Bepridil for recurrent sustained ventricular tachycardias: assessment using electrophysiologic testing

Bepridil was found to possess electrophysiologic properties common to class I and IV antiarrhythmic agents. Intravenous and oral bepridil were evaluated using serial electrophysiologic studies in a selected group of 9 patients with recurrent sustained ventricular tachycardia (VT) unresponsive to usual therapy, including amiodarone therapy in 15 patients. Intravenous bepridil treatment terminated sustained, well tolerated, pacing-induced VT in 3 of 6 patients and prevented the initiation of VT in 2 of these and in a patient in whom the drug failed to restore sinus rhythm. Oral bepridil was administered at a loading dose of 800 mg on day 1, and 500 to 600 mg the following days, and programmed electrical stimulation was repeated 2 to 6 days after initial study. Oral bepridil therapy prevented VT initiation in 6 patients (66%). The tachycardia cycle length was prolonged (30 to 105 ms) in 2 patients in whom VT remained inducible. In 1 patient the tachycardia cycle length significantly shortened after bepridil and prompt cardioversion was required. Five of the 6 patients with successful results underwent long-term oral treatment with bepridil. VT recurred in 1 patient during the hospitalization period and an adverse effect (paralytic ileus) in another patient required drug discontinuation. Three patients remain symptom-free over a follow-up of 4 to 13 months. These data suggest that bepridil may be useful in patients with recurrent, sustained VT.     

Out-of-hospital cardiac arrest in patients with no overt heart disease: electrophysiologic observations and clinical outcome

Electrophysiologic studies were performed in nine survivors of out-of-hospital cardiac arrest who had no overt heart disease on clinical, hemodynamic and angiographic evaluation. Cardiac arrest occurred during sedentary activity in seven patients and during exercise in two; no patient was on antiarrhythmic drugs at the time of cardiac arrest. Twenty-four hour ambulatory electrocardiographic monitoring demonstrated premature ventricular beats in four patients (44%). Electrophysiologic stimulation induced sustained ventricular tachycardia (VT) or fibrillation (VF) in five patients, nonsustained VT in one patient and less than five ventricular beats in the remaining three patients. Of five patients with inducible sustained VT or VF, four had complete suppression of inducible VT with antiarrhythmic therapy, and none of these four patients died suddenly or had clinical VT after an average follow-up of 27 months (range 12 to 41 months). The remaining patient with inducible sustained VT refused serial electropharmacologic testing, was treated empirically with amiodarone (400 mg/day) and died suddenly eight months later. Of the four patients with noninducible sustained VT or VF, three received no antiarrhythmic therapy and one was given a beta-blocker. None had recurrent cardiac arrest or symptomatic VT after an average follow-up of 17 months (range 13 to 20 months). Thus, inducibility of sustained VT or VF provided a reliable end point for long term antiarrhythmic therapy and noninducibility identified a subset of patients that had an excellent prognosis without specific antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of bepridil efficacy by electrophysiologic testing in patients with recurrent ventricular tachycardia: Comparison of two regimens

Summary The purpose of the study was to evaluate this effect of different doses of intravenous and oral bepridil on the induction of ventricular tachycardia. Thirty-eight patients underwent electrophysiologic evaluation for recurrent ventricular tachycardia (VT). Sustained monomorphic VT was induced by programmed ventricular stimulation, using up to three extrastimuli in all patients. The effects of intravenous bepridil (2 mg/kg) were evaluated during the initial study. Intravenous bepridil prevented the induction of sustained VT in eight patients (21%). Electrophysiologic study was repeated after oral bepridil. In six patients the study was stopped because of adverse effects or VT recurrence. Thirty-two patients underwent repeat study 7 days later, taking oral bepridil, 500 mg/day (n=16) or 900/day (n=16). A dose of 500 mg/day of bepridil prevented the induction of sustained VT in only one patient. A dose of 900 mg/day of bepridil prevented the induction of sustained VT in eight patients. There were no significant clinical adverse effects, except in one patient receiving intravenous bepridil. The response to intravenous bepridil did not predict the response to oral bepridil. The response to intravenous or oral bepridil was not related to the plasma level of bepridil but was related to a higher left ventricular ejection fraction. Eight patients (21%) in whom VTs were noninducible on oral bepridil were discharged on 300 mg/day of bepridil if their initial loading dose was 500 mg/day or on 600 mg/day if their initial loading dose was 900 mg/day. They remained free of VT during a follow-up of at least 6 months. In conclusion, this study suggests that oral bepridil at the dose of 600 mg/day may be of value in patients with recurrent VT.     

