Electrophysiologic testing and follow-up of patients with aborted sudden death

Clinical, electrophysiologic and follow-up data were analyzed for 108 patients with aborted sudden death. The mean follow-up interval was 2 years. All patients underwent baseline drug-free invasive electrophysiologic studies. Seventy-five patients (group I) had inducible ventricular arrhythmias (including nonsustained and sustained ventricular tachycardia and ventricular fibrillation) and 33 patients (group II) had no inducible arrhythmias. Noninducibility was not predictive of a favorable outcome, because the incidence of both sudden death and recurrent ventricular tachycardia was similar in the two groups. Treatment guided by electrophysiologic testing was used in 17 patients; in 13 (17%) in group I arrhythmias became noninducible, and in 4 (5%) sustained ventricular arrhythmias became nonsustained after administration of conventional drugs. There was a significantly higher incidence of sudden death and recurrent ventricular tachycardia in the 4 patients with inducible arrhythmias (n = 3, 75%) compared with the 13 patients whose arrhythmias were noninducible (n = 2, 15%) (p less than 0.05). For the group as a whole, 11% died suddenly and 15% had recurrence of ventricular tachycardia. Sixty-four patients were treated with amiodarone and, of these, four (6%) died suddenly during the follow-up period and nine (14%) had recurrent ventricular tachycardia. Ventricular arrhythmias could be induced in 69% of patients with aborted sudden death but inducibility could be suppressed in only 20% of them. The role of therapy guided by electrophysiologic testing could therefore not be fully assessed. The findings reveal a significant recurrence rate of symptomatic, potentially life-threatening ventricular arrhythmias in medically treated patients with aborted sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Prognostic value of programmed electrical stimulation in patients with a recent episode of unstable angina

Patients with a recent episode of unstable angina have a 10% 1-year risk of sudden cardiac death. To determine prospectively whether electrophysiologic testing might be useful in predicting sudden death, 20 patients admitted to our hospital underwent programmed electrical stimulation as part of their evaluation. None had persistent angina, severe congestive heart failure, or sustained arrhythmias at the time of testing. Because of their long-term benefits, beta-blocking agents were continued whenever possible (18 of 20 patients). Ten of 20 patients (50%) had inducible ventricular tachycardia. In 19.5 months' mean follow-up, three patients (15%) either died suddenly or survived an episode of ventricular fibrillation. Programmed electrical stimulation was an insensitive (33%) and nonspecific (47%) predictor of sudden death in these patients. Programmed ventricular stimulation soon after admission for unstable angina is not a useful prognostic indicator for sudden death. Such patients do have a frequent induction of ventricular arrhythmias which appears to be a nonspecific marker of underlying coronary disease.     

Electrophysiologic testing in the management of survivors of out-of-hospital cardiac arrest

Forty-five patients survived a cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF). Programmed ventricular stimulation was performed with the patients taking no antiarrhythmic medications. Sustained VT was induced in 26 patients (58%) and nonsustained VT in 8 (18%). With treatment aimed at the underlying heart disease (plus empiric antiarrhythmic therapy in 2 patients), the 11 patients who had no inducible VT have had no recurrence of symptomatic VT or cardiac arrest over a follow-up period of 19 +/- 9 months (mean +/- standard deviation). Conventional antiarrhythmic drugs suppressed the induction of VT and were used for chronic treatment in 9 of 34 patients (26%) with inducible VT. Three of these 9 patients had recurrent VT or sudden death, whereas 6 have had no recurrence over follow-up of 20 +/- 7 months. In the 25 of 34 patients in whom the induction of VT was not suppressed by conventional antiarrhythmic drugs, 23 were treated with amiodarone (daily dose 550 +/- 120 mg), and 2 underwent coronary artery bypass grafting with either aneurysmectomy or map-directed endocardial resection. One of the latter 2 patients died suddenly 12 months after surgery. Among the 23 patients treated with amiodarone, 2 had fatal VT or sudden death and 21 (91%) did not, over 18 +/- 14 months of follow-up. In survivors of a cardiac arrest, the chief value of electrophysiologic testing is in identifying patients without inducible VT, who appear to have a low risk of recurrent sudden death with treatment directed at the underlying heart disease. Serial electropharmacologic testing with conventional antiarrhythmic drugs is disappointing, with a low incidence of arrhythmia suppression.     

