolazine and propafenone produced atrial-selective prolongation of action potential duration. Propafenone depressed sodium channel-mediated parameters [maximum rate of rise of the action potential upstroke (V(max)), conduction time, and diastolic threshold of excitation] and induced postrepolarization refractoriness to a greater degree than ranolazine, and these effects, unlike those induced by ranolazine, were not or only mildly atrial-selective at normal rates (cycle length 500 ms). At fast pacing rates, however, the effects of propafenone on V(max) and conduction time became atrial-selective, because of the elimination of diastolic interval in atria, but not in ventricles. Propafenone (1.5 μM) and ranolazine (10.0 μM) were effective in preventing the initiation of persistent acetylcholine-mediated AF (6/7 and 9/11 atria, respectively), its termination (8/10 and 8/12 atria, respectively), and subsequent reinduction (8/8 and 7/8 atria, respectively). Thus, propafenone and ranolazine both suppress AF, but ranolazine, unlike propafenone, does it with minimal effects on ventricular myocardium, suggesting a reduced potential for promoting ventricular arrhythmias. |
14,763 | Protective effect of novel pyridoindole derivatives on ischemia/reperfusion injury of the isolated rat heart. | Generation of reactive oxygen species is a major, well-known cause of heart injury induced by ischemia-reperfusion. This injury is manifested through myocardial stunning, reperfusion and lethal reperfusion injury of cardiocytes. The pyridoindole stobadine has been shown to exhibit significant antioxidant, free-radical scavenging and hypoxic-tissue-protecting properties. The present study examined the effects of stobadine and two novel derivatives, SMe1 and SMe1EC2, which exhibit improved pharmacodynamic and toxicity profiles, on the functional properties and reperfusion dysrhythmias of the isolated rat heart in ischemia-reperfusion conditions. All experiments were performed on isolated Langendorff-perfused hearts isolated from 3-month-old male Wistar rats. After 15 min of stabilization, the hearts were subjected to a 30-minute period of global no-flow ischemia, followed by a 30-minute reperfusion period. Stobadine, SMe1 and SMe1EC2 were applied at a concentration of 1 x 10(-5) 10 min before the onset of ischemia, and during reperfusion through the perfusion medium. As compared to the untreated group, addition of SMe1EC2 during reperfusion significantly increased left ventricular developed pressure, decreased pathologically elevated left ventricular end-diastolic pressure and enhanced recovery of the stunned myocardium after ischemia. Both SMe1 and stobadine failed to influence these parameters; however, all derivatives tested inhibited serious life-threatening reperfusion dysrhythmias such as ventricular tachycardia and ventricular fibrillation. Our findings suggest that SMe1EC2 promotes an improved recovery of the left ventricular function following ischemia compared to either stobadine or SMe1. However, both SMe1EC2 and SMe1 manifested a significant anti-dysrhythmic effect comparable with that of stobadine and partially reduced myocardial ischemia-reperfusion-induced injury. |
14,764 | A new tissue doppler index in predicting future atrial fibrillation in patients with heart failure. | Onset of atrial fibrillation (AF) in patients with heart failure (HF) is usually associated with a high occurrence of cardiovascular complications. E/(E'×S') ratio (E=early diastolic transmitral velocity, E'=early mitral annular diastolic velocity and S'=systolic mitral annulus velocity) has been shown to reflect left ventricular filling pressure.</AbstractText>We investigate whether E/(E'×S') could be a predictor of new-onset AF in patients with HF.</AbstractText>We analyzed 113 consecutive hospitalized patients with HF, in sinus rhythm, after appropriate medical treatment. Patients with histories of AF, inadequate echocardiographic images, congenital heart disease, paced rhythm, significant primary valvular disease, acute coronary syndrome, coronary revascularization during follow-up, severe pulmonary disease or renal failure were not included. E/(E'×S') was determined using the average of septal and lateral mitral annular velocities. The primary study end-point was the new-onset AF.</AbstractText>During the follow-up period (35.7±11.2 months), 33 patients (29.2%) developed AF. Mean E/(E'×S') was 3.09±1.12 in these patients, while it was 1.72±1.34 in the other patients (p<0.001). The optimal E/(E'×S') cut-off to predict new-onset AF was 2.2 (88% sensitivity, 77% specificity). There were 64 patients (56.6%) with E/(E'×S')<2.2 and 49 (43.4%) with E/(E'×S')>2.2. New-onset AF was higher in patients with E/(E'×S')>2.2 than in patients with E/(E'×S')<2.2 [29 (59.1%) versus 4 (6.2%), p<0.001]. On multivariate Cox analysis including the variables that predicted AF on univariate analysis, E/(E'×S') was the only independent predictor of new-onset AF (hazard ratio=2.26, 95% confidence interval=1.25-4.09, p=0.007).</AbstractText>In patients with HF, E/(E'×S') seems to be a good predictor of new-onset AF.</AbstractText> |
14,765 | Effects of K201 on repolarization and arrhythmogenesis in anesthetized chronic atrioventricular block dogs susceptible to dofetilide-induced torsade de pointes. | The novel antiarrhythmic drug K201 (4-[3-{1-(4-benzyl)piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine monohydrochloride) is currently in development for treatment of atrial fibrillation. K201 not only controls intracellular calcium release by the ryanodine receptors, but also possesses a ventricular action that might predispose to torsade de pointes arrhythmias. The anti- and proarrhythmic effects of K201 were investigated in the anesthetized canine chronic atrioventricular block model. Two doses of K201 (0.1 and 0.3mg/kg/2 min followed by 0.01 and 0.03 mg/kg/30 min i.v.) were tested in 4 serial experiments in dogs with normally conducted sinus rhythm (n=10) and in torsade de pointes-susceptible dogs with chronic atrioventricular block. Susceptibility was assessed with dofetilide (0.025 mg/kg/5 min i.v.). Beat-to-beat variability of repolarization was quantified as short-term variability of left ventricular monophasic action potential duration. In dogs with normally conducted sinus rhythm, both doses of K201 prolonged ventricular repolarization whereas only the higher dose prolonged atrial repolarization. At chronic atrioventricular block, dofetilide induced torsade de pointes in 9 of 10 dogs. K201 did neither suppress nor prevent dofetilide-induced torsade de pointes. K201 dose-dependently prolonged ventricular repolarization. In contrary to the lower dose, the higher dose did increase beat-to-beat variability of repolarization (from 1.2 ± 0.3 to 2.9 ± 0.8 ms, P<0.05) and resulted in spontaneous, repetitive torsade de pointes arrhythmias in 1 of 7 dogs; Programmed electrical stimulation resulted in torsade de pointes in 2 more dogs. In conclusion, both doses of K201 showed a class III effect. No relevant antiarrhythmic effects against dofetilide-induced torsade de pointes were seen. Only at the higher dose a proarrhythmic signal was observed. |
14,766 | Evolving J waves prior to ventricular fibrillation postoperative coronary bypass. | A 74-year-old man without history of ventricular arrhythmias underwent coronary bypass surgery for 3-vessel disease. On the 4th postoperative day, he developed ventricular fibrillation (VF). His monitored ECG showed no elevation of the ST-segment and no prolongation of QT interval, but evolving J waves prior to VF were shown. These J waves gradually decreased after defibrillation. The subsequent angiography revealed patent grafts and normal left ventricular function. J waves reappeared in inferior leads when contrast medium was injected into the coronary artery. Therefore, evolving J wave can be a marker of latent ischemia and a predictor of VF. |
