Myocardial ischemia and induction of sustained ventricular tachyarrhythmias: evaluation using dobutamine stress echocardiography-electrophysiologic testing

INTRODUCTION: This study examined the relationship between dobutamine facilitation of ventricular tachyarrhythmia (VT) inducibility with programmed electrical stimulation (PES) and dobutamine stress-induced myocardial ischemia. METHODS AND RESULTS: Twenty patients with prior myocardial infarction and cardiac arrest or sustained VT but no sustained VT induced at baseline electrophysiologic testing underwent repeat PES during dobutamine infusion. Ischemia (new or worsened wall-motion abnormality) was documented by echocardiography performed in conjunction with PES. Eight patients were receiving Class I or III antiarrhythmic drugs and seven beta-blockers. Dobutamine facilitated induction of sustained VT in 16 patients (80%) and provoked ischemia in 13 patients (65%). Induction of VT was associated with ischemia in 9 patients (56%). VTs associated with ischemia were induced at higher dobutamine doses (26 +/- 11 vs 11 +/- 10 microg/kg per min, P = 0.02) than were VTs without ischemia (n = 7). Among 13 patients with provoked ischemia, 9 (69%) had VTs induced and 4 remained noninducible. The onset of ischemia occurred at the same dose as induction of VT in 5 patients and at a lower dose in 4 patients. Monomorphic VT (318 +/- 59 ms) was induced in 13 patients, of whom 8 (62%) had ischemia. The ECG morphology of VT suggested an origin in a myocardial segment that demonstrated initial viability at low doses then ischemic dysfunction at higher doses preceding VT induction in 7 (88%) of 8 patients. CONCLUSION: Dobutamine enhances inducibility of sustained VTs during PES. The temporal and anatomic association of dobutamine-induced ischemia and VT suggests that at high dobutamine doses, ischemia may contribute to ventricular arrhythmia inducibility in some patients.     

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enhanced efficacy of oral sotalol for sustained ventricular tachycardia refractory to type I antiarrhythmic drugs

Sotalol is a nonselective beta-adrenergic blocking agent with Vaughn-Williams class III activity. Its efficacy was tested in 9 patients with sustained ventricular tachycardia (VT) that had previously remained inducible during electrophysiologic testing of type I drugs (procainamide or quinidine). Eight patients had coronary artery disease with remote myocardial infarction and 1 had cardiomyopathy (ejection fraction 0.34 +/- 0.08, mean +/- standard deviation). Type I drugs prolonged the effective refractory period of the right ventricle 12 +/- 14% and prolonged the VT cycle length 41 +/- 24%. In contrast, despite an equivalent effect on the effective refractory period, a sustained VT could no longer be initiated in any of the 8 patients ultimately tested while taking oral sotalol. Daily doses averaged 600 +/- 103 mg and blood levels associated with VT suppression in electrophysiologic studies were generally greater than 3,000 ng/ml. In addition, sotalol was moderately effective at reducing ventricular ectopic activity measured by ambulatory electrocardiography. Over a mean follow-up of 23 months (range 1 to 37), mild heart failure (3 patients), symptomatic brady-cardia requiring pacemaker (1) and drug-related polymorphous VT (1) have occurred. Sudden death occurred in 1 patient and nonfatal VT recurrence was noted in 2. Five of 8 chronically treated patients currently are successfully treated with minimal side effects. Sotalol appears to be a promising antiarrhythmic drug in the treatment of serious ventricular arrhythmias, even in patients refractory to type I antiarrhythmic agents.     

Ventricular tachycardia in Chagas' disease.