Surgical coronary revascularization in survivors of prehospital cardiac arrest: its effect on inducible ventricular arrhythmias and long-term survival

In a selected subgroup of 50 survivors of cardiac arrest, the impact of surgical myocardial revascularization on inducible arrhythmias, arrhythmia recurrence and long-term survival was examined. The effects of several clinical, angiographic and electrophysiologic variables on arrhythmia recurrence and survival were also analyzed. All patients had a prehospital cardiac arrest and severe operable coronary artery disease and underwent myocardial revascularization. Preoperative electrophysiologic study was performed in 41 patients; 33 (80%) had inducible ventricular arrhythmias. Of 42 patients studied off antiarrhythmic drugs postoperatively, 19 (45%) had inducible ventricular arrhythmias. Thirty patients with inducible arrhythmias preoperatively underwent postoperative testing off antiarrhythmic drugs; arrhythmia induction was suppressed in 14 (47%). By multivariate analysis, the induction of ventricular fibrillation at the preoperative electrophysiologic study was the only significant predictor of induced ventricular arrhythmia suppression by coronary surgery (p less than 0.001). Inducible ventricular fibrillation was not present postoperatively in any of the 11 patients who manifested this arrhythmia preoperatively. In contrast, inducible ventricular tachycardia persisted in 80% of patients in whom preoperative testing induced this arrhythmia. Patients were followed up for 39 +/- 29 months. There were four arrhythmia recurrences; one was fatal. There were three nonsudden cardiac deaths and three noncardiac deaths. By life-table analysis, 5 year survival, cardiac survival and arrhythmia-free survival rates were 88%, 98%, and 88%, respectively. Depressed left ventricular ejection fraction and advanced age were predictive of death (p = 0.015 and 0.026, respectively) and cardiac death (p = 0.037 and 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular fibrillation in chronic heart disease

The objective of the work was to describe in subjects with spontaneous ventricular fibrillation, after elimination of acute cardiac disease, the strategy of antiarrhythmic treatment and to evaluate, based on prospective follow-up, the effectiveness of this treatment. The authors included in the group 36 patients (30 men and 6 women) within the range from 34 to 78 years (mean age 58 +/- 11 years) with spontaneous ventricular fibrillation. They divided the group into a subgroup (15 subjects) without revascularization of the heart muscle, into a subgroup (17 subjects) with revascularization of the myocardium (coronary angioplasty and bypasses) and a subgroup (4 subjects) where ischaemic heart disease was ruled out (mostly cardiomyopathies). In all subgroups they used programmed ventricular stimulation (apparatuses of Quinton Co. USA, Biotronik Co. GFR), in the subgroup with revascularization within 3 months. During the diagnostic procedure of ventricular stimulation they tested antiarrhythmic drugs most frequently amiodarone per os (for 4 weeks). An implantable cardioverter--defibrillator was implanted in 17 patients (8 subjects without revascularization, 6 subjects with revascularization, 3 subjects without ischaemic heart disease). All patients were followed up till death, maximum 24 months. The authors evaluated the rate of cardiac deaths (death on cardiac grounds, incl. sudden arrhythmic death) and sudden arrhythmic deaths (within one hour after the onset of symptoms or the first malignant ventricular tachyarrhythmia recorded after implantation of the defibrillator). In the subgroup without revascularization with electric instability of the ventricles according to programmed stimulation 66.7% they described seven cardiac deaths (46.7%) and 6 sudden "arrhythmic" deaths (40%) incl. 5 subjects with ineffective testing of antiarrhythmic drugs. Conversely in the subgroup with revascularization and with diagnostic programmed stimulation in 47.1% they found 3 cardiac deaths (17.7%), one sudden "arrhythmic" death (5.9%)--a subject with ineffective testing. In the subgroup without ischaemic heart disease they recorded cardiac and sudden "arrhythmic" deaths in half the subjects, in all instances in subjects without inducible ventricular tachyarrhythmia. The authors found in the course of a two-year investigation a relapse of cardiac arrest in 25% of subjects after spontaneous ventricular fibrillation. A third of these subjects (all without a cardioverter-defibrillator) died. They confirm the benefit of implantation of a defibrillator for all subjects regardless of the basic diagnosis and revascularization of the heart muscle.     