14,767 | Prevalence of heart failure with preserved ejection fraction in Latin American, Middle Eastern, and North African Regions in the I PREFER study (Identification of Patients With Heart Failure and PREserved Systolic Function: an epidemiological regional study). | The aims of the present study were to estimate the prevalence of heart failure (HF) with preserved ejection fraction (HF-PEF) in patients with HF and to compare their clinical characteristics with those with reduced ejection fraction in non-Western countries. The left ventricular ejection fraction ≥ 45% if measured < 1 year before the visit was used to qualify the patients as having HF-PEF. Of the 2,536 consecutive outpatients with HF, 1990 (79%) had the EF values recorded. Of these patients, 1291 had HF-PEF, leading to an overall prevalence of 65% (95% confidence interval 63% to 67%). Compared to the patients with HF and a reduced ejection fraction, those with HF-PEF were more likely to be older (65 vs 62 years, p < 0.001), female (50% vs 28%, p < 0.001), and obese (39% vs 27%, p < 0.001). They more frequently had a history of hypertension (78% vs 53%, p < 0.001) and atrial fibrillation (29% vs 24%, p = 0.03) and less frequently had a history of myocardial infarction (21% vs 44%, p < 0.001). Only 29% of patients with HF-PEF and hypertension had optimal blood pressure control. Left ventricular hypertrophy was less frequent in those with HF-PEF (58% vs 69%, p < 0.001). The prevalence of HF-PEF was lower in the Middle East (41%), where coronary artery disease was more often found than in Latin America (69%) and North Africa (75%), where the rate of hypertension was greater. In conclusion, in the present diverse non-Western study, HF-PEF represented almost 2/3 of all HF cases in outpatients. HF-PEF mostly affects older patients, women, and the obese. Hypertension was the most frequently associated risk factor, highlighting the need for optimal blood pressure control. |
14,768 | Impact of ischemic time on post-infarction left ventricular function in ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. | Myocardial necrosis is a time-dependent event. Nevertheless, clinical studies on association between ischemic time and left ventricle function showed inconsistent findings. Aim of current study is to evaluate the association between ischemic time and the post-infarction left ventricular function in ST-elevation myocardial infarction treated with primary PCI.</AbstractText>In 2529 patients treated with primary PCI, left ventricular ejection fraction (LVEF) was measured before discharge (median day 4) by radionuclide ventriculography or by echocardiography if patients had atrial fibrillation. Ischemic time was calculated from symptom onset to first balloon inflation.</AbstractText>The correlation between ischemic time as continuous variable and LVEF was significant but weak (P=0.002, r=-0.062). The LVEF of patients in ischemic time intervals of >6, >3-6, and ≤3 h was 45.1±11.7%, 44.6±11.9%, and 43.2±12.2%, respectively (P=0.029). Adjusted odds ratio of the ischemic time intervals for LVEF<40% was 1.14 (95% CI 1.00-1.30). TIMI flow 0 before and TIMI flow 3 after PCI were related with both longer ischemic time and low LVEF.</AbstractText>Ischemic time was associated with post infarction LVEF in patients treated with primary PCI, although this association was weak. Initial TIMI flow and post-PCI TIMI flow played important role in impact of the ischemic time on the LVEF.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,769 | Clinical features and recovery patterns of acquired non-thyrotoxic hypokalemic paralysis. | To report the clinical features and recovery patterns of patients with non-thyrotoxic acquired hypokalemic paralysis.</AbstractText>The clinical and laboratory records of 11 consecutive patients with acquired non-thyrotoxic hypokalemic paralysis were reviewed and compared with those of 3 patients with thyrotoxic periodic paralysis (TPP). The causes of potassium wasting were diarrhea (n=4), alcohol abuse (n=2), pseudoaldosteronism (n=2), primary aldosteronism (n=1), distal renal tubular acidosis associated with Sjögren's syndrome (n=1) and an unknown cause (n=1).</AbstractText>Three of the 11 patients had prominently asymmetric limb weakness, and 2 had predominant upper limb weakness. On admission, mean serum potassium and creatine kinase (CK) levels of patients with acquired hypokalemic paralysis on admission were 1.8 mEq/L and 4,075 U/mL, respectively, and the mean duration between admission and independent walking was 6.8 days (range, 2-31 days). Despite clinical recovery, 10 patients still presented with increased CK levels after several days (mean of maximum levels, 10,519 U/mL). In addition, normalization of serum potassium levels in patients with acquired hypokalemic paralysis patients was much slower compared to that in patients with TPP. One patient with acquired hypokalemic paralysis developed ventricular fibrillation, whereas all 3 patients with TPP had symmetric proximal and lower limb-dominant weakness and exhibited complete recovery from paralysis as well as normalized serum potassium levels within 24h.</AbstractText>In patients with acquired non-thyrotoxic hypokalemic paralysis, asymmetric or upper limb-dominant weakness of the extremities is observed. Despite clinical improvement after treatment, normalization of serum potassium and CK levels is often delayed, and therefore, careful monitoring for cardiac and renal complications is required.</AbstractText>Copyright © 2011 Elsevier B.V. All rights reserved.</CopyrightInformation> |
14,770 | Guidelines for genetic testing of inherited cardiac disorders. | Inherited gene variants have been implicated increasingly in cardiac disorders but the clinical impact of these discoveries has been variable. For some disorders, such as familial hypertrophic cardiomyopathy, long QT syndrome, and familial hypercholesterolaemia, genetic testing has a high yield and has become an integral part of family management. For other disorders, including dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and atrial fibrillation, relatively less is known about the genes involved and genetic testing has a lower yield. Recent advances in sequencing and array-based technologies promise to change the landscape of our understanding of the genetic basis of human disease and will dramatically increase the rate of detection of genomic variants. Since every individual is expected to harbour thousands of variants, many of which may be novel, interpretation of the functional significance of any single variant is critical, and should be undertaken by experienced personnel. Genotype results can have a wide range of medical and psychosocial implications for affected and unaffected individuals and hence, genetic testing should be performed in a specialised cardiac genetic clinic or clinical genetics service where appropriate family management and genetic counselling can be offered. |
14,771 | Is There a Relationship between Hyperkalemia and Propofol? | This is a case of a sudden cardio-pulmonary arrest in a 29 year-old female, which occurred immediately after a large bolus infusion of propofol (100 mg) intravenously during dilatation and curettage. The arrest suddenly occurred, and the patient was eventually transferred to our emergency room (ER) on cardiopulmonary resuscitation. At that time, severe hyperkalemia up to 9.1 mEq/L and ventricular fibrillation were noted. Resuscitation in ER worked successfully with conversion of electrocardiograph to sinus rhythm, but this patient expired unfortunately. On view of this acute event immediately after the bolus injection of propofol accompanied without other identified causes, severe hyperkalemia induced by propofol was strongly assumed to be the cause of death. To our understanding with the literature survey, propofol as a cause of hyperkalemia has not been well described yet. Through this case, the relationship as a cause and an effect between propofol and hyperkalemia is suggested. |
14,772 | [Aortic valve replacement for aortic stenosis in Iceland 2002-2006: Indications and short term complications]. | Information on surgical outcome of aortic valve replacement (AVR) has not been available in Iceland. We therefore studied the indications, short-term complications and operative mortality in Icelandic patients that underwent AVR with aortic stenosis.</AbstractText>This was a retrospective study including all patients that underwent AVR for aortic stenosis at Landspitali between 2002 and 2006, a total of 156 patients (average age 71.7 years, 64.7% males). Short term complications and operative mortality (≤ 30 days) were registered and risk factors analysed with multivariate analysis.</AbstractText>The most common symptoms before AVR were dyspnea (86.9%) and angina pectoris (52.6%). Preop. max aortic valve pressure gradient was on average 74 mmHg, the left ventricular ejection fraction 57.2% and EuroSCORE (st) 6.9%. The average operating time was 282 min and concomitant CABG was performed in 55% of the patients and mitral valve surgery in nine. A bioprothesis was implanted in 127 of the patients (81.4%), of which 102 were stentless valves, and a mechanical valve in 29 (18.6%) cases. The mean prosthesis size was 25.6 mm (range 21-29). Atrial fibrillation (78.0%) and acute renal injury (36.0%) were the most common complications and 20 patients (13.0%) developed multiple-organ failure. Twenty-six patients (17.0%) needed reoperation due to bleeding. Median hospital stay was 13 days and operative mortality was 6.4%.</AbstractText>The rate of short term complications following AVR was relatively high, including reoperations for bleeding and atrial fibrillation. Operative mortality is twice that of CABG, which is in line with other studies.</AbstractText> |
