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A case of an electrical storm occurring in a patient implanted with a cardioverter-defibrillator for Brugada syndrome is reported. Recurrent ventricular fibrillation was initiated by short-coupled isolated monomorphic ventricular premature beats probably originating from the right ventricular outflow tract, associated with a manifest electrocardiographic pattern of Brugada syndrome. Infusion of atropine accelerated the heart rate but did not prevent ventricular fibrillation, however, low doses of isoprenaline quickly obviated any recurrence of ventricular fibrillation. This was associated with the disappearance of the short-coupled premature beats together with a normalization of the electrocardiographic pattern. Possible mechanisms are discussed according to the accepted pathophysiological hypothesis. [ABSTRACT FROM PUBLISHER]

Conventional tilt test protocols are time consuming and there is no consensus regarding the optimal duration of the test and the provocative drug to be used. This study evaluated the diagnostic power of a short nitroglycerine test against a conventional isoproterenol protocol. A cohort of 128 patients with unexplained syncope was studied. A group of 64 consecutive patients were tilted with a short nitroglycerine test consisting of a passive phase of 15 minutes and if this proved negative, 400 microg of sublingual nitroglycerin spray for a further 15 minutes. The control group consisted of 64 patients tilted with a conventional isoproterenol protocol with a passive phase of 30 minutes and a drug-challenge phase of 20 minutes. In the nitroglycerine protocol 39 (60.9%) patients showed a positive response versus 27(42.2%) in the isoproterenol group (P = 0.034). The duration of the protocol was 23.2 +/- 7.2 minutes in the nitroglycerine group versus 41.1 +/- 15.5 minutes with isoproterenol (P = 0.001). The time until syncope was 18.87 +/- 6.1 versus 29 +/- 18, respectively (P = 0.002). For evaluating unexplained syncope the short tilt test protocol with nitroglycerine is less time consuming, easier to perform, and has a higher rate of positive response than a conventional isoproterenol protocol. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to analyze the feasibility, efficacy, and safety of epicardial radiofrequency (RF) ablation in patients with incessant ventricular tachycardia (VT).Background: Management of patients with incessant VT is a difficult clinical problem. Drugs and RF catheter ablation are not always effective. A nonsurgical transthoracic epicardial RF ablation can be an alternative in patients refractory to conventional therapy.Methods: Epicardial RF ablation was performed in 10 patients who presented with incessant VT despite the use of two or more intravenous antiarrhythmic drugs.Results: In eight patients, endocardial ablation (EdA) failed to control the tachycardia. In the remaining two patients, epicardial ablation (EpA) was first attempted because of left ventricular thrombus and severe artery disease, respectively. Eight patients had a diagnosis of coronary artery disease with healed myocardial infarction. One patient had dilated cardiomyopathy, and one patient had idiopathic, incessant VT. In patients with structural heart disease, the mean ejection fraction was 0.28 +/- 0.10%. Four patients previously received an implantable defibrillator. The EpA effectively terminated the incessant tachycardia in eight patients, which represents a success rate of 80%. In them, after a follow-up of 18 +/- 18 months, a single episode of a different VT was documented in one patient. No significant complications occurred related to the procedure.Conclusions: In patients with incessant VT despite the use of drugs or standard EdA, the epicardial approach was very effective and should be considered as an alternative in this life-threatening situation. [ABSTRACT FROM AUTHOR]

Aims To determine the effectiveness of the implantable cardioverter defibrillator (ICD) in preventing recurrence of syncope in patients with structural heart disease, previously unexplained syncope and inducible ventricular arrhythmias.Methods Thirty-eight patients with syncope, structural heart disease and inducible arrhythmias had an ICD implanted. All ICDs delivered antitachycardia pacing and shocks of adjusted energy. Detection and therapy were programmed according to uniform criteria.Results The mean age of the patients was 63±11 years and most of them were male (36/38). After a mean follow-up of 28±15 (4–61) months, six patients died and one underwent heart transplantation. Syncope recurred in three patients, but in none of them was it caused by an arrhythmic event. In 18 patients, 113 episodes of ventricular tachycardia/ventricular fibrillation were detected and appropriately treated by the ICD. The mean time from implant until first appropriate therapy was 18±14 months. The actuarial probability of receiving appropriate therapy was 20% and 42% at 12 and 24 months, respectively.Conclusions In patients with unexplained syncope, structural heart disease and inducible arrhythmias, ICD prevents syncope associated with arrhythmic events. Frequent effective use of antitachycardia pacing and shocks of adjusted energy seem essential to this aim. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved. [ABSTRACT FROM PUBLISHER]