Therapy for late post infarction ventricular tachycardia

Non-sustained ventricular tachycardia (VT) in the late post myocardial infarction (MI) period (7-21 days) has been reported to be a predictor of sudden death. We suspected that patients with 3 beat VT on Holter monitoring in the late infarction period would demonstrate electrical instability at electrophysiologic studies. Forty-seven patients were identified as having at least 3 beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred by their attending physician. The mean ejection fraction of this group was 43 +/- 16%. Eight patients have died, 3 sudden deaths in 13 +/- 5 months, a 17% incidence of sudden death. Twenty-nine patients underwent invasive electrophysiologic studies. Their mean ejection fraction was 37 +/- 7%, and 28 had inducible, 18 sustained ventricular tachycardia and 10 non-sustained VT. No complications were noted with electrophysiological testing in the post infarction patients. Using programmed electrical stimulation studies an effective antiarrhythmic agent preventing VT induction (usually experimental) could be found for each patient. After a mean follow-up of 12.5 +/- 4 months, the patient without inducible VT is alive and 26 of the 28 "inducible" patients are alive and well. Two patients died, one of stroke and one due to pump failure following a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective at the initial electrophysiologic studies. Thus, PES studies post MI are safe and may be an effective way to assess therapy for patients in the early post MI period, identified at high risk for sudden death.     

Impact of percutaneous coronary intervention or coronary artery bypass grafting on outcome after nonfatal cardiac arrest outside the hospital

Survivors of cardiac arrest due to ventricular arrhythmias are at risk for recurrent events. The role of revascularization in secondary prevention for survivors of cardiac arrest has been addressed in various studies with conflicting results. A total of 142 survivors of cardiac arrest with coronary artery disease were evaluated according to a standardized protocol, including 2-dimensional echocardiography, myocardial perfusion scintigraphy, coronary angiography, and electrophysiologic testing. Revascularization of scintigraphically documented ischemic myocardial regions was performed in 44 patients (31%). Final therapy was based on the results of electrophysiologic testing. Four-year survival rates were 100% for revascularized noninducible patients, 84% for revascularized inducible patients, 91% for nonrevascularized noninducible patients, and 72% for nonrevascularized inducible patients. Only 1 patient (<1% of study population) died suddenly. Recurrences were much more frequent in patients without revascularization (38% vs 7%, p <0.001) and the recurrence rate was 0% in the revascularized noninducible patients. Thus, revascularization of ischemically jeopardized myocardium in survivors of cardiac arrest resulted in excellent survival; moreover, in absence of inducible ventricular arrhythmias, the recurrence rate was 0%. Systematic evaluation of survivors of cardiac arrest due to ventricular arrhythmias allows risk stratification and guidance of subsequent antiarrhythmic therapy.     

Ventricular arrhythmias in congestive heart failure

Despite advances in the treatment of congestive heart failure (CHF), the mortality rate continues to be high. A large number of the deaths are sudden, presumably due to ventricular arrhythmias. Complex ventricular arrhythmias are recorded in as many as 80% of patients with CHF, with nonsustained ventricular tachycardia occurring in 40%. The latter appears to be an independent predictor of mortality. Chronic structural abnormalities responsible for CHF may be the basis for the capability of a ventricle to support life-threatening arrhythmias, which are triggered by premature ventricular contractions. The pathogenesis of arrhythmias is multifactorial. Electrolyte abnormalities, ischemia, catecholamines, inotropic and antiarrhythmic drugs may worsen arrhythmias and increase susceptibility of a ventricle to sustained arrhythmias. Beta-adrenergic blockers and angiotensin-converting enzyme inhibitors have a beneficial effect. The role of various drugs in the pathogenesis and treatment of ventricular arrhythmias is discussed. The efficacy of antiarrhythmic therapy targeted to asymptomatic nonsustained ventricular tachycardia, in order to prevent sudden death, is controversial. Pharmacotherapy guided by electrophysiologic testing is the treatment of choice for patients who have manifest sustained ventricular tachycardia, but patients resuscitated from ventricular fibrillation may require automatic implantable cardioverter defibrillator.     