14,773 | [Cardiac resynchronization therapy for patients with atrial fibrillation]. | Atrial fibrillation and chronic heart failure are two major and even growing cardiovascular conditions that often coexist. Cardiac resynchronization therapy is an important, device-based, non-pharmacological approach in a selected group of chronic heart failure patients that has been shown to improve left ventricular function and to reduce both morbidity and mortality in large randomized trials. The latest European and American guidelines have considered atrial fibrillation patients with heart failure eligible for cardiac resynchronization therapy. This review summarizes current literature concerning the following topics: prognostic relevance of atrial fibrillation in heart failure, effects of cardiac resynchronization therapy in atrial fibrillation, relevance and strategies of rhythm and rate control in this group of patients. Authors explain how atrial fibrillation may interfere with the delivery of adequate cardiac resynchronization therapy, how to reduce the burden of atrial tachyarrhythmias, and finally present a brief overview. |
14,774 | Prognostic importance of atrial fibrillation in asymptomatic aortic stenosis: the Simvastatin and Ezetimibe in Aortic Stenosis study. | The frequency and prognostic importance of atrial fibrillation (AF) in asymptomatic mild-to-moderate aortic stenosis (AS) has not been well described.</AbstractText>Clinical examination, electrocardiography and echocardiography were obtained in asymptomatic patients with mild-to-moderate AS and preserved left ventricular (LV) systolic function, randomized to simvastatin/ezetimibe combination vs. placebo in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. At inclusion, AF was categorized as episodic or longstanding. Rhythm change was assessed on annual in-study electrocardiograms. Impact of AF on cardiovascular morbidity and mortality was determined by adjusting for biomarkers, clinical- and echocardiographic covariates.</AbstractText>Mean follow-up was 4.3 ± 0.8 years (6,721 patient-years of follow-up). At baseline, episodic AF was present in 87 patients (5.6%), longstanding AF in 55 (3.5%) and no AF in 1,421 (90.9%). Incidence of new-onset AF was 1.2%/year; highest in those with impaired LV function. In multivariable analysis, longstanding AF was compared to no AF at baseline, associated with a 4.1-fold higher risk of heart failure (CI 1.2 to 13.8, p=0.02) and a 4.8-fold higher risk of non-hemorrhagic stroke (CI 1.7 to 13.6, p=0.003).</AbstractText>Rate of AF is moderate in asymptomatic AS. Longstanding but not episodic AF was, independently predictive of increased risk of heart failure and non-hemorrhagic stroke. New-onset AF was associated with cardiac decompensation.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,775 | Ambulatory external electrocardiographic monitoring: focus on atrial fibrillation. | There has been progressive development in ambulatory external electrocardiogram (AECG) monitoring technology. AECG monitors initially consisted of 24- to 48-h Holter monitors and patient-activated event and loop recorders. More recently, several ambulatory cardiovascular telemetry monitors and a patch-type 7- to 14-day Holter monitor have been introduced. These monitoring systems are reviewed along with their utility and limitations, with particular emphasis on their role in the diagnosis and evaluation of patients with atrial fibrillation (AF). AECG monitoring is necessary when asymptomatic AF is suspected (as in patients presenting with cryptogenic stroke) or when an ECG diagnosis of unexplained arrhythmic symptoms is warranted. In addition, AECG plays an important role in patients with known AF to guide ventricular rate control and anticoagulation therapy, and assess the efficacy of antiarrhythmic drug therapy and/or ablation procedures. Finally, we outline areas of uncertainty and provide recommendations for use of available AECG monitors in clinical practice. |
14,776 | Relation of serum parathyroid hormone level to severity of heart failure. | Increased parathyroid hormone (PTH) level is associated with all-cause mortality in patients with heart failure (HF). However its role for identifying advanced HF has not been previously studied. We aimed to investigate whether the assessment of serum PTH could enable clinicians to identify patients with advanced HF. One hundred fifty consecutive patients who visited our outpatient clinic with systolic HF were enrolled in the present study. Serum levels of PTH and brain natriuretic peptide (BNP) were measured across all New York Heart Association functional classes. Mean levels of PTH were 43 ± 19, 84 ± 56, 121 ± 47, and 161 ± 60 pg/ml in New York Heart Association functional classes I, II, III, and IV, respectively (p <0.001). In univariate analysis, body mass index, disease duration, PTH, BNP and hemoglobin levels, creatinine clearance, heart rate, systolic blood pressure, left ventricular ejection fraction, left ventricular diastolic diameter, left atrial size, presence of atrial fibrillation, and diuretic usage were found to be predictors of advanced HF. In multivariate logistic regression analysis, PTH level (hazard ratio 1.032, 95% confidence interval 1.003 to 1.062, p = 0.003) and body mass index (hazard ratio 0.542, 95% confidence interval 0.273 to 1.075, p = 0.079) were associated with advanced HF. Furthermore, serum PTH levels were correlated with BNP level and left ventricular ejection fraction (p <0.001 for the 2 comparisons). In receiver operator characteristics curve analysis, the optimal cut-off value of PTH to predict advanced HF was >96.4 pg/ml, with 93.3% sensitivity and 64.2% specificity. In conclusion, measurement of serum PTH could provide complementary information and a simple biomarker strategy to categorize patients with advanced HF based on increased PTH levels, allowing rapid risk stratification in these patients. |
14,777 | Beta-blockade causes a reduction in the frequency spectrum of VF but improves resuscitation outcome: A potential limitation of quantitative waveform measures. | Methods to identify appropriate treatments for the various stages of ventricular fibrillation (VF) involve differentiating groups of subjects who will respond to defibrillation with return of spontaneous circulation (ROSC) and those who require other therapies (e.g., CPR, drugs) prior to defibrillation. The use of quantitative waveform measures (QWM) which measure the frequency and fractal dimension of the VF electrocardiogram have shown success in predicting response to defibrillatory shock in animal models. Patients in cardiac arrest are often taking medications affecting adrenergic activity such as the beta blocker metoprolol and the combined alpha and beta blocker, labetalol. How this exposure might alter the QWM and ROSC rates is not known. HYOTHESIS: We sought to determine how pretreatment with adrenergic agents alters two QWM measures, the amplitude spectrum area (AMSA) and the detrended fluctuation analysis (DFA). We also examined how these medications alter the probability of ROSC after shock.</AbstractText>A swine model of ischemically induced VF cardiac arrest was used in which metoprolol and labetalol were administered prior to VF onset. 30 swine were randomly assigned to three groups of 10; control, metoprolol and labetalol. They were anesthetized, intubated and given the appropriate study drug. A balloon catheter was placed in the LAD coronary artery and inflated until VF occurred. ECG was recorded at 1000Hz for 7min of untreated VF. Closed chest compressions were then begun and after 1min a 200J shock was delivered. Resuscitation was continued with repeat defibrillation shocks as indicated for 15min or until ROSC was achieved (defined: systolic BP>60 for 10min). The Fourier frequency spectra, AMSA and DFA measures from VF onset to 7min were calculated using custom MATLAB routines. The QWM were compared over the electrical and circulatory phases of VF using generalized estimating equations. The rates of ROSC in the three groups were compared using relative risk measures.