This study examined the usefulness of the electrophysiologic approach for selecting antiarrhythmic drug therapy to improve survival in patients with ventricular tachycardia (VT) and Chagas' disease. A total of 71 consecutive chagasic patients undergoing treatment and evaluation of VT were analyzed. Programmed electrical stimulation (PES) was performed in 45 patients, sustained VT was induced in 18 of these 45 (40%); nonsustained VT was induced in 17 (38%), and in 10 patients (22%) VT was not induced at all. An average of 3 drugs per patient were tested, including mexiletine, flecainide and propafenone. At least 1 effective drug preventing VT induction was identified in 13 of 18 patients with induced sustained VT, whose outcome resulted in 2 nonsudden but cardiac deaths (15%). Eight patients received no drug therapy because the induced arrhythmia was asymptomatic nonsustained VT; none of these died. The remaining 24 patients from the PES group were empirically treated with amiodarone; 7 died (4 suddenly) during follow-up (29%). A group of 26 patients (non-PES group) did not undergo electrophysiologic evaluation. In these patients, the therapy chosen was amiodarone alone or associated with mexiletine, and the incidence of death was 7 of 26 patients (27%), 3 suddenly (p less than 0.05 at 10-year survival and p = not significant at 5-year survival). It is concluded that the electrophysiologic approach improves survival in this study population, but only 29% were eligible for guided therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Refractory ventricular tachycardia secondary to cardiac sarcoid: Electrophysiologic characteristics, mapping, and ablation

BACKGROUND: Cardiac sarcoidosis is a recognized cause of ventricular tachycardia (VT) and sudden death that has not been well studied. OBJECTIVES: The purpose of this study was to describe the clinical characteristics of a consecutive series of eight patients with recurrent monomorphic VT due to cardiac sarcoidosis and to define the electrophysiologic characteristics of the VT and its electrophysiologic substrate. METHODS/RESULTS: Of 98 patents with nonischemic cardiomyopathy and VT referred for ablation over a 7-year period, sarcoid was the etiology in 8%. Mean age was 42 +/- 8 years, and all but one patient had a reduced left ventricular ejection fraction (mean 34% +/- 15%). VT was the initial manifestation of sarcoid disease in 5 of 8 cases based on retrospective analysis. All patients had not responded to therapy with multiple antiarrhythmic drugs (mean 2.5 +/- 1). Cardiac biopsy initially was negative in 3 of 7 patients, and in 2 patients the diagnosis was not made until posttransplant examination of the heart. Two patients (25%) had a previous presumptive diagnosis of arrhythmogenic right ventricular dysplasia. Electrophysiologic study revealed evidence of scar-related reentry with multiple monomorphic VTs induced (4 +/- 2 VTs per patient) with both right bundle branch block and left bundle branch block QRS configurations. Areas of low-voltage scar were present in the right ventricle in all 8 of 8 patients, in the left ventricle in 5 (63%) of 8 patients, and in the epicardium in 2 patients undergoing epicardial mapping. Ablation abolished one or more VTs in 6 (75%) of 8 patients, but other VTs remained inducible in all but one patient. Postablation, some form of sustained VT recurred in 6 of 8 patients within 6 months. However, at longer follow-up (range 6 months to 7 years), 4 of 8 patients currently are free of VT with antiarrhythmic drugs and immunosuppression. Cardiac transplantation eventually was required in 5 of 8 patients because of either recurrent VT (n = 4) or heart failure (n = 1). CONCLUSION: Sarcoid is an important diagnostic consideration in scar-related VT. Sarcoid can be misdiagnosed as idiopathic or arrhythmogenic right ventricular cardiomyopathy. Arrhythmia control can be difficult, although ablation can be helpful in some patients.     

Long-term follow-up of postmyocardial infarction patients with ventricular tachycardia or ventricular fibrillation treated with amiodarone

Amiodarone in a low dose (200 mg/day) was administered alone or in combination with other type I antiarrhythmic drugs as a first-line agent in 33 patients with ventricular tachycardia (VT) (n = 24) or ventricular fibrillation (VF) (n = 9) secondary to coronary artery disease with healed myocardial infarction. There were 30 men and 3 women (mean age 69 +/- 9 years). Left ventricular ejection fraction ranged from 16 to 45% (mean 29 +/- 8). Therapy was guided by the results of electrophysiologic studies without the use of a control study (without drugs). Predischarge electrophysiologic studies revealed inducible sustained VT in 8 patients (24%), nonsustained VT in 7 and noninducible VT in 18 patients. Mean follow-up time was 27 +/- 7 months. Eleven patients (33%) died, 5 suddenly (15%) and 6 from nonarrhythmic causes. Five patients (15%) had nonfatal recurrences of VT. Life-table analysis showed that arrhythmic recurrences or fatalities (VT or sudden death) were related to the results of the predischarge electrophysiologic studies and not to the baseline arrhythmia (VT or VF). Toxicity from amiodarone was uncommon and no patient discontinued taking the drug.     

