Clinical Ventricular Fibrillation Research Articles

Ablation Approaches for Ventricular Fibrillation.

Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in "curing" VF are proving to be life saving for resuscitated survivors of arrhythmic death.

Modifying Ventricular Fibrillation by Targeted Rotor Substrate Ablation: Proof-of-Concept from Experimental Studies to Clinical VF.

Recent work has suggested a role for organized sources in sustaining ventricular fibrillation (VF). We assessed whether ablation of rotor substrate could modulate VF inducibility in canines, and used this proof-of-concept as a foundation to suppress antiarrhythmic drug-refractory clinical VF in a patient with structural heart disease. In 9 dogs, we introduced 64-electrode basket catheters into one or both ventricles, used rapid pacing at a recorded induction threshold to initiate VF, and then defibrillated after 18±8 seconds. Endocardial rotor sites were identified from basket recordings using phase mapping, and ablation was performed at nonrotor (sham) locations (7 ± 2 minutes) and then at rotor sites (8 ± 2 minutes, P = 0.10 vs. sham); the induction threshold was remeasured after each. Sham ablation did not alter canine VF induction threshold (preablation 150 ± 16 milliseconds, postablation 144 ± 16 milliseconds, P = 0.54). However, rotor site ablation rendered VF noninducible in 6/9 animals (P = 0.041), and increased VF induction threshold in the remaining 3. Clinical proof-of-concept was performed in a patient with repetitive ICD shocks due to VF refractory to antiarrhythmic drugs. Following biventricular basket insertion, VF was induced and then defibrillated. Mapping identified 4 rotors localized at borderzone tissue, and rotor site ablation (6.3 ± 1.5 minutes/site) rendered VF noninducible. The VF burden fell from 7 ICD shocks in 8 months preablation to zero ICD therapies at 1 year, without antiarrhythmic medications. Targeted rotor substrate ablation suppressed VF in an experimental model and a patient with refractory VF. Further studies are warranted on the efficacy of VF source modulation.

Spectral analysis-based risk score enables early prediction of mortality and cerebral performance in patients undergoing therapeutic hypothermia for ventricular fibrillation and comatose status

BackgroundEarly prognosis in comatose survivors after cardiac arrest due to ventricular fibrillation (VF) is unreliable, especially in patients undergoing mild hypothermia. We aimed at developing a reliable risk-score to enable early prediction of cerebral performance and survival. MethodsSixty-one out of 239 consecutive patients undergoing mild hypothermia after cardiac arrest, with eventual return of spontaneous circulation (ROSC), and comatose status on admission fulfilled the inclusion criteria. Background clinical variables, VF time and frequency domain fundamental variables were considered. The primary and secondary outcomes were a favorable neurological performance (FNP) during hospitalization and survival to hospital discharge, respectively. The predictive model was developed in a retrospective cohort (n=32; September 2006–September 2011, 48.5±10.5months of follow-up) and further validated in a prospective cohort (n=29; October 2011–July 2013, 5±1.8months of follow-up). ResultsFNP was present in 16 (50.0%) and 21 patients (72.4%) in the retrospective and prospective cohorts, respectively. Seventeen (53.1%) and 21 patients (72.4%), respectively, survived to hospital discharge. Both outcomes were significantly associated (p<0.001). Retrospective multivariate analysis provided a prediction model (sensitivity=0.94, specificity=1) that included spectral dominant frequency, derived power density and peak ratios between high and low frequency bands, and the number of shocks delivered before ROSC. Validation on the prospective cohort showed sensitivity=0.88 and specificity=0.91. A model-derived risk-score properly predicted 93% of FNP. Testing the model on follow-up showed a c-statistic≥0.89. ConclusionsA spectral analysis-based model reliably correlates time-dependent VF spectral changes with acute cerebral injury in comatose survivors undergoing mild hypothermia after cardiac arrest.

