Isolated noncompaction left ventricular myocardium and polymorphic ventricular tachycardia

A 57-year-old woman with syncope was admitted. She had a family history of sudden death: two brothers had died suddenly at the age of 47. Transesophageal echocardiography showed numerous prominent trabeculations and deep intertrabecular recesses in the anterior and lateroapical zones. Isotopic left ventricular ejection fraction was 46%. Cardiac catheterization showed coronary arteries with no angiographic lesions. A prominent trabecular zone and deep intertrabecular recesses were seen in the anterior wall on left ventriculography. Right ventriculography was normal. The diagnosis of isolated noncompaction left ventricular myocardium was established. Continuous 24-h electrocardiographic registry showed episodes of polymorphic ventricular tachycardia. Programmed ventricular stimulation performed at the right ventricular apex with up to three extrastimuli failed to induce ventricular arrhythmias. Treatment with beta blockers was initiated, but short runs of polymorphic ventricular tachycardia persisted. A dual-chamber automatic implantable defibrillator was implanted. We discuss the physiopathology of the arrhythmia. It appears that several factors could be responsible for the malignant arrhythmias in this entity.     

Localized right ventricular structural abnormalities in patients with idiopathic ventricular fibrillation: Magnetic resonance imaging study

Summary Lethal arrhythmias, including ventricular tachycardia and ventricular fibrillation, may occur in the absence of apparent morphological abnormalities. However, a recent study using magnetic resonance imaging (MRI) has suggested that localized, minor structural abnormalities of the right ventricle are responsible for right ventricular outflow tract ventricular tachycardia in a number of patients. We demonstrated regional wall thinning and systolic dyskinesia of the right ventricle by MRI in two patients with idiopathic ventricular fibrillation in whom other cardiac imaging modalities failed to show abnormalities. This finding implies that minor structural abnormalities do exist in patients with so-called idiopathic ventricular fibrillation.     

The “Short‐Coupled” Variant of Right Ventricular Outflow Ventricular Tachycardia: A Not‐So‐Benign Form of Benign Ventricular Tachycardia?

Idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT-VT) and idiopathic RVOT-extrasystoles are generally considered benign arrhythmias. We described three cases who originally presented with typical "benign looking" RVOT-extrasystoles or RVOT-VT but developed malignant polymorphic VT during follow-up. The unusual aspect of their RVOT-extrasystoles was their coupling interval, which appears to be intermediate between the ultra-short coupling interval of idiopathic VF and the long coupling interval seen in the truly benign RVOT-VT.     

Prognosis in Patients with Left Ventricular Dysfunction and Ventricular Tachycardia Following Programmed Ventricular Stimulation

We performed programmed ventricular stimulation on 69 patients with left ventricular ejection dysfunction (ejection fraction < 50%) and clinically recognized ventricular tachycardia including 28 patients with sustained ventricular tachycardia and 41 patients with nonsustained ventricular tachycardia. An inducible arrhythmia (> 6 beats ventricular tachycardia) was found in 74% of patients. Patients with clinically sustained arrhythmias were frequently inducible (89%) with a high incidence of inducible monomorphic ventricular tachycardia (82%). Patients with clinically nonsustained ventricular tachycardia had a lower rate of inducibility (63%) including a high incidence of inducible polymorphic ventricular tachycardia (27%). Inducible patients with left ventricular dysfunction and ventricular tachycardia had a low incidence of electrophysiologically demonstrated effective drug therapy (16%). However, if an effective drug was found, the prognosis was good. Empirical drug therapy was associated with a poor prognosis in inducible and noninducible patients. Finally, an unfavorable prognosis was associated with a clinically sustained arrhythmia, a lower ejection fraction, and the presence of a left ventricular aneurysm. An inducible arrhythmia did not predict an unfavorable course. Indeed, patients with noninducible ventricular tachycardia in this group of patients were still at risk for sudden cardiac death.     

Effects of flecainide therapy on inappropriate shocks and arrythmias in catecholaminergic polymorphic ventricular tachycardia

We report the case of a child with catecholaminergic polymorphic ventricular tachycardia, who had inappropriate electric shocks by an implantable cardioverter defibrillator and from recurrence of arrhythmias despite an appropriate β-blocking treatment. An additional treatment by flecainide completely suppressed inappropriate shocks due to sinusal tachycardia and ventricular tachyarrhythmias. We briefly discuss the potentially interesting effect of flecainide in this specific arrhythmia.     