Contemporary Clinical Trials in Ventricular Tachycardia and Fibrillation: Implications of ESVEM, CASCADE, and CASH for Clinical Management

Trials in Ventricular Tachycardias. Recent clinical trials in patients with ventricular tachycardia (VT) or fibrillation (VF) have occurred in the setting of the disappointing results of postinfarction secondary prevention studies using Class I antiarrhythmics (e.g., CAST). ESVEM addressed in a randomized trial whether electrophysiologic study (EPS) or Hotter monitoring (HM) is a more accurate predictor of long-term antiarrhythmic drug efficacy in VT/VF patients (N = 486) and what the relative efficacy of various antiarrhythmic agents is for VT/VF. Surprisingly, arrhythmia recurrence rates were not significantly different by the method of determining an efficacy prediction. However, arrhythmia recurrence and mortality were lower (by about 50% at 1 year) in patients treated with sotalol (a mixed Class II/III agent) than with other drugs (Class I). CASCADE evaluated empiric amiodarone versus guided (EPS or HM) standard (Class I) therapy in survivors of out-of-hospital cardiac arrest due to VF. The primary endpoint of cardiac death, resuscitated VF, or syncopal shock (in ICD patients) was reduced by amiodarone compared with conventional therapy (9% vs 23% at 1 year). An interim report of the ongoing CASH study suggested in 230 survivors of cardiac arrest that propafenone (Class IC) provided less effective prophylaxis (approximately 20% 1-year mortality) compared with randomly assigned therapies with amiodarone, metoprolol, or an ICD (approximately 14% mortality rates) and was excluded from further study. These studies have led to a paradigm shift in the approach to antiarrhythmic therapy of VT/VF: drugs with antisympathetic plus Class III (refractoriness prolonging) action (i.e., sotalol, amiodarone) are superior to traditional drugs with Class I (conduction slowing) effects, even when guided by EPS or HM.     

Evaluation of proarrhythmic effect of antiarrhythmic drugs on ventricular tachycardia associated with congestive heart failure.

The usefulness and limitations of antiarrhythmic drugs in ventricular tachycardias (VT) associated with congestive heart failure remain uncertain. The purpose of this study is to evaluate the proarrhythmic effects of antiarrhythmic drugs in patients with refractory VT associated with left ventricular dysfunction using electrophysiologic study (EPS). Twenty-four patients with left ventricular dysfunction, defined by left ventricular ejection fraction (LVEF) lower than 40% using left ventriculography, were studied. The average LVEF was 29.5%. As for underlying heart disease, 14 had old myocardial infarction, 8 cases had dilated cardiomyopathy and 2 had aortic regurgitation. As a control to this group, 23 cases with underlying heart disease and LVEF higher than 40%, and 27 cases with no obvious heart disease were studied. We considered a drug to have proarrhythmic effects if 1) it decreased by one the number of stimuli needed to induce VT, 2) induced non-sustained VT in the control study which changed to induced sustained VT, 3) the sustained VT or ventricular fibrillation was newly induced, or 4) the induced sustained VT which was stopped by pacing in the control study changed to induced VT which could not be terminated by pacing and required DC shock. Proarrhythmic effects were recognized in 17 of 24 cases with left ventricular dysfunction. Of the 67 drug trials, proarrythmic effects were seen in 26. Proarrhythmias were observed in 9 of 23 cases (39.1%) with organic heart disease associated with LVEF higher than 40%. In 12 of 69 drug trials (17.4%) proarrhythmias were observed. Of 27 cases with no obvious heart disease 10 cases (37%) had proarrhythmias. In 14 of 130 drug trials (10.8%), proarrhythmias were recognized.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.     

Effects of Electrophysiologic-Guided Therapy with Class IA Antiarrhythmic Drugs on the Long-Term Outcome of Patients with Idiopathic Ventricular Fibrillation with or without the Brugada Syndrome