</AbstractText>All 10 control animals fibrillated after coronary occlusion, 8 metoprolol and 7 labetalol animals fibrillated. The frequency spectrum in metoprolol treated animals demonstrated a reduction in mean frequencies from 1 to 3min (electrical phase) and from 3 to 7min (circulatory phase). Labetalol produced an even greater reduction in frequencies in these intervals. The decline in AMSA was similar in all three groups over the first 3min. From 3 to 7min the metoprolol group was significantly lower than the control group (p<0.001) and the labetalol group was lower still (p<0.001). The DFA demonstrated little difference between the control and metoprolol groups, but showed a linear increase over 7min in the labetalol group (p<0.001 vs compared to control and metoprolol groups). ROSC was noted in 2/10 in the control group, 7/8 in metoprolol group and 2/7 in the labetalol group. The frequentist analysis of ROSC showed a relative risk (RR) of ROSC of 4.4 when comparing control to metoprolol animals and 1.4 comparing control to labetalol animals.</AbstractText>Metoprolol results in a reduction in frequencies in the Fourier spectrum of VF as compared with controls. There is a further decrease in frequencies with labetalol. The AMSA reflects this reduction in frequencies with lower AMSA values from 3 to 7min of VF. The DFA demonstrates consistent changes with labetalol treated animals over the 7min, but the metoprolol treated animals do not differ from the controls. The marked improvement in ROSC seen with metoprolol (RR 4.4) is unexpected and is not seen in labetalol treated animals. Adrenergic blockade prior to VF induction affects quantitative measures of the VF waveform and may limit the ability of such measures to predict downtime or defibrillation outcome.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,778 | Implantation of a completely subcutaneous ICD system: case report of a patient with Brugada syndrome and state of the art. | Complications of implantable cardioverter-defibrillator (ICD) therapy are often linked to transvenous lead insertion, lead failure, or infections. An entirely subcutaneous ICD system (S-ICD) avoids the need for the placement of electrodes within the heart and can provide clinical advantages.</AbstractText>A 45-year-old patient with Brugada syndrome (spontaneous type 1 Brugada ECG, syncope during fever, family history of sudden death <45 years old) was implanted with an entirely S-ICD. A left lateral incision was made over the sixth rib in the anterior axillary line for pocket formation and pulse generator placement. The subcutaneous electrode was placed subcutaneously, parallel to and 2 cm to the left of the sternal midline, and was connected to the generator. The insertion of the system was guided only by anatomical landmarks, and no fluoroscopy was required. Ventricular fibrillation was induced and terminated by a 65-J shock (15-J safety margin). No complication occurred, and subsequent course was uneventful.</AbstractText>S-ICD is a new system for delivering lifesaving shock therapy in patients at risk of sudden cardiac death, without the need of intracardiac leads. Young patients with inherited arrhythmogenic syndromes could benefit the most from this system. This is the first case of Brugada syndrome implanted with a first-generation S-ICD in Italy.</AbstractText> |
14,779 | Relationship between electroanatomical voltage mapping characteristics and breakout site of ventricular activation in idiopathic ventricular tachyarrhythmia originating from the right ventricular outflow tract septum. | To assess the electrophysiological characteristics of the breakout site of ventricular activation using electroanatomical voltage mapping (EVM) and its relation to the optimal ablation site in idiopathic ventricular tachyarrhythmias originating from the outflow tract of the (RVOT) septum.</AbstractText>Twenty-eight patients with symptomatic drug-refractory premature ventricular complexes (PVCs) and/or ventricular tachycardia (VT) originating from the RVOT septum and 5 control subjects with WPW syndrome were included. Low-voltage areas (LVAs) were defined as signal amplitudes between 0.1 and 1.5 mV. The borderline between the normal area and the LVA was defined as "border," and the distance from the LVA to the border (length of LVA) was measured.</AbstractText>In all 28 patients and control subjects, there was an LVA below the pulmonary valve. There was no significant difference in length of LVA between patients with idiopathic ventricular arrhythmias and control subjects (2.0 ± 0.6 vs. 1.9 ± 0.1 cm). In 19 of the 28 patients, the optimal ablation site was identical to the border area. In all 11 patients who had pre-potentials at the successful ablation site, there were two cases with polymorphic VT and/or ventricular fibrillation associated with PVCs. In these two cases, length of LVA was longer than in other patients (4.0 and 3.9 cm vs. 1.8 ± 0.5 cm (n = 26)), and the optimal ablation site was located at the border area.</AbstractText>The border area, including the LVA, tends to be the breakout site and/or origin of ventricular arrhythmias in idiopathic ventricular tachyarrhythmia originating from the RVOT septum.</AbstractText> |
14,780 | How to use implantable loop recorders in clinical trials and hybrid therapy. | Epidemiological studies show that atrial fibrillation (AF) is associated with a doubling of mortality, even after adjustment for confounders. AF can be asymptomatic, but this does not decrease the thromboembolic risk of the patient. Office ECGs, occasional 24-h Holter recordings and long-term ECG event recording might not be sensitive and accurate enough in patients with AF, especially in those with paroxysmal episodes. In one study, 7 days of continuous monitoring with event recorders detected paroxysmal AF in 20 of 65 patients with a previous negative 24-h Holter recording. Over the last decade, enormous improvements have been made in the technology of implantable devices, which can now store significant information regarding heart rhythm. The first subcutaneous implantable monitor (Reveal XT, Medtronic) was validated for continuous AF monitoring by the XPECT study. The dedicated AF detection algorithm uses irregularity and incoherence of R-R intervals to identify and classify patterns in ventricular conduction. Its sensitivity in identifying patients with AF is >96%. Numerous clinical data from continuous monitoring of AF have recently been published. The first applications of this technology have been in the field of surgical and catheter AF ablation. With regard to cryptogenic stroke, an international randomized trial is ongoing to compare standard care with standard care plus the implantable cardiac monitor for AF detection in patients discharged with the diagnosis of cryptogenic stroke: the Crystal AF trial. Continuous AF monitoring provides an optimal picture of daily AF burden, both symptomatic and asymptomatic. Implantable cardiac monitors have high sensitivity, enable better assessment of therapy success and may guide further AF therapy. |
14,781 | [Cardiocirculatory arrest caused by electric shock: importance of semi-automatic defibrillator]. | Accidental electrical burn injuries are serious because they can cause death by cardiocirculatory arrest. Cardiocirculatory arrest induced by low-voltage current is generally due to ventricular fibrillation, and the prognosis is fairly good if the survival chain is efficient. It is necessary to give priority to early defibrillation using an automated external defibrillator. Early defibrillation can immediately restore spontaneous circulation.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Siah</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Unité fonctionnelle d'anesthésie-réanimation des brûlés.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fouadi</LastName><ForeName>F E</ForeName><Initials>FE</Initials></Author><Author ValidYN="Y"><LastName>Ababou</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Ihrai</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Drissi</LastName><ForeName>N K</ForeName><Initials>NK</Initials></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Arrêt cardiocirculatoire par accidents d'électrisations: intérêt du défibrillateur semi-automatique.</VernacularTitle></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Ann Burns Fire Disasters</MedlineTA><NlmUniqueID>101251186</NlmUniqueID><ISSNLinking>1592-9558</ISSNLinking></MedlineJournalInfo><OtherAbstract Type="Publisher" Language="fre">Les brûlures par accidents électriques sont graves car elles peuvent entraîner le décès par arrêt cardiocirculatoire. Les arrêts cardiocirculatoires induits par le courant de basse tension sont en règle générale dûs à une fibrillation ventriculaire, plutôt de bon pronostic si la chaîne des secours est efficace. Il faut donner la priorité à la défibrillation systématique d’emblée en utilisant un défibrillateur semi-automatique. La défibrillation électrique est susceptible de procurer immédiatement une restauration de l’activité circulatoire spontanée. |