Aims To analyse whether the proportion of patients with lone atrial fibrillation engaged in chronic sport practice was higher than that observed in the general population.Methods and Results The records of 1160 patients, seen at the arrhythmia outpatient clinic, were reviewed. A total of 70 patients (6%) suffered lone atrial fibrillation and were younger than 65 years. Thirty two of them had been engaged in long-term sport practice. All patients in the sport group were men as compared to only 50% in the sedentary group (P<0·0001). To avoid the confounding effect of sex distribution, women were excluded. Sportsmen started their episodes of atrial fibrillation at a younger age, they had a lower incidence of mild hypertension and their episodes of atrial fibrillation were predominantly vagal in contrast to the sedentary patients. The echocardiographic parameters were similar to those observed in the sedentary patients, but when compared with 20 healthy controls, they showed greater atrial and ventricular dimensions and a higher ventricular mass. The proportion of sportsmen among patients with lone atrial fibrillation is much higher than that reported in the general population of Catalonia: 63% vs 15% (P<0·05).Conclusion Long-term vigorous exercise may predispose to atrial fibrillation. [ABSTRACT FROM PUBLISHER]

Background The syndrome with an electrocardiographic pattern of right bundle branch block, ST segment elevation in leads V1to V3and sudden death is genetically determined and caused by mutations in the cardiac sodium channel. The inheritance of the disease is autosomal dominant. Sudden death may, however, occur from a variety of causes in relatives and patients with this syndrome.Patients and Methods Twenty-five Flemish families with this syndrome with a total of 334 members were studied. Affected members were recognized by means of a typical electrocardiogram either occurring spontaneously or after the intravenous administration of antiarrhythmic drugs. Sudden deaths in these families were classified as related or not to the syndrome by analysis of the data at the time of the event, mode of inheritance of the disease, and data provided by survivors.Results Of the 25 families with the syndrome, 18 were symptomatic (at least one sudden death related to the syndrome) and seven were asymptomatic (no sudden deaths related to the syndrome). In total, there were 42 sudden cardiac deaths (12% incidence). Twenty-four sudden deaths were related to the syndrome and all occurred in symptomatic families. Eighteen sudden deaths (43% of total sudden deaths) were not related to the syndrome (nine cases) or were of unclear cause (nine cases). Three of them occurred in two asymptomatic families and the remaining 15 in five symptomatic families. Twenty-four of the 50 affected members (47%) suffered (aborted) sudden death and 18 of the 284 unaffected members (6%). This difference in the incidence of sudden death was statistically significant (P<0·0001). Patients with (aborted) sudden death caused by the syndrome were younger than patients with sudden death of other or unclear causes (38±4 years vs 59±3 years respectively,P =0·0003).Conclusions In families at high risk of sudden death because of genetically determined diseases, the main cause of sudden death remains the disease. However, almost the half of sudden deaths are caused by unrelated diseases or are of unclear cause. Accurate classification of the causes of sudden death is mandatory for appropriate analysis of the causes of death when designing preventive treatments. [ABSTRACT FROM PUBLISHER]

Patients with an implantable cardioverter defibrillator (ICD) can undergo inappropriate therapies if electrical activity not originating in the ventricle is wrongly recognized as ventricular by the device. Inappropriate therapy can be the result of detection of supraventricular tachycardias or over-sensing of other artifacts by the device. Enhanced detection criteria in third-generation ICD have been implemented to recognize fast supraventricular arrhythmias. Analysis of the use of these criteria in patients with an ICD has shown that arrhythmias detected in the ventricular tachycardia zone are frequently supraventricular (193 supraventricular of 690 tachycardia episodes in 23 of 59 patients). Use of sudden onset was very effective in detecting sinus tachycardia (65 of 67 episodes) and stability was very useful in detecting atrial fibrillation (31 of 32 episodes). However sensitivity in detecting ventricular tachycardia was only 90% (451 of 497 episodes). Application of the sustained, rate duration criteria allowed appropriate treatment of all ventricular tachycardia episodes, increasing sensitivity to 100%; however, specificity in appropriate nontreatment of supraventricular episodes decreased from 96% to 83%. Subsequent analysis of different algorithms showed that sudden onset > 9% and stability < 40 msec was the algorithm with the best specificity and sensitivity. Programming sudden onset and stability detection criteria with a sustained, rate duration safety net for triggering tachycardia therapy results in appropriate device management in most patients with supraventricular and relatively slow ventricular tachycardia. [ABSTRACT FROM AUTHOR]