Long-term continuous electrocardiographic recordings and electrophysiologic testing to select patients with ventricular arrhythmias for drug trials and to determine antiarrhythmic drug efficacy

Long-term continuous electrocardiographic recordings (Holter recordings) and electrophysiologic testing are useful for selecting patients for antiarrhythmic drug trials and for evaluating efficacy and adverse effects during therapy. These 2 methods are used to establish patient eligibility and to stratify patients during randomization. Both noninvasive testing and electrophysiologic studies help to classify arrhythmias as benign, potentially malignant or malignant. Holter monitoring and electrophysiologic studies each have unique advantages and disadvantages for baseline evaluation before starting antiarrhythmic drug treatment and for evaluation of efficacy or adverse effects during follow-up. Both methods have been shown to predict outcome of treatment in patients with malignant ventricular arrhythmias (i.e., can be used as surrogates for sudden death). Several ongoing studies are attempting to extend our knowledge of these 2 techniques. A multicenter study in the United States is comparing the 2 methods for applicability, predictive accuracy and cost. Investigators in the Netherlands are testing the validity of electrophysiologic studies by continuing antiarrhythmic drug treatment whether or not programmed ventricular stimulation predicts success or failure. Finally, new proposals have been made for conducting randomized, controlled studies in selected patients with malignant ventricular arrhythmias using time to drug failure as the endpoint.     

Comparison of noninvasive arrhythmia induction techniques with electrophysiologic studies and evaluation of lorcainide in patients with symptomatic ventricular tachycardia

Twenty-six patients (19 men and 7 women) with symptomatic ventricular tachycardia (VT) were studied using invasive and noninvasive techniques to induce VT. Of the study population, 12% had syncope and VT on Holter monitoring, 30% had cardiac arrest and 58% had symptomatic VT. All patients had antiarrhythmic agents stopped 5 half-lives before evaluation and then had autonomic profile (upright tilt, cold pressor test, exercise testing and hand grip) as well as programmed electrical stimulation studies performed. Autonomic profile testing induced VT in 5 of 26 patients (19%) and in only 1 patient was the arrhythmia reproducibly induced. All 26 patients had VT induced on electrophysiologic testing; 9 patients had nonsustained and 17 had sustained VT. Lorcainide administered intravenously prevented VT induction in 20 of 26 patients tested, whereas procainamide was effective in 11 of 24 patients. Ten of the 13 not protected by procainamide were protected by lorcainide. Twenty patients were started on long-term lorcainide therapy and followed up for 29 +/- 3.4 months. Five patients have discontinued therapy, 2 because of breakthrough arrhythmias, 2 because of severe sleep-wake disturbances and 1 because of private physician preference. An additional 3 patients died during therapy because of myocardial infarction in 1, progressive myopathy in 1 and sudden death in 1. Sixty percent of patients started on lorcainide therapy have continued. In this patient population, noninvasive induction of VT is not a sensitive or reproducible technique in assessing antiarrhythmic therapy. Furthermore, when selected on the basis of electrophysiologic testing, lorcainide is a well-tolerated and effective antiarrhythmic agent.     