Dispersion of repolarization following double and triple programmed stimulation: A clinical study using the monophasic action potential recording technique

To study the dispersion of ventricular repolarization followingdouble and triple programmed stimulation and its correlationwith the inducibility of ventricular arrhythmias, monophasicaction potentials were simultaneously recorded from the rightventricular apex and outflow tract during programmed stimulationin 12 patients with ventricular arrhythmias and a normal QTinterval. The time difference between the ends of the two monophasicaction potentials were used as a measure of the dispersion ofventricular repolarization, which consists of the activationtime difference and the monophasic action potential durationdifference. During double and triple programmed stimulation, the dispersionof ventricular repolarization increased significantly with theshortening of the coupling interval but decreased slightly withthe shortening of the coupling interval but decreased slightlywith the shortening of the preceding interval. The inductionof the ventricular arrhythmias in these patients was invariablyassociated with a marked increase in the dispersion of ventricularrepolarization. The maximal dispersion of ventricular repolarizationwas significantly larger in the seven patients with polymorphicventricular tachycardia and/or ventricular flutter/fibrillationinduced than in the four patients with monomorphic ventriculartachycardia induced. Analysis of the two components of the dispersionof ventricular repolarization revealed that the increased dispersionof ventricular repolarization was mainly caused by an increasein the activation time difference in the monomorphic ventriculartachycardia subgroup, and by increases in both the activationtime difference and monophasic action potential duration differencein the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricularrepolarization is one of the underlying mechanisms accountingfor the myocardial vulnerability to ventricular arrhythmiasand that repolarization disturbance is important for the genesisof polymorphic ventricular tachycardia/fibrillation.     

Analysis of the pattern of initiation of sustained ventricular arrhythmias in patients with implantable defibrillators

INTRODUCTION: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease. METHODS AND RESULTS: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating beat of all ventricular arrhythmias was 523 +/- 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty-two (85%) of the arrhythmia episodes were initiated by a late-coupled premature beat, 33 (13%) were initiated by an early-coupled premature beat, and 5 episodes (2%) were initiated with a short-long-short sequence. The pattern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias. CONCLUSION: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late-coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia.     

Signed value of monophasic action potential duration difference: A useful measure in evaluation of dispersion of repolarization in patients with ventricular arrhythmias

AIMS: To evaluate the usefulness of the signed value of monophasicaction potential duration difference in analysing the causeof dispersion of ventricular repolarization. METHODS AND RESULTS: Monophasic action potentials were simultaneously recorded fromthe right ventricular apex and outflow tract during programmedstimulation in 36 patients with ventricular arrhythmias. Thetime difference between the ends of repolarization on the twomonophasic action potentials was used as a measure of the dispersionof ventricular repolarization, and the signed value of the monophasicaction potential duration difference was used to specify thecontributions of the activation time difference and the monophasicaction potential duration difference to the dispersion of ventricularrepolarization. During right ventricular pacing, single anddouble programmed stimulation and at the induction of ventriculararrhythmias, the dispersion of ventricular repolarization andthe signed value of monophasic action potential duration differencewere markedly greater in the 11 patients with polymorphic ventriculartachycardia/ventricular fibrillation induced than in the 13patients with monomorphic ventricular tachycardia induced, andin the 10 patients with clinical polymorphic ventricular tachycardia/ventricularfibrillation/cardiac arrest than in the 12 patients with sustainedmonomorphic ventricular tachycardia. This disclosed that theincreased dispersion of ventricular repolarization was causedby increases in both the activation time difference and themonophasic action potential duration difference in the former,but mainly by an increased activation time difference in thelatter groups. CONCLUSION: The signed value of monophasic action potential duration differencecan specify whether an increased dispersion of ventricular repolarizationis caused by in-homogeneous repolarization, inhomogeneous conductionor both, and thereby it is useful in study of the mechanismof ventricular arrhythmias.     

Calcium channel antagonism reduces exercise-induced ventricular arrhythmias in catecholaminergic polymorphic ventricular tachycardia patients with RyR2 mutations