In 1992 a new syndrome was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and an electrocardiogram (ECG) characteristic of right bundle branch block with ST segment elevation in leads V1to V3. The disease is genetically determined, with an autosomal dominant pattern of transmission. Three different mutations that affect the structure and function of the cardiac sodium channel gene SCN5A have been identified. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The incidence of the disease is difficult to estimate, but it causes 4 to 10 sudden deaths per 10 000 inhabitants per year in areas like Thailand and Laos. In these countries, the disease represents the most frequent cause of death in young adults. Up to 50% of the yearly sudden deaths in patients with a structurally normal heart are caused by this syndrome. The diagnosis is easily made by means of the ECG. The presence of concealed and intermittent forms, however, make the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the ECG, while intravenous ajmaline, flecainide or procainamide accentuate ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. Recent data suggest that loss of the action potential dome in the right ventricular epicardium but not the endocardium underlies ST segment elevation seen in the Brugada syndrome. Also, electrical heterogeneity within the right ventricular epicardium leads to the development of closely coupled extrasystoles via a phase 2 reentrant mechanism, which then precipitates ventricular tachycardia–ventricular fibrillation. Right ventricular epicardium is preferentially affected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs like amiodarone and beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals. Gene therapy may offer a cure in future years. Implantation of an automatic cardioverter–defibrillator is the only currently proven effective therapy. [ABSTRACT FROM PUBLISHER]

The possibility that an asynchronous increase in the ventricular monophasic action potential duration is the basis of the quinidine-induced torsade de pointes, has led us to study the electrophysiological effects of increasing doses of intravenous quinidine. We measured the monophasic action potential duration and the ventricular effective refractory period at several right ventricular myocardial sites in the anaesthetized dog. Our results showed that quinidine induces a dose-dependent prolongation in ventricular effective refractory period and in ventricular monophasic action potential duration. These increases were uniform throughout the right ventricle. No variations in repolarization or in refractoriness were observed between the four ventricular sites studied. The results suggest that quinidine does not have a direct effect on dispersion of repolarization, and that mechanisms other than its direct electrophysiological action are involved in the development of torsade de pointes. [ABSTRACT FROM PUBLISHER]

Background: Cardiac resynchronization therapy (CRT) has been shown to reduce functional mitral regurgitation (MR). It has been proposed that the mechanism of MR reduction relates to geometric change or, alternatively, changes in left ventricular (LV) contractile function. Normal mitral valve (MV) function relies on a balance between tethering and closing forces on the MV leaflets. Functional MR results from a derangement of this force–balance relationship, and CRT may be an important modulator of MV function by its ability to enhance the force–balance relationship on the MV. We hypothesized that CRT improves the comprehensive force balance acting on the valve, including favorable changes in both geometry and LV contractile function. Methods and Results: We examined the effect of CRT on 34 patients with functional MR before and after CRT (209±81 days). MR regurgitant volume, closing forces on MV (derived from Doppler transmitral pressure gradients), including dP/dt and a factor (closing pressure ratio) expressing how long the peak closing gradient is maintained over systole (closing pressure ratio=velocity time integral/MR peak velocity×mitral regurgitation time), and dyssynchrony by tissue Doppler were measured. End-diastolic volume, end-systolic volume, mitral valve annular area (MAA) and contraction (percent change in MAA from end-diastole to midsystole), leaflet closing area (leaflet area during valve closure), and tenting volume (volume under leaflets to annular plane) were measured by 3D echocardiography. After CRT, end-diastolic volume (253±111 versus 221±110 mL, P<0.001) and end-systolic volume (206±97 versus 167±91 mL, P<0.001) decreased and ejection fraction (19±6 versus 27±9%, P<0.001) increased. MR regurgitant volume decreased from 35±17 to 23±14 mL (P<0.001), MAA from 11.6±3.5 to 10.5±3.1 cm2 (P<0.001), leaflet closing area from 15.4±5 to 13.7±3.8 cm2 (P<0.001), and tenting volume from 5.7±2.6 to 4.6±2.2 mL (P<0.001). Peak velocity (and therefore transmitral closing pressure) was more sustained throughout systole, as reflected by the increase in the closing pressure ratio (0.77±0.1 versus 0.84±0.1 before CRT versus after CRT, P=0.01); dP/dt also improved after CRT. There was no change in dyssynchrony or MAA contraction. Conclusions: Reduction in MR after CRT is associated with favorable changes in MV geometry and closing forces on the MV. It does so by favorably affecting the force balance acting on the MV in 2 ways: reducing tethering through reversal of LV remodeling and increasing the systolic duration of peak transmitral closing pressures.