Prognostic significance of nonsustained ventricular tachycardia after revascularization

INTRODUCTION: Two randomized trials (Multicenter Automatic Defibrillator Implantation Trial [MADIT] and Multicenter Unsustained Tachycardia Trial [MUSTT]) suggest that implantable cardioverter defibrillator (ICD) placement is associated with improved survival in patients with coronary artery disease, depressed left ventricular function, and nonsustained ventricular tachycardia (VT) who also have inducible sustained VT. However, neither study directly addresses the management of such patients who develop nonsustained VT early after revascularization. METHODS AND RESULTS: We evaluated 109 consecutive patients who underwent electrophysiologic testing to evaluate nonsustained VT, which occurred 5 +/- 4 days following revascularization. Sustained monomorphic VT was inducible in 46 (42%) patients; these patients received an ICD. The remaining 63 (58%) noninducible patients received neither antiarrhythmic drug therapy nor an ICD. During 27 +/- 12 months of follow-up, 15 (33%) of 45 patients with an implanted ICD received at least one appropriate therapy from the device and 26 (24%) of the 109 study patients died. The 1- and 2-year freedom from ventricular tachycardia/fibrillation or sudden death in noninducible patients (97% and 93%) was significantly greater than that of inducible patients (84% and 71%; P = 0.001). However, no difference was observed in total mortality. CONCLUSION: Patients with nonsustained VT during the early postrevascularization period who have inducible VT have a high incidence of arrhythmic events. Although this study was not designed to assess the impact of ICD placement on the total mortality of inducible patients, the finding that one third of these patients received appropriate ICD therapy suggests that the device may have a protective effect in these patients.     

Idiopathic dilated cardiomyopathy: prognostic significance of electrocardiographic and electrophysiologic findings in the nineties.

BACKGROUND: With the exception of a few cases such as aborted sudden cardiac death, sustained ventricular tachycardia, and syncope of unexplained origin, there is no consensus on the clinical findings identifying patients with idiopathic dilated cardiomyopathy with an increased risk of sudden cardiac death or malignant ventricular arrhythmias. METHODS: To verify whether electrocardiographic and arrhythmologic features could be useful for prognostic stratification, 78 consecutive patients with an invasive diagnosis of idiopathic dilated cardiomyopathy, but without symptomatic ventricular arrhythmias, were enrolled in a prospective study. Signal-averaged ECG, 24 to 48 hour ECG monitoring and electrophysiologic study were performed at the time of diagnosis to identify arrhythmogenic predictors of outcome. Transplant-free and arrhythmic event-free survival was evaluated on the basis of initial parameters. RESULTS: During a mean follow-up of 85 months, 9 patients died (6 of sudden cardiac death and 3 of congestive heart failure), 10 patients underwent cardiac transplantation for refractory heart failure, and 3 presented with sustained ventricular tachycardia. The independent predictors for death and cardiac transplantation were an HV interval > 55 ms and the combination of frequent repetitive ventricular ectopics with a poor left ventricular function. A strong index of arrhythmic events proved to be the association of a prolonged HV interval with a wide (> 110 ms) QRS complex (odds ratio 4.53, 95% confidence interval 1.57-13.04, p < 0.005). CONCLUSIONS: An accurate measurement of the HV interval and QRS duration at baseline evaluation may add prognostic information in patients with idiopathic dilated cardiomyopathy. In our experience, abnormal values of both parameters identified a group of patients with a very high risk of late occurring arrhythmic events.     

Arrhythmias in heart failure: current concepts of mechanisms and therapy

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.     

Treatment of choice and long-term prognosis for ventricular arrhythmias

Treatment of choice and long-term prognosis of the patients with ventricular arrhythmias are described in terms of prevention of sudden cardiac death and/or recurrence of life-threatening arrhythmias(ventricular tachycardia and ventricular fibrillation). 1) As to the long-term prognosis of ventricular tachyarrhythmias, presence of organic heart disease and degree of cardiac dysfunction are major determining factors. 2) The prognosis of patients with ventricular arrhythmias depends on how sudden cardiac death and life-threatening arrhythmias can be prevented. Among various methods, the electrophysiological test and its guided-therapy for antiarrhythmic drugs are now believed to be the most effective method for the prediction and prevention of the life-threatening events. We propose that the signal averaged electrocardiography is the best screening method as non-invasive approach for the selection of patients undergoing the electrophysiological test. 3) There are still certain limitations as to the prediction of sudden cardiac death and/or prevention of recurrent life-threatening arrhythmias by antiarrhythmic drug treatments in the certain numbers of patients depending on their basal cardiac disease and functional impairment. At present, catheter ablation procedure and implantable cardioverter defibrillator are the choice of the treatment in these cases. 4) In addition to conventional antiarrhythmic drugs, the treatment for the basal cardiac condition is mandatory for the long-term prognosis in the patients with ventricular arrhythmias.     