Encainide in lethal ventricular arrhythmias evaluated by electrophysiologic testing and decrease in symptoms

Encainide hydrochloride has distinct electrophysiologic properties that suggest active antiarrhythmic properties. Encainide has been administered both intravenously (0.5 to 1.7 mg/kg) and orally (100 to 300 mg/day) to patients with lethal ventricular arrhythmias--ventricular tachycardia (VT) and ventricular fibrillation--and evaluated by electrophysiologic testing. In 62 patients with inducible sustained VT, intravenous encainide prevented initiation in 13 (21%). In 57 patients with refractory sustained VT, oral encainide prevented initiation of VT by programmed stimulation in 17 (30%). The results obtained with intravenous and oral encainide in the same patient were usually concordant (93%). Encainide may worsen ventricular arrhythmia, most typically by converting nonsustained VT into sustained VT during electrophysiologic testing. In patients with lethal ventricular arrhythmia, analysis of symptoms before and during chronic encainide therapy showed that the number and severity of arrhythmia-related symptoms were reduced. Encainide appears to be a useful antiarrhythmic agent.     

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.     

Efficacy and tolerance of high-dose intravenous amiodarone for recurrent, refractory ventricular tachycardia

High-dose intravenous amiodarone was given to 35 patients with recurrent life-threatening ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents. Intravenous amiodarone was given as a 5 mg/kg dose over 30 minutes followed by 20 to 30 mg/kg/day as a constant infusion for 5 days. Twenty-two (63%) patients responded to intravenous amiodarone. All 22 responders received oral amiodarone. Thirteen (59%) continue to receive oral amiodarone after an average follow-up of 19 months, 4 (18%) had sudden cardiac death on oral amiodarone, 2 (9%) died while receiving amiodarone, secondary to left ventricular failure, and 3 (14%) discontinued amiodarone because of side effects. Of the 13 (37%) nonresponders, 10 died in the hospital while receiving intravenous amiodarone, secondary to lethal arrhythmia. Three nonresponders were discharged from the hospital; 2 with automatic cardioverter/defibrillators and 1 receiving a combination of antiarrhythmic agents. Serious adverse events occurred in 13 (37%) patients during intravenous amiodarone therapy. These included hypotension in 8 patients, symptomatic bradycardia in 4 patients and sinus arrest with bradycardia and hypotension in 1 patient. Minor side effects occurred in 23 (66%) patients. In conclusion, high dose intravenous amiodarone is effective in most patients with recurrent, sustained VT but is associated with an unacceptably high incidence of serious adverse events. The optimal dose and duration of intravenous amiodarone for patients with recurrent, refractory sustained VT remain unknown.     

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.     

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)     

Electrophysiological anti-arrhythmia effects of tiracizine in ventricular tachycardia]

The electrophysiologic effects and antiarrhythmic efficacy of tiracizine, a new class I antiarrhythmic drug, were studied in 16 patients with documented sustained ventricular tachycardia (VT) after intravenous drug application and in 6 patients after oral drug administration by means of programmed ventricular stimulation (PVS). After intravenous tiracizine (0.3 mg/kg) the VT was no longer inducible by PVS in 3 of 16 patients and became nonsustained in another patient. In 11 of 13 patients with further inducible VT the cycle duration of VT increased after tiracizine (mean 29 ms). After oral tiracizine (150-225 mg/day) the VT induction was suppressed in one patient. In a second patient the VT became nonsustained. Cycle length of VT in 4 patients with persistent induction of VT was longer after therapy (mean 88 ms). Antiarrhythmic efficacy of intravenous or oral tiracizine can be expected in at least one third of patients with VT.     

Electrophysiologic testing of bretylium tosylate in sustained ventricular tachycardia

We used programmed ventricular stimulation to test intravenous bretylium tosylate in 10 consecutive patients with inducible sustained ventricular tachycardia (usually refractory to type I antiarrhythmic agents). These 10 patients had previously documented sustained ventricular tachycardia and/or ventricular fibrillation complicating stable heart disease. Following control inductions of sustained ventricular tachycardia, bretylium 10 mg/kg was infused over 30 minutes. Thirty minutes after this infusion, sustained ventricular tachycardia could be induced in 9 of the 10 patients (one of these nine patients also had bretylium-potentiated spontaneous ventricular tachycardia). Tachycardia induced in the nine patients after bretylium was similar to control tachycardia with respect to morphology and cycle length (333 +/- 16 msec after bretylium versus 330 +/- 16 msec during control). However, five of the nine patients tolerated induced tachycardia less well after bretylium (exacerbated hypotension). In one patient, ventricular tachycardia could not be induced after intravenous bretylium.     