INTRODUCTION: Implantation of a implantable cardioverter defibrillator (ICD) is viewed universally as the "gold standard" therapy for patients with idiopathic ventricular fibrillation (VF). We sought to study the long-term value of electrophysiologic (EP)-guided therapy with Class IA antiarrhythmic drugs in patients with idiopathic VF with or without the Brugada syndrome. METHODS AND RESULTS: We performed EP studies in 34 consecutive patients who had idiopathic VF with (n = 5) or without (n = 29) the Brugada syndrome. All patients with inducible sustained polymorphic ventricular tachycardia (SPVT) or VF underwent repeated EP evaluation after oral administration of a Class IA antiarrhythmic drug (mainly quinidine). Patients rendered noninducible received this therapy on a long-term basis. SPVT/VF were induced in 27 (79.4%) patients at baseline studies. Class IA drugs effectively prevented induction of SPVT/VF in 26 (96%) patients. Of the 23 patients treated with these medications, no patient died or had a sustained ventricular arrhythmia during a mean follow-up period of 9.1 +/- 5.6 years (7 to 20 years in 15 patients). Two deaths occurred in patients without inducible SPVT/VF at baseline studies who had been treated empirically. CONCLUSION: Our results suggest that EP-guided therapy with Class IA agents is a reasonable, safe, and effective approach for the long-term management of patients with idiopathic VF. A randomized prospective study of EP-guided Class IA therapy in patients with ICDs seems warranted.     

Estimation of the long-term efficacy of anti-arrhythmia treatment with flecainide in ventricular tachycardia

Flecainide, a Class IC antiarrhythmic agent, was used in 12 patients with an average age of 57 years to treat spontaneous monomorphic sustained ventricular tachycardia (S-VT, n = 9), with a ventricular rhythm of 203 +/- 41 bpm (5 right bundle branch and 4 left bundle branch block pattern) and non-sustained ventricular tachycardia (NS-VT, n = 3). The patients had ischaemic heart disease (n = 5, including 2 cases of aneurysm), idiopathic dilated cardiomyopathy (n = 1), ventricular dysplasia (right, n = 1; left n = 2; biventricular, n = 1). The remaining 2 patients had no overt cardiac disease on coronary angiography. None of the patients had signs of cardiac failure; the left ventricular ejection fraction was 0.49 +/- 0.7. Before treatment, programmed ventricular stimulation (PVS) induced 12 S-VT (214 +/- 41 bpm) which reproduced the clinical VT in 8 out of 10 cases. A second series of electrophysiological studies was performed after an average of 5 weeks treatment with Flecainide 300 mg/day (200-400 mg). It was not possible to induce VT in 2 patients (17% total prevention); NS-VT replaced S-VT in 4 patients (33%); S-VT was less rapid in 5 patients (at least 50 bpm slower) (41%); one patient had S-VT as rapid as before treatment (9%). The 12 patients were prescribed long-term Flecainide therapy. During follow-up there were 4 early (7, 10 and 15 days) and one late recurrence (16 months) (42% failure rate) whilst the other 7 patients had no further attacks of VT (follow-up of 19.1 +/- 5 months) (58% success rate).(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of electrophysiologic testing in evaluation of amiodarone therapy for sustained ventricular tachyarrhythmias associated with coronary heart disease

The prognostic importance of electrophysiologic studies in patients with sustained ventricular tachyarrhythmias treated with amiodarone was prospectively studied in 100 consecutive patients. Sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) was inducible in all patients before amiodarone therapy. After amiodarone administration 2 groups of patients were identified. In group 1 patients the ventricular tachyarrhythmia was no longer inducible and in group 2 patients the arrhythmia remained inducible. In group 1, no recurrent arrhythmia occurred during a follow-up of 18 +/- 10 months. In group 2, 38 of 80 patients (48%) had arrhythmia recurrence during a follow-up of 12 +/- 9 months. The difference between group 1 and 2 could not be explained by clinical variables, amiodarone doses or plasma concentrations, or electrocardiographic variables. In patients in whom cardiovascular collapse or other severe symptoms where noted during electrophysiologic study after amiodarone treatment, recurrences caused sudden death (n = 12). However, in patients in whom the induced arrhythmia produced moderate symptoms, the recurrent arrhythmia was nonfatal VT (n = 26). Electrophysiologic testing provides clinical guidance and predicts prognosis in patients treated with amiodarone as it does for the evaluation of other antiarrhythmic agents.     

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.     

Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

The efficacy and safety of sotalol were assessed by electrophysiologic testing and ambulatory recordings in 16 patients with recurrent sustained ventricular tachycardia (VT) or nonfatal cardiac arrest who were refractory to an average of 4.8 conventional antiarrhythmic agents. Twenty-four-hour ambulatory recordings were performed before and after sotalol therapy. Fourteen patients underwent baseline electrophysiologic study and sustained VT was inducible in 12. Oral sotalol (320 to 960 mg/day) completely suppressed inducible sustained VT in 7 patients (58%), with modification in 3 (25%). Ventricular premature complexes were suppressed from baseline (mean +/- standard deviation) 431 +/- 616 to 60 +/- 110/hr (p less than 0.03). After a mean follow-up of 19 +/- 7 months, 12 of 14 patients receiving sotalol treatment had successful suppression of ventricular premature complexes (60 +/- 85/hr) and remained clinically free of sustained VT, except 2 who needed additional antiarrhythmic drugs to suppress the recurrent sustained VT. One patient died suddenly after 25 months of sotalol treatment. No severe side effects were noted during sotalol therapy. This study demonstrates that sotalol is a well-tolerated, effective antiarrhythmic agent in patients at high-risk for sudden death. It appears to be beneficial in patients who did not benefit from multiple drug treatment.     

Mode of Induction of Ventricular Tachycardia and Prognosis in Patients with Coronary Disease: The Multicenter UnSustained Tachycardia Trial (MUSTT)

Introduction: Programmed stimulation is an important prognostic tool in the evaluation of patients with an ejection fraction ≤40% after myocardial infarction. Many believe that ventricular tachycardia (VT) requiring 3 ventricular extrastimuli (VES) for induction is less likely to occur spontaneously and has less predictive value. However, it is unknown whether the mode of VT induction is associated with long-term prognosis.
Methods and Results: We analyzed a cohort of 371 patients enrolled in MUSTT who had inducible monomorphic VT and who were not treated with antiarrhythmic drugs or an implantable cardioverter defibrillator during the trial. Patients in whom sustained VT was induced with 1 or 2 VES or burst pacing (single VES n = 15, double VES n = 127, burst n = 7, total n = 149) were compared with those in whom VT was induced with 3 VES (n = 222). Compared with the others, patients requiring 3 VES were closer to their most recent myocardial infarction (17 vs 51 months, P = 0.035) and showed a trend toward a lower ejection fraction (26% vs 30%, P = 0.057). VT requiring 3 VES had a shorter cycle length (240 vs 260 ms, P < 0.001). Despite these findings, there was no difference in the incidence of arrhythmic death or cardiac arrest (HR 1.02; 95% CI 0.69-1.51) or all-cause mortality (HR 1.03; 95% CI 0.76-1.39) according to the mode of induction in adjusted analyses.
Conclusions: The prognostic significance of VT induced by 3 VES is similar to that of VT induced by 1 or 2 VES, or burst pacing, in patients with coronary disease and abnormal LV function.     

Clinical characteristics and results of electrophysiologic testing in young adults with ventricular tachycardia or ventricular fibrillation

Thirty-one patients 16 to 40 years of age (mean +/- SD = 30.7 +/- 7 years) had one or more episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Underlying cardiac abnormalities consisted most commonly of cardiomyopathy (nine), long QT syndrome (LQTS) (five), and mitral valve prolapse (five); no identifiable heart disease was found in four patients. Programmed ventricular stimulation induced VT in only one of four patients with the LQTS but induced VT in 64% of 22 patients with other abnormalities. Chronic drug treatment was based either on serial electropharmacologic testing or was empiric when electrophysiologic testing failed to provoke an arrhythmia. Using this approach, we found a 13% incidence of recurrent VT and a 10% mortality over a follow-up period of 18.1 +/- 13.9 months. In young adults with VT or VF, an underlying cardiac abnormality can usually be found. Extensive evaluation should be performed to uncover the underlying cardiac abnormality as this may influence chronic management.     

