Signal-averaged electrocardiographic late potentials in patients with ventricular fibrillation or ventricular tachycardia: correlation with clinical arrhythmia and electrophysiologic study

High-frequency potentials measured in the terminal 40 ms of the signal-averaged QRS complex during sinus rhythm are of abnormally low amplitude in most patients with ventricular tachycardia (VT). However, less is known about high-frequency late potentials in patients with ventricular fibrillation (VF), and the relation between late potentials and arrhythmia inducibility during electrophysiologic study has not been established. Signal-averaged electrocardiography was used to measure high-frequency (more than 25 Hz) late potentials in 24 patients with spontaneous VF, 27 patients with spontaneous sustained VT, and 19 normal subjects, none of whom were receiving antiarrhythmic drugs. Late-potential amplitude in patients with VT was significantly lower than that in patients with VF (p less than 0.02). Late-potential amplitude in patients with VF was not significantly different from that in normal subjects. Ventricular arrhythmia induction was attempted during electrophysiologic study in 46 of the patients with VF or VT. Late-potential amplitude was significantly lower in 26 patients with reproducibly inducible sustained ventricular arrhythmias than in 20 without (p less than 0.001). The correlation between late-potential amplitude and arrhythmia inducibility was independent of that between late-potential amplitude and clinical arrhythmia (VT vs VF).     

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.     

Electrophysiologic drug testing in symptomatic ventricular arrhythmias after repair of tetralogy of Fallot

Nine patients with symptomatic ventricular arrhythmias were evaluated a mean interval of 16 years after surgical repair of tetralogy of Fallot. The clinical arrhythmia was sustained ventricular tachycardia (VT) in 4 patients (group I) and premature ventricular contractions in 5 (group II). All patients underwent cardiac catheterization and electrophysiologic studies. Ventricular tachycardia was induced at electrophysiologic study in all patients in group I and in 3 patients in group II. Six patients with inducible sustained monomorphic VT underwent chronic drug testing based on electrophysiologic study. A mean of 3.3 drugs per patient was tested. Patients with right ventricular systolic hypertension did not respond to any drug tested, and underwent surgery. Five patients received drug treatment based on the results of electrophysiologic study. During a mean follow-up period of 2.2 years, no patient in either group had recurrent episodes of VT or syncope. In the postoperative patient with tetralogy of Fallot with symptomatic ventricular arrhythmias, it is concluded that electrophysiologic study is useful in reproducing clinical episodes of VT and in selecting effective antiarrhythmic medication; a small number of patients with ventricular premature complexes alone will have inducible sustained VT during electrophysiologic study; prognosis of these patients may be improved by treatment that results in prevention of VT induction; and in patients with right ventricular hypertension, VT is likely to be refractory to drug treatment.     

Day-to-day reproducibility of antiarrhythmic drug trials using programmed extrastimulus techniques for ventricular tachyarrhythmias associated with coronary artery disease

Forty-nine patients with coronary artery disease and documented clinical sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) were studied twice in the drug-free state and twice during treatment with an identical antiarrhythmic medication at therapeutic plasma concentrations using an identical programmed electrical stimulation protocol. Tested drugs included procainamide, quinidine, disopyramide and phenytoin. During their 2 paired tests, 11 patients had nearly identical therapeutic plasma concentrations of antiarrhythmic agents (group I) and 38 patients had therapeutic plasma concentrations, but with more variation in drug levels between otherwise identical paired drug tests (group II). Overall, 71% of patients had inducible sustained VT or VF during drug testing. Induced ventricular arrhythmias were not reproducible in 45% of group I patients, despite restudy at nearly identical therapeutic plasma concentrations of an identical antiarrhythmic agent. Induced arrhythmias were also not reproducible in 16% of group II patients. This variability could not be attributed to the electrophysiologic characteristics of the patients studied. Drug trials directed by programmed stimulation should be cautiously interpreted because time-associated changes can mimic a change attributed to a beneficial or deleterious drug effect.     

Electropharmacology of nonsustained ventricular tachycardia: effects of class I antiarrhythmic agents, verapamil and propranolol

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p less than 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.     