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.     

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.     

Electrophysiologic and clinical factors influencing response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia

Clinical and electrophysiologic data from 51 consecutive patients with sustained monomorphic ventricular tachycardia inducible during programmed ventricular stimulation were evaluated to determine what variables predict the response to intravenous class IA antiarrhythmic agents. All patients received acute drug testing in the electrophysiologic laboratory with either intravenous procainamide or intravenous quinidine. Ventricular tachycardia suppression was achieved in 9 out of 51 patients (18%). The age, gender, left ventricular ejection fraction, baseline right ventricular effective refractory period, baseline HV interval, and baseline ventricular tachycardia cycle length were not predictive of ventricular tachycardia suppression with intravenous procainamide or quinidine during programmed ventricular stimulation. The degree of prolongation of the right ventricular effective refractory period after drug administration did not predict success or failure to suppress inducible ventricular tachycardia. The degree of prolongation of the HV interval was also not predictive. In addition, the degree of prolongation of the right ventricular effective refractory period or the HV interval did not predict the change in the ventricular tachycardia cycle length after drug administration in patients who remained inducible. These data indicate that the response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia cannot be predicted on the basis of various clinical and electrophysiologic parameters.     

Usefulness of the electrophysiology laboratory for evaluation of proarrhythmic drug response in coronary artery disease.

Two potential manifestations of proarrhythmic responses to type IA antiarrhythmic agents in the electrophysiology laboratory were evaluated in 122 patients with chronic coronary artery disease and previous myocardial infarction: (1) conversion of uniform nonsustained ventricular tachycardia (VT) into sustained VT after drug administration, and (2) induction of sustained VT by fewer extrastimuli after drug administration. Forty-two patients were evaluated for nonsustained VT. Eighty patients were evaluated for sustained VT: 30 of these had spontaneous sustained VT only while receiving empiric therapy with quinidine or procainamide, whereas the remaining 50 developed spontaneous VT in the absence of antiarrhythmic drugs. All patients underwent programmed stimulation in the baseline state and after procainamide. Four patients had conversion of induced uniform nonsustained VT into the same morphology, but sustained VT after procainamide administration. These responses only occurred in patients evaluated for nonsustained VT. Over 90% of patients presenting with sustained VT had uniform sustained VT induced at the baseline study and after procainamide, regardless of whether the spontaneous arrhythmia occurred only in the presence or absence of antiarrhythmic drugs. There was no significant difference in the change in mode of induction from baseline to procainamide study, regardless of whether patients had developed spontaneous VT only in the presence or absence of antiarrhythmic drugs. One patient with no inducible VT at the baseline study had inducible uniform sustained VT after procainamide administration, and 1 patient with inducible VT at baseline developed spontaneous sustained uniform VT after procainamide administration. Both patients had developed spontaneous sustained VT only while receiving therapy with type IA agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular tachycardia: prediction of response to oral aprindine with intravenous aprindine

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.     

Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.     

Clinical and electrophysiologic assessment of oral flecainide acetate for recurrent ventricular tachycardia: Evidence for exacerbation of electrical instability

Four patients with recurrent, symptomatic ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents were given flecainide acetate to control arrhythmias. Ventricular stimulation studies were performed in all patients before and 1 to 2 weeks after initiation of oral flecainide therapy. Before flecainide, all patients had easily inducible VT that was morphologically identical to their spontaneously occurring arrhythmia. Flecainide increased the mean PR interval (from 0.17 to 0.23 second), mean QRS duration (from 0.08 to 0.12 second) and mean ventricular effective refractory period (from 235 to 270 ms). Mean corrected QT interval did not change (0.51 second).In 2 patients, VT could not be induced during follow-up stimulation studies. One patient has been treated successfully for 10 months, with no clinically apparent episodes of VT. One patient had recurrent nonsustained VT and was withdrawn from the study as a treatment failure after 6 months of therapy. Two patients had inducible, polymorphous VT that degenerated into ventricular fibrillation that required 2 countershocks before the successful restoration of sinus rhythm. One of these patients had VT stimulation by atrial pacing at a cycle length of 320 ms in the postflecainide electrophysiologic study. VT was not inducible by atrial pacing during this patient's preflecainide study.Thus, sustained oral flecainide administration may precipitate serious electrical instability in susceptible patients, and ventricular stimulation studies and other clinical variables may be useful in selecting patients with recurrent VT who may benefit or may be endangered by oral flecainide therapy.     