14,782 | Echocardiographic diastolic parameters and risk of atrial fibrillation: the Cardiovascular Health Study. | Atrial fibrillation (AF) is the most common sustained arrhythmia in the elderly, and shares several risk factors with diastolic dysfunction, including hypertension and advanced age. The purpose of this study is to examine diastolic dysfunction as a risk for incident AF.</AbstractText>We examined the association of echocardiographic parameters of diastolic function with the incidence of AF in 4480 participants enrolled in the Cardiovascular Health Study, an ongoing cohort of community-dwelling older adults from four US communities. Participants underwent baseline echocardiography in 1989-1990 and were followed for incident AF on routine follow-up and hospitalizations. After 50 941 person-years of follow-up (median follow-up time 12.1 years), 1219 participants developed AF. In multivariable-adjusted age-stratified Cox models, diastolic echocardiographic parameters were significantly associated with the risk of incident AF. The most significant parameters were the Doppler peak E-wave velocity and left atrial diameter, which demonstrated a positive nonlinear association [HR 1.5 (CI 1.3-1.9) and HR 1.7 (CI 1.4-2.1) for highest vs. lowest quintile, respectively], and Doppler A-wave velocity time integral, which displayed a U-shaped relationship with the risk of AF [HR 0.7 (CI 0.6-0.9) for middle vs. lowest quintile]. Each diastolic parameter displayed a significant association with adjusted NT-proBNP levels, although the nature of the association did not entirely parallel the risk of AF. Further cluster analysis revealed unique patterns of diastolic function that may identify patients at risk for AF.</AbstractText>In a community-based population of older adults, echocardiographic measures of diastolic function are significantly associated with an increased risk of AF.</AbstractText> |
14,783 | Arrhythmogenic effect of sympathetic histamine in mouse hearts subjected to acute ischemia. | The role of histamine as a newly recognized sympathetic neurotransmitter has been presented previously, and its postsynaptic effects greatly depended on the activities of sympathetic nerves. Cardiac sympathetic nerves become overactivated under acute myocardial ischemic conditions and release neurotransmitters in large amounts, inducing ventricular arrhythmia. Therefore, it is proposed that cardiac sympathetic histamine, in addition to norepinephrine, may have a significant arrhythmogenic effect. To test this hypothesis, we observed the release of cardiac sympathetic histamine and associated ventricular arrhythmogenesis that was induced by acute ischemia in isolated mouse hearts. Mast cell-deficient mice (MCDM) and histidine decarboxylase knockout (HDC(-/-)) mice were used to exclude the potential involvement of mast cells. Electrical field stimulation and acute ischemia-reperfusion evoked chemical sympathectomy-sensitive histamine release from the hearts of both MCDM and wild-type (WT) mice but not from HDC(-/-) mice. The release of histamine from the hearts of MCDM and WT mice was associated with the development of acute ischemia-induced ventricular tachycardia and ventricular fibrillation. The incidence and duration of induced ventricular arrhythmias were found to decrease in the presence of the selective histamine H(2) receptor antagonist famotidine. Additionally, the released histamine facilitated the arrhythmogenic effect of simultaneously released norepinephrine. We conclude that, under acute ischemic conditions, cardiac sympathetic histamine released by overactive sympathetic nerve terminals plays a certain arrhythmogenic role via H(2) receptors. These findings provided novel insight into the pathophysiological roles of sympathetic histamine, which may be a new therapeutic target for acute ischemia-induced arrhythmias. |
14,784 | Left atrial dimension and risk of stroke in women without atrial fibrillation: the Chin-Shan Community Cardiovascular Cohort study. | Evidence on the relationship between left atrial dimension and cardiovascular events is inconclusive. We explored the association between left atrial dimension and stroke and all-cause death in an ethnic Chinese population.</AbstractText>We recruited 1,937 subjects undertaking echocardiographic examination without prior atrial fibrillation/stroke in the Chin-Shan Community Cardiovascular Cohort study. Left atrial dimension indexed by body mass index was used as left atrial dimension index (LADI) for analysis. The end points were stroke and all-cause death. A multivariate Cox regression analysis was used to estimate the relative risks between participants stratified by tertile of LADI within each gender.</AbstractText>During a median follow-up of 11.9 years, 21,733 person-years were accrued and 114 subjects with stroke and 364 all-cause deaths were identified. The adjusted relative risk of stroke was 2.44 (95% CI, 1.11 to 5.36, P for trend = 0.029) among women in the upper tertile of LADI compared with women in the lower tertile of LADI. Further adjusting for left ventricular mass index attenuated the relationship of LADI to stroke (adjusted relative risk 2.11, 95% CI, 0.88 to 5.02, P for trend = 0.09). In men, tertile of LADI was not associated with stroke. LADI was not associated with risk of all-cause death in both genders.</AbstractText>We found an association between increased LADI and incident stroke in women but not in men in this ethnic Chinese population. LADI was not associated with all-cause death in both genders.</AbstractText>© 2011, Wiley Periodicals, Inc.</CopyrightInformation> |
14,785 | Cardiac ion channels and mechanisms for protection against atrial fibrillation. | Atrial fibrillation (AF) is recognised as the most common sustained cardiac arrhythmia in clinical practice. Ongoing drug development is aiming at obtaining atrial specific effects in order to prevent pro-arrhythmic, devastating ventricular effects. In principle, this is possible due to a different ion channel composition in the atria and ventricles. The present text will review the aetiology of arrhythmias with focus on AF and include a description of cardiac ion channels. Channels that constitute potentially atria-selective targets will be described in details. Specific focus is addressed to the recent discovery that Ca(2+)-activated small conductance K(+) channels (SK channels) are important for the repolarisation of atrial action potentials. Finally, an overview of current pharmacological treatment of AF is included. |