Programmed ventricular stimulation for arrhythmia risk prediction in patients with idiopathic dilated cardiomyopathy and nonsustained ventricular tachycardia

Objectives. This study investigated the role of programmed ventricular stimulation (PVS) for arrhythmia risk prediction in patients with idiopathic dilated cardiomyopathy (IDC) and spontaneous nonsustained ventricular tachycardia (VT).Background. Nonsustained VT in patients with IDC has been associated with a high incidence of sudden cardiac death.Methods. Over the course of 4 years, 34 patients with IDC, a left ventricular (LV) ejection fraction ≤35%, and spontaneous nonsustained VT underwent PVS. All patients were prospectively followed for 24 ± 13 months.Results. Sustained ventricular arrhythmias were induced in 13 patients (38%). Sustained monomorphic VT was induced in three patients (9%), and polymorphic VT or ventricular fibrillation (VF) in another 10 patients (29%). No sustained ventricular arrhythmia could be induced in 21 study patients (62%). Prophylactic implantation of third-generation defibrillators (ICDs) with electrogram storage capability was performed in all 13 patients with inducible sustained VT or VF, and in nine of 21 patients (43%) without inducible sustained VT or VF. There were no significant differences between the additional use of amiodarone, d,I-sotalol, and beta-blocker therapy during follow-up in patients with and without inducible VT or VF. During 24 ± 13 months of follow-up, arrhythmic events were observed in nine patients (26%) including sudden cardiac deaths in two patients and ICD shocks for rapid VT or VF in seven patients. Arrhythmic events during follow-up occurred in four of 13 patients with inducible ventricular arrhythmias compared with five of 21 patients without inducible ventricular arrhythmias at PVS (31% vs. 24%, p = NS).Conclusion. PVS does not appear to be helpful for arrhythmia risk stratification in patients with IDC, a left ventricular ejection fraction ≤35%, and spontaneous nonsustained VT. Due to the limited number of patients, however, the power of this study is too small to exclude moderately large differences in outcome between patients with IDC with and without inducible VT or VF.     

Clinical and electrophysiologic predictors of ventricular tachyarrhythmia recurrence in patients with implantable cardioverter defibrillators

INTRODUCTION: Not all patients experience recurrent sustained ventricular tachyarrhythmias after placement of an implantable cardioverter defibrillator (ICD). We evaluated the clinical and electrophysiologic predictors of ventricular tachycardia (VT) and ventricular fibrillation (VF) recurrence following ICD implantation. METHODS AND RESULTS: Consecutive patients (n = 133) underwent 4 +/- 3 serial electrophysiologic studies (EPS) over 50 +/- 26 months following ICD implantation. Sustained VT/VF could always be induced during follow-up EPS in 49 patients; sustained VT/VF was sometimes induced during follow-up EPS in 47 patients; and sustained VT/VF could never be induced during follow-up EPS in 37 patients. Spontaneous VT/VF requiring ICD therapy occurred in 107 patients during follow-up. Patients with sustained VT/VF that was always inducible or sometimes inducible during follow-up experienced more frequent episodes of VT/VF following ICD implant (20.5, 95% CI 12.7-33.0; and 17.8, 95% CI 11.3-28.1 episodes/patient respectively; vs 3.0, 95% CI 2.0-4.6 episodes/patient for patients with VT/VF never induced, P < 0.001). Inducibility of sustained VT/VF post-ICD implant (P < 0.001) and sustained VT as the presenting arrhythmia (P = 0.02) were independent predictors of spontaneous VT/VF recurrence. CONCLUSION: Reproducibly inducible VT/VF following ICD implantation predicts a high probability of VT/VF recurrence and identifies a cohort of patients who experience frequent episodes of VT/VF over time. Persistent noninducibility of sustained VT/VF identifies a group of patients who experience no or very few episodes of VT/VF recurrence.     

Noninvasive electrophysiologic study using standard permanent pacemakers in patients with spontaneous sustained ventricular tachycardia or ventricular fibrillation

Permanent pacemakers capable of noninvasive electrophysiologic testing were used to study and treat 26 patients with spontaneous sustained ventricular tachycardia (VT) or fibrillation (VF). One hundred nine episodes of sustained VT or VF were induced in these patients. In 8 patients spontaneous VT was reverted by noninvasive means. Drug changes based on noninvasive testing were made in 12 patients. In the 1- to 67-month follow-up period, drug therapy based on noninvasive electrophysiologic testing was predictive of outcome in patients with spontaneous arrhythmias. Thus, noninvasive electrophysiologic testing using permanent pacemakers is a useful method for studying and treating patients with recurrent sustained ventricular arrhythmias.     