Abstract 17810: Spectral Analysis-Based Risk Score to Early Predict Mortality and Cerebral Performance in Patients Undergoing Therapeutic Hypothermia for Ventricular Fibrillation and Comatose Status

Introduction: Early reliable prognostication in comatose survivors after cardiac arrest due to ventricular fibrillation (VF) is very limited, especially in patients undergoing mild hypothermia. Hypothesis: Spectral analysis of VF before a DC shock will reflect the degree of acute cerebral injury as a consequence of time in VF and concomitant myocardial ischemia. Methods: We included consecutive patients undergoing mild hypothermia after cardiac arrest due to VF, eventually with return of spontaneous circulation (ROSC), and a comatose status on admission. Background clinical variables, VF time and frequency domain fundamental variables were considered in the analysis. The primary and secondary outcomes were a favorable neurological performance (FNP) during hospitalization and survival to hospital discharge, respectively. The predictive model was developed in a retrospective cohort (September 2006 to September 2011) and further validated in a prospective cohort (October 2011 to July 2013). The model was also tested at follow-up. Results: Sixty-one patients out of 239 who underwent mild hypothermia fulfilled the inclusion criteria. FNP was present in 16 (50.0%) and 21 patients (72.4%) in the retrospective and prospective cohorts, respectively. Seventeen (53.1%) and 21 patients (72.4%), respectively, survived to hospital discharge. Both outcomes were significantly associated (p&lt;0.001). Multivariate analysis on the retrospective cohort provided a prediction model (sensitivity=0.94, specificity=1) including dominant frequency, ratio between number of peaks in high and low frequency bands, power spectral density ratio between high and low frequency bands and the number of shocks delivered before ROSC. Validation on the prospective cohort showed sensitivity=0.88 and specificity=0.91 for both primary and secondary outcomes. A model-derived risk score properly predicted 93% of FNP. The model showed cstatistic ≥0.89 after a median follow-up of 48.5±10.5 and 5±1.8 months in the retrospective and prospective cohorts, respectively. Conclusions: A spectral analysis-based model reliably correlates time-dependent VF spectral changes with acute cerebral injury in comatose survivors after cardiac arrest undergoing mild hypothermia.

Underdetection of ventricular fibrillation despite ICD testing and high sinus R wave

Apart from monitoring shock efficacy, proof of flawless detection of induced ventricular fibrillation (VF) is a decisive argument in favor of implantable cardioverter defibrillator (ICD) testing. On the other hand, it has been observed that undersensing of VF is extremely rare with good sensing of the intrinsic R wave of ≥ 5-7mV. The case presented here shows limitations in both argumentations: Neither optimal R wave sensing during sinus rhythm nor repeated ICD testing could rule out or predict multiple erroneous detections of clinical VF episodes. This must be taken into consideration in the current discussion on the necessity of defibrillation testing. Further optimization of sensing technology should be a focus in the development of modern ICD systems so as to improve the safety and efficacy of ICD therapy.

Spectral methods to distinguish ventricular fibrillation from artefact in implantable cardioverter-defibrillators

Despite the proven benefit of implantable cardioverter-defibrillators (ICDs), inappropriate shocks remain a significant problem. Recent trends have shown an increased incidence of lead failure and an increased exposure of devices to extreme electromagnetic interference environments. The goal of the current study is to evaluate the spectral characteristics of ventricular fibrillation (VF) detected in an ICD at time of defibrillation threshold testing and use of the findings to predict event types from a population of clinical VF and artefact events. A modelling group was created from induced VF and artefact events at time of ICD implantation and DFT testing. Power spectral density evaluation was performed on each event and used to calculate an energy ratio (ER; the ratio of energy under the first three harmonics to the entire spectrum). The model was then applied to a database of clinical VF and artefact events to determine its sensitivity and specificity. The far-field ER of the modelling group was significantly larger for VF (0.888 ± 0.110) than artefact (0.265 ± 0.156, P < 0.0001). In the test group, the far-field ER of VF (0.882 ± 0.088) was also significantly larger than artefact (0.344 ± 0.128, P < 0.0001). At a cut-off of >0.526, the far-field ER had a sensitivity of 100% [confidence interval (CI) 100-100%] and a specificity of 92.4% (CI 84.9-98.5%) to distinguish clinical VF from clinical artefact. Far-field signal during VF detected by an ICD has a distinct spectral pattern that can distinguish VF from artefact.