Lymphocytic myocarditis presenting as unexplained ventricular arrhythmias: diagnosis with endomyocardial biopsy and response to immunosuppression

During a period of 18 months beginning in January 1982, a total of 65 patients were referred to the Miami Heart Institute for evaluation of either aborted out of hospital sudden death, ventricular tachycardia resistant to standard clinically directed antiarrhythmic medication programs or high grade ventricular arrhythmia (Lown class greater than or equal to IV B) with or without syncope. After complete evaluation including cardiac catheterization in all but 1 patient, 17 patients were identified in whom no obvious cardiac disease could be found. Twelve of the 17 underwent right ventricular endomyocardial biopsy. Six of the 12 biopsies demonstrated clinically unsuspected lymphocytic myocarditis (Group A). Findings in three of the remaining six biopsies were consistent with an early cardiomyopathy and in three were completely normal (Group B). Retrospective review of the clinical, laboratory, electrophysiologic, hemodynamic and angiographic data failed to identify a marker that reliably separated Group A from Group B patients. In addition to antiarrhythmic therapy guided by laboratory electrophysiologic study, all Group A patients were treated with prednisone and azathioprine. After 6 months of immunosuppression, all patients with myocarditis were reevaluated in the hospital without antiarrhythmic medication. Ventricular tachycardia/fibrillation could not be provoked in the laboratory during repeat electrophysiologic testing in five of the six patients. Repeat myocardial biopsy after all immunosuppressive therapy had been discontinued revealed absence of inflammation associated with varying degrees of residual interstitial fibrosis. There were no deaths. It was concluded that a patient with an otherwise clinically silent lymphocytic myocarditis can present with potentially life-threatening ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)     

Short- and long-term experience with flecainide acetate in the management of refractory life-threatening ventricular arrhythmias

Thirty-eight patients with organic heart disease and history of sudden cardiac arrest or recurrent sustained ventricular tachycardia were treated with flecainide. Coronary artery disease was present in 33 patients. Previous antiarrhythmic therapy consisted of two to eight drugs (mean four). Fourteen patients were resuscitated from sudden cardiac death and 24 patients had chronic recurrent sustained ventricular tachycardia. Twenty-eight patients had electrophysiologic testing before and during flecainide treatment. Sustained ventricular tachycardia became noninducible in 5 patients, nonsustained in 5 patients and slowed in 13 patients (cycle length increased from 278 +/- 64 to 395 +/- 91 ms; p = 0.002). Three of the 14 patients with sudden cardiac death and 15 of the 24 patients with recurrent sustained ventricular tachycardia remained on long-term flecainide treatment. The mean left ventricular ejection fraction in 16 of these 18 patients was 37%. Nonlimiting side effects occurred in seven patients (18%). Proarrhythmic effects were seen in four patients (10%). At a mean follow-up time of 11 +/- 3 months, 15 patients (39%) had had no recurrence, including 5 who had inducible sustained ventricular tachycardia and 5 who did not on retesting during treatment. In the 18 patients who received long-term therapy, 3 late deaths occurred, 1 of which was of arrhythmic origin. These data suggest that flecainide is effective in about 40% of patients with severe refractory ventricular arrhythmias. Its value as a single drug in the treatment of sudden cardiac death remains to be defined.     