Long-term reproducibility of responses to programmed cardiac stimulation in spontaneous ventricular tachyarrhythmias

Programmed electrical stimulation (PES) of the heart has been used to initiate and terminate ventricular tachyarrhythmias under controlled conditions in patients in whom these arrhythmias have occurred spontaneously. The long-term reproducibility of the response to programmed cardiac stimulation in patients with ventricular arrhythmias is unknown. Seventeen patients with previously documented spontaneously occurring ventricular tachyarrhythmias were evaluated: 5 with nonsustained ventricular tachycardia (VT), 10 with sustained VT and 2 with ventricular fibrillation. The underlying cardiac diagnosis was atherosclerotic coronary heart disease (CAD) in 11 patients, dilated cardiomyopathy in 2 patients, congenital heart disease in 1 patient and no structural heart disease in 3. All patients underwent PES in the absence of antiarrhythmic drug treatment, and patients with inducible VT underwent serial electrophysiologic-pharmacologic testing in an attempt to suppress the arrhythmia. All 17 patients were reexamined with PES at a mean of 18 months (range 2 to 42) after their initial electrophysiologic study, during which time none had a myocardial infarction or intervening cardiac surgery. Repeat electrophysiologic studies, performed in the absence of antiarrhythmic agents, were undertaken because of drug intolerance, availability of new drugs, recurrent arrhythmia or preoperative reevaluation. All 11 patients with CAD had inducible VT on both the first and second electrophysiologic evaluation. Of the 6 patients with no CAD, only 1 had inducible VT on both occasions. Thus, long-term reproducibility of PES-induced VT in patients with stable CAD appears to be high.     

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.     

Programmed ventricular stimulation in mitral valve prolapse: analysis of 36 patients

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.     

Predictive value of ventricular arrhythmia inducibility for subsequent ventricular tachycardia or ventricular fibrillation in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients.

In the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II, implantable cardioverter-defibrillator (ICD)-randomized patients underwent electrophysiologic testing. Both inducible and noninducible patients received an ICD. We correlated inducibility with the occurrence of subsequent ventricular tachycardia (VT) or ventricular fibrillation (VF). Intracardiac ICD electrograms for subsequent events were analyzed to categorize the spontaneous arrhythmia as VT or VF. The two-year Kaplan-Meier event rate for VT in inducible patients was 29.0% versus 19.3% in noninducible patients. However, ICD therapy for spontaneous VF was less common at two years in inducible patients (3.2%) than in noninducible patients (8.6%). In the MADIT II study, inducibility predicted an increased likelihood of VT but decreased VF. OBJECTIVES: We correlated electrophysiologic inducibility with spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II. BACKGROUND: In the MADIT II study, 593 (82%) of 720 implantable cardioverter-defibrillator (ICD) randomized patients underwent electrophysiologic testing. Patients received an ICD whether they were inducible or not. METHODS: A "standard" inducibility definition included sustained monomorphic or polymorphic VT induced with three or fewer extrastimuli or VF induced with two or fewer extrastimuli. We compared a narrow inducibility definition (only monomorphic VT) and a broad definition (standard definition plus VF with three extrastimuli). We used ICD-stored electrograms to categorize spontaneous VT or VF. RESULTS: Inducible patients (standard definition) had a greater likelihood of experiencing ICD therapy for VT than noninducible patients (p = 0.023). Unexpectedly, ICD therapy for spontaneous VF was less common (p = 0.021) in inducible patients than in noninducible patients. The two-year Kaplan-Meier event rate for VT or VF was 29.4% for inducible patients and 25.5% for noninducible patients. Standard inducibility did not predict the combined end point of VT or VF (p = 0.280, by log-rank analysis). The narrow inducibility definition outperformed the standard definition, whereas the broad definition appeared inferior to the standard definition. CONCLUSIONS: In the MADIT II study patients, inducibility was associated with an increased likelihood of VT. Noninducible MADIT II study subjects using this electrophysiologic protocol had a considerable VT event rate and a higher VF event rate than inducible patients. Induction of polymorphic VT or VF, even with double extrastimuli, appears less relevant than induction of monomorphic VT.     