Clinical Significance of Macroscopic T‐Wave Alternans After Sodium Channel Blocker Administration in Patients with Brugada Syndrome

Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after pilsicainide, a sodium channel blocker administration in BS patients. We administered pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. TWA after pilsicainide administration is associated with a high risk of clinical VF in patients with BS.

The effect of ischemia on ventricular fibrillation as measured by fractal dimension and frequency measures

Most animal studies of ventricular fibrillation (VF) waveform characteristics involve healthy animals with VF initiated by electric shock. However, clinical VF is usually the result of ischemia. The waveform characteristics in these two types of VF may differ. The angular velocity (AV), frequency ratio (FR) and median frequency (MF) are three frequency-based measures of VF. The scaling exponent (ScE), the logarithm of the absolute correlations (LAC) and the Hurst exponent (HE) are three measures of the fractal dimension of VF. We hypothesized that these quantitative measures would differ between ischemic and electrically initiated VF. VF was induced in 14 swine by electric shock and in 12 swine by ischemia. For ischemia induced VF animals, an angioplasty catheter was positioned in the mid-LAD and the balloon inflated. A mean of 891+/-608 (S.D.)s later, VF occurred. For electrically induced animals, an AC current was passed through a catheter in the RV. Following initiation by either method, VF was recorded for 7min. Sequential 5s epochs were analyzed for AV, FR, MF and fractal dimension measures. Ischemic VF demonstrated a significantly higher fractal dimension as estimated by the ScE for the first 0-90s (p=0.021) and for 90-180s (p=0.016). The Hurst exponent was significantly higher for ischemic VF for both 0-90s (p<0.0001) and 90-180s (p<0.0001). The fractal dimension as estimated by the LAC method was not significantly different for 0-90s (p=0.056) but was highly significant for 90-180s (p=0.001). During the initial 90s the groups did differ in all measures of frequency as follows: AV (p<0.001), FR (p<0.001), MF (p<0.001). These differences did not persist beyond 90s except for a mild elevation of the FR after 270s (p<0.02). Fractal based measures indicate an increase in the fractal dimension of ischemia induced VF for the first 180s when compared to electrically induced VF. Frequency-based measures uniformly demonstrate a pattern of higher frequencies for electrically induced VF for the first 90s. The increased fractal dimension and decreased frequencies associated with ischemia induced VF may reflect changes in the underlying myocardial physiology that can be used to guide therapies.

Tpeak-Tend interval as a new risk factor for arrhythmic event in patient with Brugada syndrome

Objective To evaluate Tpeak-Tend(Tp-e) interval in surface standard ECG as a new risk factor for arrhythmic event in patient with Brugada syndrome. Methods 23 male patients with Brugada syndrome and 20 male patients with paroxysmal supraventricular tachycardia(PSVT) as the control group were investigated in this study. Tp-e interval in surface standard ECG was compared between BrS and PSVT patients. Results Tp-e interval in BrS patients was significantly longer than that in PSVT patients (109.57 ± 2.86 ms vs. 88.50 ± 3.08ms, P < 0.05). There was significant difference in Tp-e interval between 16 BrS patients with arrhythmic events (including syncope, clinical ventricular fibrillation [VF] and programmed electrical stimulation [PES]-induced VF) and 7 BrS patients without arrhythmic events and PSVT patients(118.12 ± 0.40ms vs. 90.00 ± 5.27ms, P < 0.05; 118.12 ± 0.40ms vs. 88.50 ± 3.08ms, P <0.05). However, Tp-e interval was similar in BrS patients without arrhythmic events and PSVT patients (90.00 ± 5.27ms vs. 88.50 ± 3.08ms, P > 0.05). Conclusion The prolongation of Tp-e interval could serve as a new noninvasive event predictor for arrhyth- mic events in patients with Brugada syndrome.