14,786 | The importance of class-I antiarrhythmic drug test in the evaluation of patients with syncope: unmasking Brugada syndrome. | The Brugada syndrome (BrS) can first present with syncope. Class-I antiarrhythmic drug (AAD) test is used to unmask the diagnostic coved-type ECG pattern in case it is not spontaneously present. The aim of the study was to analyze patients with BrS presenting with syncope as first manifestation and compare patients with syncope and a spontaneous coved-type ECG to patients with syncope in whom a class-I AAD test unmasked the disease.</AbstractText>Fifty-eight of 157 probands (36.9%) had syncope as first manifestation of the disease. Twenty-six patients (44.8%, group A) showed a spontaneous coved-type ECG diagnostic for BrS at first presentation. In 32 patients (55.2%, group B) without spontaneous coved-type ECG pattern at first presentation (36% normal ECGs and 19% type-II ECG pattern), a class-I AAD test unmasked the disease. Twenty-one patients of group A and 29 patients of group B underwent implantable cardioverter defibrillator (ICD) implantation. The mean follow up as 9.7 ± 55.7 month. Four patients in group A (15.4%) and 3 patients (9.3%) in group B had appropriate ICD shock delivery due to ventricular fibrillation or ventricular tachycardia (P = NS).</AbstractText>One of 3 patients with BrS presents first with syncope. More than one-third of these patients have a normal ECG at investigation for syncope and the correct diagnosis would have been missed without a class-I AAD test. Patients presenting with syncope are at similar risk irrespective of the presence of a spontaneous coved-type ECG. </AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,787 | Electrogram fractionation: the relationship between spatiotemporal variation of tissue excitation and electrode spatial resolution. | Fractionated electrograms are used by some as targets for ablation in atrial and ventricular arrhythmias. Fractionation has been demonstrated to result when there is repetitive or asynchronous activation of separate groups of cells within the recording region of a mapping electrode(s).</AbstractText>Using a computer model, we generated tissue activation patterns with increasing spatiotemporal variation and calculated virtual electrograms from electrodes with decreasing resolution. We then quantified electrogram fractionation. In addition, we recorded unipolar electrograms during atrial fibrillation in 20 patients undergoing atrial fibrillation ablation. From these we constructed bipolar electrograms with increasing interelectrode spacing and quantified fractionation. During modeling of spatiotemporal variation, fractionation varied directly with electrode length, diameter, height, and interelectrode spacing. When resolution was held constant, fractionation increased with increasing spatiotemporal variation. In the absence of spatial variation, fractionation was independent of resolution and proportional to excitation frequency. In patients with atrial fibrillation, fractionation increased as interelectrode spacing increased.</AbstractText>We created a model for distinguishing the roles of spatial and temporal electric variation and electrode resolution in producing electrogram fractionation. Spatial resolution affects fractionation attributable to spatiotemporal variation but not temporal variation alone. Electrogram fractionation was directly proportional to spatiotemporal variation and inversely proportional to spatial resolution. Spatial resolution limits the ability to distinguish high-frequency excitation from overcounting. In patients with atrial fibrillation, complex fractionated atrial electrogram detection varies with spatial resolution. Electrode resolution must therefore be considered when interpreting and comparing studies of fractionation.</AbstractText> |
14,788 | Use of the impedance threshold device improves survival rate and neurological outcome in a swine model of asphyxial cardiac arrest*. | To assess whether intermittent impedance of inspiratory gas exchange improves hemodynamic parameters, 48-hr survival, and neurologic outcome in a swine model of asphyxial cardiac arrest treated with active compression-decompression cardiopulmonary resuscitation.</AbstractText>Prospective, randomized, double-blind study.</AbstractText>Laboratory investigation.</AbstractText>Thirty healthy Landrace/Large-White piglets of both sexes, aged 10 to 15 wks, whose average weight was 19 ± 2 kg.</AbstractText>At approximately 7 mins following endotracheal tube clamping, ventricular fibrillation was induced and remained untreated for another 8 mins. Before initiation of cardiopulmonary resuscitation, animals were randomly assigned to either receive active compression-decompression cardiopulmonary resuscitation plus a sham impedance threshold device (control group, n = 15), or active compression-decompression cardiopulmonary resuscitation plus an active impedance threshold device (experimental group, n = 15). Electrical defibrillation was attempted every 2 mins until return of spontaneous circulation or asystole.</AbstractText>Return of spontaneous circulation was observed in six (40%) animals treated with the sham valve and 14 (93.3%) animals treated with the active valve (p = .005, odds ratio 21.0, 95% confidence interval 2.16-204.6). Neuron-specific enolase and S-100 levels increased in the ensuing 4 hrs post resuscitation in both groups, but they were significantly elevated in animals treated with the sham valve (p < .01). At 48 hrs, neurologic alertness score was significantly better in animals treated with the active valve (79.1 ± 18.7 vs. 50 ± 10, p < .05) and was strongly negatively correlated with 1- and 4-hr postresuscitation neuron-specific enolase (r = -.86, p < .001 and r = -.87, p < .001, respectively) and S-100 (r = -.77, p < .001 and r = -0.8, p = .001) values.</AbstractText>In this model of asphyxial cardiac arrest, intermittent airway occlusion with the impedance threshold device during the decompression phase of active compression-decompression cardiopulmonary resuscitation significantly improved hemodynamic parameters, 24- and 48-hr survival, and neurologic outcome evaluated both with clinical and biochemical parameters (neuron-specific enolase, S-100).</AbstractText> |
14,789 | Cardiac sarcoidosis mimicking arrhythmogenic right ventricular dysplasia with high defibrillation threshold requiring subcutaneous shocking coil implantation. | Cardiac involvement in patients with sarcoidosis has been reported in up to 25-39% of patients and is responsible for up to 85% of deaths attributed to the disease, often due to sudden cardiac death. An established diagnosis of cardiac sarcoidosis (CS) portends an ominous prognosis, with an estimated five year-survival of 44%. We report a case that was initially diagnosed as arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), but extra-cardiac biopsies later on were consistent with sarcoidosis and a final diagnosis of CS was made. The patient received an implantable cardioverter defibrillator (ICD) with a subcutaneous lead array implant for high defibrillation threshold (DFT). Exclusive right ventricular (RV) involvement is atypical for CS. The predominant RV involvement based on echocardiogram, cardiac magnetic resonance imaging (MRI) and right precordial electrocardiogram changes can lead to misdiagnosis as ARVD/C based on the modified task force criteria. Cardiac sarcoidosis is an under-diagnosed disease and the delay in its diagnosis and appropriate therapy can lead to a fatal outcome. High defibrillation thresholds have not been previously reported in patients with CS, but given the natural progression of the disease and the limitations in current pharmacotherapy, implanters who diagnose and treat such patients must be prepared to deal with this issue. |
14,790 | The occurrence of new arrhythmias after catheter-ablation of accessory pathway: delayed arrhythmic side-effect of curative radiofrequency lesion? | New arrhythmias (NA) may appear late after accessory pathway (AP) ablation, but their relation to curative radiofrequency (RF) lesion is unknown.</AbstractText>The aim of this study was to determine the prevalence and predictors for NA occurrence after AP ablation and to investigate pro-arrhythmic effect of RF.</AbstractText>Total of 124 patients (88 males, mean age 43 +/- 14 years) with Wolff-Parkinson-White syndrome and single AP have been followed after successful RF ablation. Post-ablation finding of arrhythmia, not recorded before the procedure, was considered a NA. The origin of NA was assessed by analysis of P-wave and/or QRS-complex morphology, and, thereafter, it was compared with locations of previously ablated APs.</AbstractText>Over the follow-up of 4.3 +/- 3.9 years, NA was registered in 20 patients (16%). The prevalence of specific NAs was as follows: atrioventricular (AV) block 0.8%, atrial premature beats 1.6%, atrial fibrillation 5.4%, atrial flutter 0.8%, sinus tachycardia 4.8%, ventricular premature beats (VPBs) 7.3%. Multivariate Cox-regression analysis identified (1) pre-ablation history of pathway-mediated tachyarrhythmias >10 years (HR = 3.54, p = 0.016) and (2) septal AP location (HR = 4.25, p = 0.003), as the independent predictors for NA occurrence. In four NA cases (two cases of septal VPBs, one of typical AFL and one of AV-block) presumed NA origin was identified in the vicinity of previous ablation target.</AbstractText>NAs were found in 16% of patients after AP elimination. In few of these cases, late on-site arrhythmic effect of initially curative RF lesion might be possible. While earlier intervention could prevent NA occurrence, closer follow-up is advised after ablation of septal AP.</AbstractText> |