Decline in inducibility of sustained ventricular tachycardia from two to twenty weeks after acute myocardial infarction

To determine temporal evolution of sustained ventricular arrhythmias inducible after acute myocardial infarction (AMI), serial programmed ventricular stimulation (PVS) was performed in 27 patients 15 +/- 4 and 150 +/- 28 days after AMI. These patients did not have worsening of congestive heart failure or angina, coronary artery bypass surgery or spontaneous sustained ventricular tachycardia (VT) in the period between 2 PVS studies. During initial PVS, sustained VT or ventricular fibrillation (VF) was inducible in 17 patients (group I) and was not inducible in 10 (group II). Late PVS in group I induced sustained VT or VF in 8 patients (47%) and nonsustained VT or no VT in 9 (53%). A decrease in late inducibility of sustained VT/VF was greater for arrhythmias induced during initial PVS by triple extrastimuli and burst pacing than for those induced by double extrastimuli (88% vs 25%, p less than 0.04), but appeared to be unrelated to the morphologic characteristics or cycle length of the initially induced sustained VT or VF and to other clinical, hemodynamic or angiographic variables. During late PVS in 10 group II patients, sustained VT or VF remained noninducible in 9 (90% concordance); in 1 patient sustained VT was induced. During a mean follow-up of 14 +/- 5 months since late PVS, none of 27 patients had spontaneous sustained VT and 2 patients in group I died suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias

Twenty-four patients, mean age 42 years, with idiopathic dilated cardiomyopathy (DC) and no history of symptomatic ventricular arrhythmias underwent right ventricular programmed stimulation with up to 3 extrastimuli. Ventricular tachycardia (VT) was induced in 8 patients and ventricular fibrillation (VF) in 2. The VT was unimorphic in 2 and polymorphic in 6. No significant differences were noted between patients in whom arrhythmias were inducible and and those in whom they were not with regard to age, symptomatic class, arrhythmia severity or hemodynamic indexes. Over a mean follow-up of 12 months, 4 patients died, 3 suddenly and 1 with progressive heart failure. Only 1 of the 3 who died suddenly had inducible VT. One other patient with induced sustained unimorphic VT later presented with spontaneous sustained VT similar in rate and configuration to induced VT. In conclusion, VT or VF may be induced in approximately 40% of patients with DC and no history of symptomatic VT or VF. Inducibility of polymorphic VT or VF does not correlate with clinical or hemodynamic variables or with the risk of sudden death. However, induction of unimorphic VT may predict later occurrence of spontaneous unimorphic VT.     

Intolerance and ineffectiveness of mexiletine in patients with serious ventricular arrhythmias

Fifty-one patients were treated with mexiletine over 10.4 +/- 16 months. The clinical arrhythmia in 25 (49%) was ventricular fibrillation (VF), 11 (22%) had sustained ventricular tachycardia (VT), and 15 (29%) had symptomatic nonsustained VT. Ischemic heart disease was present in 33 patients (66%), cardiomyopathy in nine (17%), and valvular or congenital heart disease in nine (17%). Only six (12%) remain on the drug. Arrhythmias recurred in 21 patients (41%): seven (14%) with VF, three (5%) with sustained VT, and 11 (22%) with symptomatic nonsustained VT. Intolerable side effects occurred in another 17 (33%). Seven patients (14%) died from nonarrhythmic-related deaths while taking mexiletine. Mexiletine was combined with a conventional type IA antiarrhythmic agent in 25 patients (49%). In 12 of these 25 patients (48%), ventricular arrhythmias recurred. These findings were not significantly different from those of the group treated with mexiletine alone, where arrhythmias recurred in 9 of 26 patients (35%) (p = NS). Thus mexiletine, alone or in combination with a type IA antiarrhythmic agent, has limited clinical utility in patients with life-threatening ventricular arrhythmias.     