Predictive Impact of the Inducibility of Ventricular Fibrillation in Patients With Brugada-Type ECG

The natural history of asymptomatic individuals with a Brugada-type electrocardiogram (ECG) is still controversial. In this study, we evaluated ventricular fibrillation (VF) inducibility in Brugada-type ECG patients and compared it with other risk factors to clarify the significance of these data on their prognosis. The study population consisted of 38 patients who presented with a typical ST-segment elevation in the precordial leads and underwent an electrophysiological study (EPS). The patients were divided into 3 groups; group A: patients with spontaneous ventricular fibrillation (VF) (n = 5), group B: patients without clinical VF but with inducible VF in EPS (n = 16), and group C: patients with neither clinical nor inducible VF (n = 17). The clinical features, diagnostic results, and prognosis were compared among these groups. During the follow-up period of 26 +/- 19 months, 2/5 (group A), 1/16 (group B), and 0/17 (group C) patients suffered fatal arrhythmic events. None of the clinical features showed any significant difference, although the incidence of positive results in a drug challenge test was higher in groups A and B than in group C (P < 0.05). On the other hand, VF inducibility was higher in patients with positive results in the drug challenge test than in patients with negative results (59% versus 13%; P < 0.05). No VF episodes were observed in patients without VF induction, although one was observed in 1 of 16 patients with VF induction in asymptomatic Brugada syndrome. The drug challenge test appears to be useful for predicting VF inducibility even though it is a noninvasive test.

A Model of Ischemically Induced Ventricular Fibrillation for Comparison of Fixed‐dose and Escalating‐dose Defibrillation Strategies

Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J-300 J-360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with < or =3 shocks. VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with < or =3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with < or =3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with < or =3 shocks ranging from 200 to 360 J. In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks.

Malignant sustained ventricular tachyarrhythmias in women: characteristics and outcome of treatment with an implantable cardioverter defibrillator.

Clinical rhythm, heart disease, ejection fraction, defibrillation threshold, recurrent arrhythmias, and mortality were compared in 268 consecutive recipients (213 men and 55 women) of their first implantable cardioverter defibrillator for life-threatening ventricular tachycardia or fibrillation. Women were younger than men, less likely to have structural heart disease, and more likely to have clinical ventricular fibrillation, a higher ejection fraction, and a lower defibrillation threshold. Complications of defibrillator placement were similar in both sexes. Unadjusted survival tended to be higher in women than in men (97% vs 90%, respectively, at 2 years, P = 0.08), largely due to fewer deaths from noncardiac causes or cardiac causes other than arrhythmia (P = 0.04). Women also tended to be at lower, albeit still substantial, risk for recurrent arrhythmias during follow-up (37% vs 52% in men at 2 years, P = 0.11). After adjustment for baseline differences, overall survival, arrhythmia death-free survival, nonarrhythmia death-free survival, and frequency of recurrent arrhythmias were not found to be gender related. Despite their apparent "lower risk" status on initial presentation, women remained at substantial risk for recurrent arrhythmias. This underscores the need to avoid being unduly biased by the "appearance" of health in managing women with malignant arrhythmias. That survival and other clinical endpoints were all ultimately independent of gender emphasizes the importance of other clinical variables in assessing risk from ventricular tachyarrhythmias.

Treatment and prevention of ventricular fibrillation: Are there better agents?