14,791 | Role of KATP channels in the maintenance of ventricular fibrillation in cardiomyopathic human hearts. | Ventricular fibrillation (VF) leads to global ischemia. The modulation of ischemia-dependent pathways may alter the electrophysiological evolution of VF.</AbstractText>We addressed the hypotheses that there is regional disease-related expression of K(ATP) channels in human cardiomyopathic hearts and that K(ATP) channel blockade promotes spontaneous VF termination by attenuating spatiotemporal dispersion of refractoriness.</AbstractText>In a human Langendorff model, electric mapping of 6 control and 9 treatment (10 μmol/L glibenclamide) isolated cardiomyopathic hearts was performed. Spontaneous defibrillation was studied and mean VF cycle length was compared regionally at VF onset and after 180 seconds between control and treatment groups. K(ATP) subunit gene expression was compared between LV endocardium versus epicardium in myopathic hearts. Spontaneous VF termination occurred in 1 of 6 control hearts and 7 of 8 glibenclamide-treated hearts (P=0.026). After 180 seconds of ischemia, a transmural dispersion in VF cycle length was observed between epicardium and endocardium (P=0.001), which was attenuated by glibenclamide. There was greater gene expression of all K(ATP) subunit on the endocardium compared with the epicardium (P<0.02). In an ischemic rat heart model, transmural dispersion of refractoriness (ΔERP(Transmural)=ERP(Epicardium)-ERP(Endocardium)) was verified with pacing protocols. ΔERP(Transmural) in control was 5 ± 2 ms and increased to 36 ± 5 ms with ischemia. This effect was greatly attenuated by glibenclamide (ΔERP(Transmural) for glibenclamide+ischemia=4.9 ± 4 ms, P=0.019 versus control ischemia).</AbstractText>K(ATP) channel subunit gene expression is heterogeneously altered in the cardiomyopathic human heart. Blockade of K(ATP) channels promotes spontaneous defibrillation in cardiomyopathic human hearts by attenuating the ischemia-dependent spatiotemporal heterogeneity of refractoriness during early VF.</AbstractText> |
14,792 | Role of implantable cardioverter defibrillator therapy in patients with acquired long QT syndrome: a long-term follow-up. | The use of implantable cardioverter defibrillators (ICD) in patients with torsade de pointes (TdP) and ventricular fibrillation in the presence of acquired long QT syndrome (aLQTS) is under debate, partly due to the fact that aLQTS is potentially reversible and currently no long-term follow-up data are available. We aimed to evaluate the long-term follow-up of patients with acquired long QT syndrome (aLQTS) who had received an implantable cardioverter defibrillator (ICD) for secondary prevention of sudden cardiac arrest (SCA).</AbstractText>Over a 10 year period, 43 patients with an ICD after survived cardiac arrest (SCA) due to an aLQTS were included [female n= 27 (63%); mean age 61 ± 16 years]. There was no clinical evidence for congenital LQTS (Schwartz score 1.25 ± 0.8). Structural heart disease was present in 29 patients (47%; ischaemic n= 13; dilated cardiomyopathy n= 9; mean EF 41%± 12). The most common proarrhythmic trigger happened to be antiarrhythmic drugs (n= 34; 79%). Other triggers included contrast agent (n= 1), haloperidol (n= 2), severe hypokalaemia (n= 2), drug abuse/alcohol (n= 2), and mere severe bradycardia (n= 2). Under trigger QTc interval measured 536 ± 58 vs. 438 ± 33 ms without trigger (P< 0.001). During a mean follow-up of 84 ± 55 months, appropriate shocks occurred in 19 patients (44%); inappropriate shocks in 13 patients (30%; only inappropriate n= 3). Appropriate shocks were almost as common in patients without as in those with structural heart disease (35 vs. 48%; P= 0.32). None of the patients were re-exposed to the initial trigger during the follow-up period. Beta-blocker medication did not prevent ICD shocks (12 of 19 vs. 11 of 24 on medication).</AbstractText>Appropriate ICD shocks are a common finding in patients with aLQTS and SCA irrespective of the underlying cause or structural heart disease. Thus, even in the presence of relevant acquired proarrhythmia ICD may be beneficial.</AbstractText> |
14,793 | Celivarone in patients with an implantable cardioverter-defibrillator: adjunctive therapy for the reduction of ventricular arrhythmia-triggered implantable cardioverter-defibrillator interventions. | Implantable cardioverter-defibrillators (ICDs) remain the treatment of choice for the prevention of life-threatening arrhythmias. However, many patients with ICDs require additional antiarrhythmic therapy to reduce the morbidity associated with recurrent arrhythmia-triggered ICD interventions.</AbstractText>Our study aimed to evaluate the safety and efficacy of celivarone in reducing these interventions.</AbstractText>A total of 153 eligible ICD recipients were randomized to receive either placebo or celivarone 100 or 300 mg once daily for 6 months. The primary end point was the prevention of arrhythmia-triggered ICD therapies.</AbstractText>Fewer ventricular tachycardia and ventricular fibrillation episodes were observed in the 300-mg celivarone group than in the placebo group, with a relative risk reduction of 46%, which was not statistically significant. The analysis of all-cause shocks showed a trend toward a decreased number of events in the celivarone 300-mg group. A post hoc analysis of the primary end point in a subgroup of patients in the celivarone 300-mg group, who had received ICD therapy within 1 month of randomization, showed a significant benefit (P = .032). Celivarone was not associated with an increased risk of torsades de pointes, thyroid dysfunction, or pulmonary events. More heart failure events were reported in the celivarone groups than in the placebo group, but the difference was not statistically significant.</AbstractText>Celivarone tends to reduce ventricular tachycardia-/ventricular fibrillation-triggered ICD therapies. This effect was not statistically significant. There was a trend toward greater efficacy in the 300-mg group, especially in patients undergoing ICD therapy within 30 days prior to randomization. Overall, celivarone was well tolerated.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,794 | Prognostic impact of left ventricular mass severity according to the classification proposed by the American Society of Echocardiography/European Association of Echocardiography. | The American Society of Echocardiography (ASE) and European Association of Echocardiography (EAE) recommend the use of quantitative estimation of left ventricular (LV) mass and defined partition values for mild, moderate, and severe hypertrophy. However, the prognostic implications associated with this categorization are unknown.</AbstractText>In this observational cohort study of unselected adults undergoing echocardiography for any indication, LV hypertrophy was assessed using the ASE/EAE-recommended formula and measurement convention from LV linear dimensions indexed to body surface area. Mortality and incident hospitalizations for cardiovascular disease were the outcomes of this study.</AbstractText>Of 2,545 subjects (mean age, 61.9 ± 15.8 years; 56.3% women), 52.9% had normal LV mass, and 15.4% had mild, 12.1% moderate, and 19.6% severe LV hypertrophy. During a mean follow-up period of 2.5 ± 1.2 years, 121 deaths and 292 incident hospitalizations for cardiovascular disease occurred. In multivariate models including age, gender, LV ejection fraction, wall motion score index, significant valvular disease, and atrial fibrillation, the adjusted hazard ratios for death were 1.81 (95% confidence interval [CI], 1.03-3.20; P = .041) for mild, 2.31 (95% CI, 1.33-4.01; P = .003) for moderate, and 2.30 (95% CI, 1.39-3.79, P = .001) for severe LV hypertrophy. The adjusted hazard ratios for incident cardiovascular hospitalizations were 1.24 (95% CI, 0.84-1.82; P = .277) for mild, 2.02 (95% CI, 1.42-2.88; P = .0001) for moderate, and 2.38 (95% CI, 1.75-3.22, P < .0001) for severe LV hypertrophy. After adjustment for known risk predictors, there was a 1.3-fold risk for death and cardiovascular disease events per category of LV mass (P = .001).</AbstractText>In a cohort study of unselected adult outpatients, the categorization of LV mass according to the ASE/EAE recommendations offered prognostic information independently of age, gender, and other known predictors.</AbstractText>Copyright © 2011 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.</CopyrightInformation> |