Calcium channel antagonism in RyR2 defects. INTRODUCTION: Recently, gain-of-function mutations of cardiac ryanodine receptor RyR2 gene have been identified as a cause of familial or catecholaminergic polymorphic ventricular tachycardia. We examined the influence of the calcium channel blockers, verapamil and magnesium, on exercise-induced ventricular arrhythmias in patients with RyR2 mutations. METHODS AND RESULTS: Six molecularly defined catecholaminergic polymorphic ventricular tachycardia patients, all carrying a RyR2 mutation and on beta-adrenergic blocker therapy, underwent exercise stress test four times: at baseline, after verapamil and magnesium sulphate infusions, and finally, without interventions. The number of isolated and successive premature ventricular complexes during exercise ranged from 40 to 374 beats (mean 165 beats) at baseline, and was reduced during verapamil by 76+/-17% (P<0.05). Premature ventricular complexes appeared later and at higher heart rate during verapamil than at baseline (119+/-21 vs. 127+/-27 min-1, P<0.05). Magnesium did not inhibit the arrhythmias. Results in the fourth exercise stress test without interventions were similar to those in the first baseline study. CONCLUSIONS: This study provides the first in vivo demonstration that a calcium channel antagonist, verapamil, can suppress premature ventricular complexes and nonsustained ventricular salvoes in catecholaminergic polymorphic ventricular tachycardia caused by RyR2 mutations. Modifying the abnormal calcium handling by calcium antagonists might have therapeutic value.     

致心律失常性右室发育不良室性心动过速的电生理检查和外科治疗（附一例报告）

报告药物治疗无效、射频导管消融失败的致心律失常性右室发育不良（ＡＲＶＤ）顽固性室性心动过速（简称室速）１例患者，在电生理导引下行右室前游离壁隔离术治疗成功。术后随访７个月无室速发作，左室收缩功能正常。提示部分右室隔离术对有生命危险和药物治疗无效及射频导管消融失败的ＡＲＶＤ室速患者是安全、有效的     

Ventricular Arrhythmias after LV Remodelling: Surgical Ventricular Restoration or ICD?

Ventricular arrhythmias cause ~50% of deaths in remodeled ventricles after myocardial infarction, and the Multicenter Automatic Defibrillator Implantation Trial (MADIT II) showed that the Implantable Cardioverter Defibrillator (ICD) saved lives in high risk coronary patients with advanced left ventricular dysfunction. We studied 382 patients with remodeled hearts by preoperative Ventricular stimulation (PVS) to evaluate surgical ventricular restoration (SVR) that excludes scar and lower ventricular volume alters the early and late arrhythmia process without ICD utilization.Methods: Clinical and hemodynamic results before and after SVR in post-infarction patients, are compared to contrast spontaneous and/or inducible ventricular tachycardia to patients without arrhythmias. Study arrhythmia groups included: Spontaneous in 87 patients with clinical documented ventricular arrhythmias and inducible or not inducible ventricular tachycardia: Inducible in 105 patients without clinical ventricular arrhythmias but PVS inducible ventricular tachycardia; and No arrhythmias in 190 patients without spontaneous or PVS inducible ventricular tachycardia.Results: Preoperative LV end systolic volume index helped define preoperative arrythmia potential: Spontaneous > 120/m², inducible > 100 ml/m², and none < 100ml/m². Overall operative mortality rate was 7.6% (29/382). Sudden cardiac death rate was 2.5% causing 18.7% of all deaths. Surgical management reduced inducible ventricular tachycardia, from 41% preoperatively (144/352) to 8% (26/307) at early study, and 8% (14/177) one year later. Cardiac mortality was low at 5-years and not different between groups, despite use of only one late ICD device.Conclusions: Favorable electrical success rate and low mortality always included volume reduction to interrupt functional re-entry circuits, but also added endocardiectomy, cryoablation, CABG and mitral repair when needed. Overall SVR findings show volume and shape alteration limits ventricular arrhythmias that impair prognosis, and suggests ICD devices are not needed.     

Devices for the management of ventricular arrhythmias in cardiac failure

Heart failure is a common clinical syndrome with a high morbidity and mortality. Despite advances in medical treatment, death from dangerous ventricular arrhythmias is frequently implicated. Emerging evidence supports the use of the implantable cardioverter defibrillator for selected patients. This includes secondary prevention indications for patients who have survived life-threatening ventricular arrhythmias. In addition, patients who have not suffered spontaneous sustained ventricular arrhythmias, but who are at high risk for sudden arrhythmic death are starting to be recognized as candidates for ICD therapy. At present the only primary prevention indication with a good evidence base is the presence of inducible ventricular arrhythmias at electrophysiologic testing in patients with prior myocardial infarction, impaired left ventricular systolic function and non-sustained ventricular tachycardia on Holter monitoring. Studies planned or in progress are likely to expand further the role of device therapy in the treatment of patients with cardiac failure.     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