Ventricular tachycardia in arrhythmogenic right ventricular dysplasia/cardiomyopathy: clinical presentation, risk stratification and results of long-term follow-up

BACKGROUND: Not all patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are at risk for sudden cardiac death. The aim of the study was to evaluate the risk stratification in patients with ARVD/C. METHODS AND RESULTS: Programmed ventricular stimulation (PVS) was performed in 34 ARVD/C patients. Twenty-two, 7 and 4 patients had documented sustained monomorphic ventricular tachycardia (smVT), non-smVT and ventricular fibrillation, respectively. One patient experienced syncope only. An implantable cardioverter defibrillator (ICD) was implanted in 11 patients inducible in smVT with hemodynamic compromise, in 4 patients with documented ventricular fibrillation and in one patient with non-smVT (194 ms tachycardia cycle length) (ICD group, n = 16). Ten patients were left without any antiarrhythmic therapy, 5 patients received antiarrhythmic drugs and 3 patients underwent successful VT ablation (non-ICD group, n = 18). Thirteen patients had an abnormal signal averaged ECG. During 6.5 +/- 2.4 years 69% of ICD patients received appropriate discharges and one non-ICD patient had a hemodynamically tolerated smVT recurrence (no sudden cardiac death in both groups). Comparison between the cycle lengths of clinical VT, induced VT and follow-up VT revealed a strong relationship (R = 0.62-0.88). On multivariate analysis abnormal signal averaged ECG and decreased left ventricular ejection fraction were statistically significant predictors for VT recurrence. CONCLUSIONS: In ARVD/C the tachycardia cycle length of clinical VT, PVS-induced VT and follow-up VT correlate well implicating that a PVS-guided approach does not provide additional information. Spontaneous arrhythmia in combination with clinical presentation allows identification of patients in need for an ICD.     

Comparative effects of anti-arrhythmia agents on ventricular refractory period and prevention of ventricular tachycardia induced by stimulation]

The efficacy of antiarrhythmic drugs is attributed to their actions on the refractory periods or conduction velocity in the reentry circuit. The aim of this study was to determine the relationship between these factors and the prevention of electrically inducible ventricular tachycardia (VT). Twenty-seven patients with sustained monomorphic postinfarction VT underwent programmed stimulation under basal conditions and after administration of oral Class I antiarrhythmic drugs. The protocol of stimulation consisted of delivering one to three extrastimuli to the right ventricular apex on two basic cycle lengths. Sustained VT was induced in all patients. After the same protocol under antiarrhythmic therapy (1 to 5 tests, average 2.9 +/- 1) sustained VT could not be induced in 12 patients (44%). The effective right ventricular refractory period was significantly increased in patients without inducible VT under treatment (247 +/- 18 versus 302 +/- 26 ms). The increase in the right ventricular effective refractory period in patients with persistence of inducible VT was much less (from 270 +/- 28 to 287 +/- 30 ms). In all patients in whom several antiarrhythmic drugs were tested the right ventricular effective refractory period was higher when the treatment was judged to be effective (299 +/- 27 ms) than ineffective (272 +/- 27, p < 0.02). The prevention of inducible VT by class I antiarrhythmic agents seems therefore to be related to their effect on the ventricular refractory period.     

Prolongation of ventricular refractoriness by class Ia antiarrhythmic drugs in the prevention of ventricular tachycardia induction

The effects of class la antiarrhythmic drugs (procainamide, quinidine) on the right ventricular effective refractory period (VERP) and intraventricular conduction time were assessed during serial invasive electrophysiologic studies for sustained monomorphic ventricular tachycardia (VT). In 47 patients with remote myocardial infarction, sustained VT was inducible by up to two extrastimuli after the basic drive at one of two basic cycle lengths at the right ventricular apex. With oral drug administration, sustained VT was no longer inducible (group I) in 27 patients but remained inducible (group II) in 20 with the same protocol. Class la drugs prolonged the VERP in both groups, but there was greater lengthening when drugs were effective (e.g., +32 +/- 14 msec in group I vs +12 +/- 19 msec in group II; p less than 0.005, basic cycle length 600 to 700 msec). Prolongation of the VERP by greater than 30 msec had an 88% positive predictive value for prevention of sustained VT induction. In all except one patient in group I, drugs prolonged the VERP such that the coupling intervals that had resulted in sustained VT induction under control conditions were no longer attainable. In contrast, conduction time through the ventricle (surface QRS duration) in sinus rhythm and during right ventricular pacing was prolonged similarly regardless of efficacy (e.g., +33 +/- 21 msec vs +27 +/- 27 msec at a cycle length of 400 msec). The presence of similar plasma levels of drug did not imply equivalent prolongation of the VERP in the two groups. These results suggest that greater prolongation of the VERP by oral procainamide or quinidine correlates with drug efficacy against VT induction and is a better predictor of drug effect than achievement of a "therapeutic plasma level."