Ventricular fibrillation occurs in diverse clinical settings and differing pathogenic mechanisms make it unlikely that a single drug treatment will be universally effective. Drugs may be used as an adjunct to electrical defibrillation in circulatory collapse, to prevent recurrence after successful resuscitation or as a prophylactic treatment in high-risk patients. Various drugs are available for intravenous administration in the acute management of ventricular fibrillation and the choice among them will depend on several factors: proven efficacy, comparative efficacy and their safety including haemodynamic effects. Although several drugs have been shown to suppress ventricular ectopic beats and ventricular tachycardia, ventricular fibrillation and sudden death can occur despite abolition of these less serious ventricular arrhythmias [ 11. Animal studies have suggested the concept of separate ‘antiarrhythmic’ and ‘antilibrillatory’ action of drugs. Drugs with antifibrillatory properties increase the energy threshold for production of ventricular fibrillation while many conventional antiarrhythmic drugs have no effect [2,3]. However, an effect on fibrillation threshold does not necessarily indicate a reduction in energy requirements for successful electrical defibrillation. The major criticism of such models is that the substrate for generation of ventricular fibrillation is usually different in clinical ventricular fibrillation. Lignocaine and bretylium are the current standard drugs for management of acute ventricular fibrillation. This review examines the claims of other antiarrhythmic drugs to supplant or supplement these agents (Table I). Figure 1 shows a representation of the normal cardiac action potential. Initial depolarisation (phase 0) is achieved by rapid influx of sodium ions which is slowed by agents which belong to class 1 of the Vaughan Williams and Singh classification. These compounds are subdivided by their effect on the duration of the action potential: Class la drugs lengthen it, Class lb shorten it, while Class lc have no effect. Class II drugs are the beta blockers which have no direct effect on the action potential but antagonise myocardial stimulation by catecholamines. The Class III agents delay phase 3 repolarisation and prolong the duration of the action potential. Class IV drugs are calcium channel blockers which reduce the influx of calcium into cells, in particular reducing the spontaneous depolarisation of phase 4 in the atrio-

Spontaneous sustained ventricular tachyarrhythmias during treatment with type IA antiarrhythmic agents

Twenty-six patients who developed their first clinical episode of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) while taking type IA antiarrhythmic agents for more benign rhythm disturbances were rechallenged with the identical drug during electrophysiologic testing. Patients with these new drug-associated spontaneous ventricular arrhythmias often manifested a preexisting substrate for such arrhythmias: sustained VT or VF was induced in 65% of patients at baseline, and in 58% of patients when tested with their previously taken antiarrhythmic drug. Among those without inducible sustained ventricular arrhythmias in the drug-free state, 78% remained free of inducible sustained arrhythmias when tested with the same drug they had been taking at the time of the clinical arrhythmia. Even patients without a definable electrophysiologic substrate for sustained VT or VF remained at risk for arrhythmia recurrence if treated with alternative antiarrhythmic medications: 40% of such patients who continued to receive an antiarrhythmic agent different from that being administered when their clinical VT or VF occurred had recurrent spontaneous ventricular tachyarrhythmias during follow-up. Thus, patients with drug-associated clinical sustained ventricular tachycardias form a heterogenous group that should be evaluated individually and not empirically managed for a “proarrhythmic effect” simply by antiarrhythmic drug withdrawal or drug substitution.

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmaco logic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 ± 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 ± 9 months was 32% (p < 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Programmed ventricular stimulation in predicting vulnerability to ventricular arrhythmias and their response to antiarrhythmic therapy

In predicting vulnerability to ventricular arrhythmias and their response to antiarrhythmic therapy, several factors and questions need to be considered, including the following. (1) Ventricular tachycardia (VT) can be induced in most patients who have recurrent sustained VT. (2) Because induced VT can often be pace terminated, termination by pacing should be attempted before cardioversion is applied. (3) Acutely effective antiarrhythmic agents are no longer being found for the majority of patients undergoing electrophysiologic-pharmacologic study in our series. (4) Specific VT-induction programs affect both the inducibility of VT and the acute efficacy of drugs at electrophysiologic study; this point requires examination. (5) Arrhythmia-induction studies may not produce high yield in patients with clinical ventricular fibrillation or unsustained VT. (6) It is as yet unclear whether some drugs, such as amiodarone, can be accurately evaluated by using arrhythmia-induction techniques. (7) Induction of the repetitive ventricular response by V 2 stimulation is not a useful method for antiarrhythmic drug selection in patients with recurrent ventricular tachyarrhythmias. (8) Adequate data do not yet exist to identify either the ECG-monitoring technique or the arrhythmia-induction technique as the preferred method for selecting antiarrhythmic drugs for chronic therapy of patients with recurrent ventricular tachyarrhythmias. A study to compare the accuracies of the two techniques is both feasible and needed.