Heterogeneity and cardiac arrhythmias: An overview

This lecture examines the hypothesis that amplification of spatial dispersion of repolarization in the form of transmural dispersion of repolarization (TDR) underlies the development of life-threatening ventricular arrhythmias associated with inherited ion channelopathies, including the long QT, short QT, and Brugada syndromes as well as catecholaminergic polymorphic ventricular tachycardia. In the long QT syndrome, amplification of TDR often is secondary to preferential prolongation of the action potential duration of M cells, whereas in Brugada syndrome, it is thought to be due to selective abbreviation of the action potential duration of right ventricular epicardium. In the short QT syndrome, preferential abbreviation of action potential duration of either endocardium or epicardium appears to be responsible for amplification of TDR. In catecholaminergic polymorphic ventricular tachycardia, reversal of the direction of activation of the ventricular wall is responsible for the increase in TDR. Thus, the long QT, short QT, Brugada, and catecholaminergic ventricular tachycardia syndromes are pathologies with very different phenotypes and etiologies. However, these syndromes share a common final pathway in their predisposition to sudden cardiac death.     

Influence of calcium preconditioning and streptomycin on ventricular dilation-induced arrhythmias in isolated rat hearts

Objective To investigate the mechanism of ventricular dilation-induced arrhythmias by dilating isolated rat hearts. Methods Isolated rat hearts were perfused by Langerdorff method. After equilibration,80 hearts were randomly divided into four groups as follows:(1) control group(n=20) ,(2) Ca2 preconditioning(CPC) group(n=20) ,(3) streptomycin group(n=20) ,and(4) CPC streptomycin group(n=20) . A latex balloon which can be filled with fluid was anchored in the left ventricle through the left atrium and mitral valve. Epicardial ECG of the left ventricle,left ventricular pressure,coronary flow and heart rate were recorded before and during ventricular dilation by injecting fluid into the latex balloon. The rate and duration of ventricular dilation-induced arrhythmias were recorded. Results Under the same increase in ventricular end-diastolic pressure made by inflation of the balloon,the rate of arrhythmias was 100% and duration of arrhythmias was 2. 56±0.46s in the control group. Both the rates of premature ventricular beat(90%) and ventricular tachycardia 70%) were high. Compared with the control group,the total rate(60%) of arrhythmias was lower,and duration(1.67±0.61s) of arrhythmias was shorter in the CPC group. Both the rates of premature ventricular beat(60%) and ventricular tachycardia(40%) were low comparatively. The rate of arrhythmias(45%) was lower and duration(1.64±0.42s) of arrhythmias was shorter,and the rates of premature ventricular beat(30%) or ventricular tachycardia(35%) were lower in the streptomycin group than in the control one. The least ventricular dilation-induced arrhythmias occurred in the CPC streptomycin group. The rate of arrhythmias(10%) was the lowest and duration(1.01±0.37s) of arrhythmias was the shortest;both the rates of premature ventricular beat(5%) and ventricular tachycardia(10%) were the lowest. Conclusions Ventricular dilation may induce arrhythmias in isolated rat hearts. Stretch-activated ion channel and the increase in [Ca2 ]i are supposed to play important roles in the pathological mechanism.     

Ventricular Arrhythmias in the North American Multidisciplinary Study of ARVC : Predictors,Characteristics, and Treatment

Background

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is associated with sudden cardiac death. However, the selection of patients for implanted cardioverter-defibrillators (ICDs), as well as programming of the ICD, is unclear.

Objectives

The objective of this study was to identify predictors, characteristics, and treatment of ventricular arrhythmias in patients with ARVC.

Methods

The Multidisciplinary Study of Right Ventricular Cardiomyopathy established the North American ARVC Registry and enrolled patients with a diagnosis of ARVC. Patients were followed prospectively.

Results

Of 137 patients enrolled, 108 received ICDs. Forty-eight patients had 502 sustained episodes of ventricular arrhythmias, including 489 that were monomorphic and 13 that were polymorphic. In the patients with ICDs, independent predictors of ventricular arrhythmias in follow-up included spontaneous sustained ventricular arrhythmias before ICD implantation and T-wave inversions inferiorly. The only independent predictor for life-threatening arrhythmias, defined as sustained ventricular tachycardia (VT) ≥240 beats/min or ventricular fibrillation, was a younger age at enrollment. Anti-tachycardia pacing (ATP), independent of the cycle length of the VT, was successful in terminating 92% of VT episodes.

Conclusions

In the North American ARVC Registry, the majority of ventricular arrhythmias in follow-up are monomorphic. Risk factors for ventricular arrhythmias were spontaneous ventricular arrhythmias before enrollment and a younger age at ICD implantation. ATP is highly successful in terminating VT, and all ICDs should be programmed for ATP, even for rapid VT.     