Antifibrillatory versus antiectopic therapy

The concept of antifibrillatory action distinct from antiarrhythmic effect has recently been recognized. An antiarrhythmic (antiectopic) action leads to a decrease in the frequency of ventricular ectopic beats. In contrast, an antifibrillatory drug action increases myocardial electric stability, decreasing the propensity for ventricular fibrillation. Agents with predominant antiarrhythmic action (designated class I) include lidocaine, quinidine, procainamide and disopyramide. Bretylium is an agent with predominant antifibrillatory action (class III). Amiodarone and sotalol are experimental class III drugs. The beta-blockers (class II) also possess antifibrillatory action, particularly in ischemic heart disease. The rationale for the use of agents with antiarrhythmic (antiectopic) effects is the reduction of triggering events for more complex ventricular tachyarrhythmias. These agents act by slowing conduction, decreasing abnormal automaticity and affecting phase IV depolarization. In contrast, agents with antifibrillatory action may exert little effect on cardiac conduction and automaticity. However, they raise the energy threshold required for premature electrical discharge to initiate ventricular fibrillation (ventricular fibrillation threshold). The inhomogeneity of electrophysiologic properties and adrenergic tone in different portions of the heart may be reduced or eliminated. Direct electrophysiologic effects of agents such as bretyllum include a general lengthening of the refractory period and the action potential duration in the heart and a diminution in the disparity of their durations between normal and abnormal myocardium.Clinical studies are incomplete, but they support the concept of antifibrillatory therapy. In postmyocardial infarction patients at intermediate risk of sudden death, the broad use of oral antiarrhythmic agents has not decreased the incidence of sudden death, whereas high-dose β-blocker therapy, which exerts experimental antifibrillatory effects, may reduce sudden death by 30 to 70%. For survivors of sudden death and sustained ventricular arrhythmias at high risk of recurrence, clinical evidence suggests that antifibrillatory therapy with amiodarone is generally more effective in reducing recurrence than is therapy with both standard and newer antiarrhythmic agents. In therapy or prophylaxis of acute ventricular fibrillation, bretylium is unexcelled. Unlike standard antiectopic agents, bretylium reduces the experimental defibrillation threshold. Ventricular fibrillation recurring despite standard therapy responds to bretylium in up to 75 % of patients, based on several clinical studies.     

Ventricular arrhythmias in dilated cardiomyopathy: efficacy of amiodarone

Sixty-five patients with dilated cardiomyopathy were studied by means of 24-hour ECG monitoring. Ventricular arrhythmias were present in 62 (95.4%), of whom 52 (80%) showed a complex form (multiform ventricular extrasystoles, pairs, and ventricular tachycardia). Forty-one patients, presenting with complex ventricular arrhythmias, received antiarrhythmic treatment with amiodarone (600 mg/day in the first week, 400 mg/day in the second week, and 200 to 400 mg/day chronically), and were then controlled with periodic 24-hour ambulatory monitoring. A significant reduction in the number of ventricular extrasystoles was seen in over 70% of patients during a 3-year period. There was also a significant decrease in the incidence of complex ventricular arrhythmias (particularly of ventricular tachycardia). Adverse effects were noted in 23 patients, but only four had to stop treatment. During the follow-up period, 19 patients died: 14 of heart failure, four of sudden death, and one of a noncardiac cause; all patients who died suddenly were not treated with amiodarone (p = 0.022). Complex ventricular arrhythmias are frequent in dilated cardiomyopathy and it is suggested that amiodarone is effective in short- and long-term control of these arrhythmias.     

The impact of transtelephonic documentation of arrhythmia on morbidity and mortality rate in sudden death survivors

A post hospital follow-up system based on predetermined antiarrhythmic strategies and telephone transmitters used to record ECGs was helpful in managing post hospital course and improved survival in patients with a history of out-of-hospital sudden death. All patients underwent therapy guided by serial electrophysiologic testing. Of the 47 patients, 19 used the telephone transmitter system and 28 did not. During follow-up, residual symptomatic and silent ventricular arrhythmia was documented in 78% of patients using telephone transmitters. Ventricular tachycardia was transmitted in six patients--all survived. During an average 15-month follow-up, 1 of 19 patients using the telephone transmitter system died vs 12 deaths among the 28 patients who did not use the system (p less than 0.005). These results were independent of ejection fraction, presence of congestive heart failure, amiodarone therapy, and the outcome on electrophysiologic therapy. Thus, patients with a history of out-of-hospital sudden death, discharged following electrophysiologic guided therapy, require repeated antiarrhythmic dose titration for side effects or residual ventricular arrhythmia. Prompt diagnosis and treatment of potentially fatal arrhythmia is crucial and feasible, especially with regular ECG checks through telephone transmission.