14,795 | Stroke mechanism in patients with non-valvular atrial fibrillation according to the CHADS2 and CHA2 DS2 -VASc scores. | The CHADS(2) and CHA(2) DS(2) -VASc scores are useful to stratify embolic risks in patients with non-valvular atrial fibrillation (NVAF) and to identify patients eligible for anticoagulation. Although the risk of stoke increases in patients with higher CHADS(2) or CHA(2) DS(2) -VASc scores, it is uncertain why the stroke rate increases in them. Concomitant potential cardiac sources of embolism (PCSE) may be more frequent in patients with higher CHADS(2) or CHA(2) DS(2) -VASc scores because stroke risks increase when concomitant PCSE is present in Atrial fibrillation (AF). On the other hand, atherothrombosis may be the cause when considering that most components of the CHADS(2) and CHA(2) DS(2) -VASc scores are risk factors for atherosclerosis.</AbstractText>Amongst 5493 stroke patients who were prospectively registered with the stroke registry for 11years, 860 consecutive patients with NVAF were included for this study. We investigated the mechanisms of stroke according to the CHADS(2) /CHA(2) DS(2) -VASc score in stroke patients with NVAF.</AbstractText>Amongst 860 patients, concomitant PCSE were found in 334 patients (38.8%). The number of PCSE increased as the CHADS(2) /CHA(2) DS(2) -VASc score increased (P<0.001). Of individual PCSE, akinetic left ventricular segment, hypokinetic left ventricular segment and myocardial infarction <4weeks were associated with the CHADS(2) /CHA(2) DS(2) -VASc score. The presence of possible atherothrombotic mechanism, in addition to AF, was suggested in 27.3%. The proportion of patients with concomitant presence of possible atherothrombosis was increased as the CHADS(2) /CHA(2) DS(2) -VASc score increased (P<0.001).</AbstractText>Increased frequency of concomitant PCSE and that of the atherothrombotic mechanism may explain the high risk of stroke in patients with higher CHADS(2) /CHA(2) DS(2) -VASc score.</AbstractText>© 2011 The Author(s). European Journal of Neurology © 2011 EFNS.</CopyrightInformation> |
14,796 | Pre-hospital discharge testing after implantable cardioverter defibrillator implantation: a measure of safety or out of date? A retrospective analysis of 975 patients. | The present study evaluates the relevance and additional safety value of pre-hospital discharge (PHD) testing in patients with implantable cardioverter defibrillator (ICD) therapy.</AbstractText>From June 1998 to May 2009, 975 patients (830 male, 145 female) with ICD were screened retrospectively for failed PHD and analysed for its consequences, risk factors, and patient characteristics after successful intra-operative testing in the implantation procedure.</AbstractText>Pre-hospital discharge testing procedure was performed in 809 cases. No serious adverse events (e.g. death, persistant ventricular fibrillation or ventricular tachycardia, stroke) occurred. The overall incidence of failed PHD was 1.4% (n = 11). The underlying mechanisms were defibrillation threshold failure in 9/11 cases and sensing failure in 2/11 cases.</AbstractText>In this study predictors for PHD-failure are: (i) cardiomyopathy other than ischaemic or dilative, (ii) young age, and (iii) small or very large left ventricular end-diastolic diameter ( < 40 or > 65 mm). Particularly, (i) manufacture of device or leads, (ii) lead design, (iii) medical treatment, or (iv) gender have no significant influence on PHD failure.</AbstractText> |
14,797 | Upright T waves in lead aVR are associated with cardiac death or hospitalization for heart failure in patients with a prior myocardial infarction. | The aim of the present study was to clarify the prognostic significance of upright T waves (amplitude > 0 mV) in lead aVR in patients with a prior myocardial infarction (MI). We retrospectively examined 167 patients with a prior MI. The primary end point was cardiac death or hospitalization for heart failure. During a follow-up period of 6.5 ± 2.8 years, 34 patients developed the primary end point. A Kaplan-Meier analysis showed a lower primary event-free rate in patients with upright T waves in lead aVR than in those with nonupright T waves in lead aVR (P = 0.001). Univariate Cox proportional hazards regression analyses showed that age, gender, chronic kidney disease, anterior wall MI, upright T waves in lead aVR, left ventricular ejection fraction, loop diuretic use, and spironolactone use were significantly associated with the primary end point. A multivariate Cox proportional hazards regression analysis selected age [hazard ratio (HR) 1.10, 95% confidence interval (CI) 1.05-1.16, P < 0.001], upright T waves in lead aVR (HR 3.10, 95% CI 1.23-7.82, P = 0.017), and loop diuretic use (HR 4.61, 95% CI 1.55-13.67, P = 0.006) as independent predictors of the primary end point. In conclusion, the presence of upright T waves in lead aVR is an independent predictor of cardiac death or hospitalization for heart failure in patients with a prior MI. The analysis of T-wave amplitude in lead aVR provides useful prognostic information in patients with a prior MI. |
14,798 | Stimulation of the intra-cardiac vagal nerves innervating the AV-node to control ventricular rate during AF: specificity, parameter optimization and chronic use up to 3 months. | Stimulation of the intra-cardiac vagal nerves innervating the AV-node (AVNS) is a promising approach to slow down ventricular rate (VR) during atrial fibrillation (AF). Our purpose was to demonstrate that effects on R-R-interval during stable AF can be maintained for several months once optimized and that AVNS affects specifically the nerves innervating the AV-node.</AbstractText>Our study included both an acute and chronic phase. Fifteen goats were implanted with a pacemaker connected to an atrial and ventricular lead and a neurostimulator connected to an atrial lead placed at a certain septal site, to induce an AV prolongation. In the chronic experiments (n = 9), after assessment of optimal AVNS parameters, the effect of continuous AVNS on VR was studied during stable AF for up to 3 months. The mechanism of AVNS was studied using atropine and esmolol. Next, the effects of AVNS during the atrial refractory period on electrophysiological and hemodynamic parameters were investigated acutely (n = 7).</AbstractText>The maximal effect was found at a stimulation frequency of 40 Hz, and increased with increasing pulse width (at lower voltages) and increasing voltage. After 0, 1, and 3 months of AVNS during stable AF, AVNS decreased average VR, respectively, 55% (n = 9), 48% (n = 8), and 28% (n = 6). The AVNS effect appeared to be dominantly parasympathetic. AVNS did not influence (1) the sinus node, (2) the refractory period of the atrial, ventricular tissue, and His and (3) hemodynamic parameters.</AbstractText>AVNS is efficient in reducing ventricular rate for at least 3 months using optimized parameters and specifically affects the parasympathetic nerves innervating the AV-node.</AbstractText> |
14,799 | The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity. | The purpose of this study is to test the role that parasympathetic postganglionic neurons could play on the adaptive electrophysiological changes produced by physical training on intrinsic myocardial automatism, conduction and refractoriness. Trained rabbits were submitted to a physical training protocol on treadmill during 6 weeks. The electrophysiological study was performed in an isolated heart preparation. The investigated myocardial properties were: (a) sinus automatism, (b) atrioventricular and ventriculoatrial conduction, (c) atrial, conduction system and ventricular refractoriness. The parameters to study the refractoriness were obtained by means of extrastimulus test at four different pacing cycle lengths (10% shorter than spontaneous sinus cycle length, 250, 200 and 150 ms) and (d) mean dominant frequency (DF) of the induced ventricular fibrillation (VF), using a spectral method. The electrophysiological protocol was performed before and during continuous atropine administration (1 μM), in order to block cholinergic receptors. Cholinergic receptor blockade did not modify either the increase in sinus cycle length, atrioventricular conduction and refractoriness (left ventricular and atrioventricular conduction system functional refractory periods) or the decrease of DF of VF. These findings reveal that the myocardial electrophysiological modifications produced by physical training are not mediated by intrinsic cardiac parasympathetic activity. |
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