Vasospastic Angina with J‐Wave Pattern and Polymorphic Ventricular Tachycardia Effectively Treated with Quinidine

Background: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J‐wave pattern was suggested to be a marker of a disorder associated with life‐threatening arrhythmias. Results: We report the case of a patient with vasospastic angina and J‐wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine—vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. Conclusion: The J‐wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina—quinidine can effectively prevent such arrhythmias in these patients.     

Inducibility of life-threatening ventricular arrhythmias is related to maximum left ventricular thickness and clinical markers of sudden cardiac death in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the alpha-tropomyosin gene

We investigated inducibility of life-threatening arrhythmias with programmed ventricular stimulation (PVS) in relation to clinical markers of sudden cardiac death (SCD) in subjects with hypertrophic cardiomyopathy (HCM) attributable to the Asp175Asn mutation in the α-tropomyosin gene (TPM1-Asp175Asn). PVS was performed with up to three extrastimuli and distribution of markers of SCD was evaluated in 21 adult subjects with the TPM1-Asp175Asn. Sustained polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) was induced in seven of 21 subjects (33%). Inducible subjects had more severe left ventricular hypertrophy (LVH) and an increased number of markers of SCD (family history of SCD, syncope or presyncope, fall in systolic blood pressure (BP) during exercise, documented non-sustained VT (NSVT), and marked LVH) compared to non-inducible subjects (IVS 2.4 ± 0.3 cm vs. 1.6 ± 0.5 cm, P < 0.001; and two to three vs. one to two markers of SCD, P = 0.007, respectively). In conclusion, in HCM attributable to the Asp175Asn mutation in the α-tropomyosin gene, life-threatening arrhythmias were induced in one third of the patients. Inducibility was associated with the maximum left ventricular (LV) thickness and the number of markers of SCD, suggesting that in HCM patients with an identical causative mutation, susceptibility to ventricular arrhythmias is related to the cardiomyopathic phenotype.     

Successful treatment of aconitine induced life threatening ventricular tachyarrhythmia with amiodarone

With the increasing trend of cross mixing of populations, aconitine induced poisoning and its related arrhythmias may be more frequently encountered worldwide. However, the clinical experience is often too limited to draw any conclusion on the optimal treatment for tachycardia induced by aconitine intoxication. The clinical presentation, serial electrocardiographic changes, and responses to antiarrhythmic agents are reported in a patient with aconitine induced life threatening ventricular tachyarrhythmia. Amiodarone was effective in suppressing polymorphic ventricular tachycardia, which might provide an example of successful pharmacological intervention in aconitine induced ventricular tachyarrhythmia.


Keywords: aconitine; herbal medicine; life threatening ventricular tachyarrhythmia; amiodarone     

Programmed electrical stimulation in hypertrophic cardiomyopathy. Results in patients with and without cardiac arrest or syncope

Programmed electrical stimulation was performed in 54 consecutivepatients with hypertrophic cardiomyopathy. There were 11 ‘symptomatic’patients: three had a history of cardiac arrest due to ventriculartachyarrhythmias (group A), and eight had a history of syncopeof unknown origin (group B); 43 patients were ‘asymptomatic’,i.e. they had no documented or suspected symptomatic ventriculararrhythmias (group C). There were no differences among the groupswith respect to electrocardiographic, echocardiographic or hemodynamicdata. Ventricular arrhythmias were induced by atrial and rightand left ventricular stimulation with a maximum of two extrastimuliin 18 patients. Induced arrhythmias were repetitive ventricularresponse in six patients, nonsustained ventricular tachycardiain four, sustained ventricular tachycardia in five, and ventricularfibrillation in three patients. With one exception, ventriculartachycardia was always rapid (cycle lengths ranged from 180to 250 ms); it was polymorphic in six patients and monomorphicin three. Atrial stimulation induced rapid monomorphic ventriculartachycardia in one group A patient. The type and incidence ofinduced ventricular arrhythmias did not differ among the threegroups. It is concluded that programmed electrical stimulationinduces the same type of ventricular arrhythmia (rapid polymorphicventricular tachycardia or ventricular fibrillation) in ‘symptomatic’and ‘asymptomatic’ patients with hypertrophic cardiomyopathy,the incidence in the latter group being 19%. Induction by atrialstimulation of a rapid ventricular tachycardia may be a specificfinding to identify patients with hypertrophic cardiomyopathyat risk for exercise-induced ventricular fibrillation.