Electrophysiologic and antiarrhythmic properties of bepridil

Bepridil has been shown to block both slow- and fast-channel activity in the heart. Electrophysiologic studies in man demonstrate that oral and intravenous bepridil prolongs sinus cycle length, PR interval and QT interval, without apparently changing the QRS interval. In addition, the drug depresses atrioventricular (AV) nodal conduction, resulting in an increased AH interval. Refractoriness in the AV node, atrium and ventricle is increased. There is usually little or no change in the HV interval. The antiarrhythmic properties of bepridil have been noted in patients with supraventricular tachycardia, ventricular premature complexes (VPCs) and sustained ventricular tachycardia (VT). In 17 patients, intravenous bepridil was compared with either verapamil or ajmaline. AV nodal reentrant tachycardia was terminated in all patients with bepridil and verapamil. However, ajmaline was somewhat more effective than bepridil in patients with AV reentry (8 of 8 versus 5 of 8). In 12 of these 17 patients, oral bepridil (500 mg/day for 3 days) suppressed the induction of tachycardia or slowed its rate. In 3 studies of oral bepridil for VPCs, the drug was effective in 68%, 69% and 70% of patients. Another group of studies evaluated bepridil in a total of 30 patients with sustained VT. Intravenous bepridil terminated VT in 17 of 26 patients. The induction of VT by programmed ventricular stimulation was also prevented in 7 of 17 patients. Although torsade de pointes has been reported, its incidence appears to be low.     

Long-term clinical outcome of ventricular tachycardia or fibrillation treated with amiodarone

The determinants of long-term clinical outcome were studied in 42 patients with recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) who were treated with amiodarone as the sole antiarrhythmic agent. Of the 42 patients, 11 (26%) either died suddenly or had recurrent, symptomatic, sustained VT during a mean follow-up period of 10 months (range 0.3 to 45). Of the 19 patients without inducible VT/VF during electrophysiologic study while receiving amiodarone, 1 patient died suddenly but no patient had recurrent VT/VF. Ten of the 23 patients (43%) with persistently inducible arrhythmia have died suddenly or have had recurrent VT/VF. Using survival and stepwise logistic regression analyses, 2 significant independent predictors of recurrent arrhythmia were identified; persistently inducible VT during electrophysiologic testing in patients receiving amiodarone therapy (p < 0.002) and the left ventricular ejection fraction at rest (p < 0.05). The predictive accuracy of the response to serial electrophysiologic testing during amiodarone therapy was 67%, the sensitivity was 58% and the specificity was 91%. Thus, serial electrophysiologic testing is useful for determining the prognosis in patients with inducible VT/VF treated with amiodarone.     

Effectiveness of propranolol added to a type I antiarrhythmic agent for sustained ventricular tachycardia secondary to coronary artery disease

The effect of adding propranolol to procainamide, quinidine, propafenone or disopyramide was prospectively evaluated in 37 patients, all with prior infarction and inducible ventricular tachycardia (VT). After showing that VT remained inducible during therapy with a type I drug, 23 patients received intravenous propranolol. The ventricular effective refractory period, prolonged by the type I agent, was further increased by propranolol. The cycle length of the VT also increased after the type I drug and propranolol exaggerated this effect. Seven of the 23 patients were rendered noninducible after propranolol and another 10 manifested a greater than 100 ms increase in induced VT cycle length. In the other 14 patients, propranolol was infused immediately after the basal study. If VT remained inducible, testing was repeated after a type I drug was added. The ventricular effective refractory period, as well as the VT cycle length, increased after propranolol and was further prolonged after the addition of a type I agent. Seven of these 14 patients were rendered noninducible, 3 with propranolol alone and 4 others with the combination, and in 4, the VT cycle length was prolonged by greater than 100 ms. A total of 17 patients were discharged on either propranolol alone (3 patients) or on an effective combination (14 patients). During a mean follow-up of 20 months, 1 patient died suddenly, 2 had recurrence of well-tolerated VT and 9 remain on therapy. Thus, propranolol has a demonstrable antiarrhythmic effect in the invasive laboratory and may supplement the antiarrhythmic efficacy of conventional type I antiarrhythmic drugs.