Flecainide: electrophysiologic and antiarrhythmic properties in refractory ventricular tachycardia

Twenty-two patients with coronary artery disease and spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent intracardiac electrophysiologic evaluation and, when possible, ambulatory monitoring before and after therapy with flecainide (mean dose 418 +/- 87 mg [mean +/- standard deviation]). An average of 4 antiarrhythmic agents were used and were unsuccessful before therapy with flecainide was begun. During 64 +/- 16 hours of control Holter monitoring in 16 patients, all had 1 or more salvos of VT, as well as ventricular premature complexes (VPCs). Programmed stimulation during the control period induced VT in 17 of 22 patients. After flecainide therapy, Holter monitoring showed elimination of all forms of VT in all but 1 patient, as well as significant reduction of paired VPCs by 95% (p less than 0.03) and single VPCs by 70% (p less than 0.005). Electrophysiologic study during flecainide therapy showed significant increases in AH, HV, PR, QRS and QTc intervals, and the ventricular effective refractory period. Programmed stimulation in 17 patients taking flecainide, with a mean plasma level of 1,075 +/- 521 ng/ml, showed ablation of inducible VT in only 2 patients, a worsening in 5 and continued VT inducibility in 10. Adverse effects that required drug withdrawal were infrequent and encountered in patients who received higher drug levels: 1 patient with congestive heart failure and 1 with severe sinus bradycardia. Thus, although flecainide suppresses complex ventricular arrhythmias on Holter recordings, it rarely alters the response to programmed stimulation. Caution is recommended in its use for recurrent sustained VT or VF and in the interpretation of electrophysiologic studies until the predictive value of programmed stimulation with flecainide therapy is established.     

Prediction of response to class I antiarrhythmic drugs during electrophysiologic study of ventricular tachycardia

We have retrospectively examined data from 41 patients studied in our laboratory for symptomatic ventricular arrhythmia in order to test whether any clinical or electrophysiologic variables could be identified which would predict the patient's response to class I antiarrhythmic drugs. All patients had (1) clinically documented paroxysmal sustained ventricular tachycardia (VT) or ventricular fibrillation remote from acute myocardial infarction, (2) inducible sustained VT during control electrophysiologic study (EPS), and (3) EPS after one or more of the following class I antiarrhythmic drugs: intravenous procainamide (36 patients), oral quinidine (30 patients), and oral disopyramide (36 patients). Initially, patients were divided into those who had noninducible or only nonsustained VT after any of the tested drugs (responders), and those who continued to have inducible sustained VT after all tested drugs (nonresponders). A logistic regression technique demonstrated no independent contribution to drug response by any of the following variables: sex, arteriosclerotic heart disease, cardiomegaly, age, time since the initial episode of VT, and cycle length of VT during control study. The number of antiarrhythmic drugs the patient had received prior to study was found to be a significant independent contributor (p < 0.03), with responders having received an average of 2.5 drugs compared with 4.2 for nonresponders. In addition to the logistic regression, 12 other clinical and electrophysiologic variables were not predictors of drug response. The question was also asked, “Does response or nonresponse to one class I drug predict response or nonresponse to the others?” Significant concordance of response and nonresponse was demonstrated for procainamide and quinidine, but not for either of these drugs and disopyramide. Drug therapy for inducible sustained VT therefore remains empiric.     

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.     

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)     

Suppression of sustained ventricular tachyarrhythmias: a comparison of d,l-sotalol with no antiarrhythmic drug treatment

Objectives. This study evaluates the clinical efficacy of d,l-sotalol in patients with sustained ventricular tachyarrhythmias.Background. D,l-sotalol is an important antiarrhythmic agent to prevent recurrences of sustained ventricular tachyarrhythmias (VT/VF). However, evidence is lacking that an antiarrhythmic agent like d,l-sotalol can reduce the incidence of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.Methods. A prospective study was performed in 146 consecutive patients with inducible sustained ventricular tachycardia or ventricular fibrillation. In 53 patients, oral d,l-sotalol prevented induction of VT/VF during electrophysiological testing and patients were discharged on oral d,l-sotalol (sotalol group). In 93 patients, VT/VF remained inducible and a defibrillator (ICD) was implanted. After implantation of the device patients were randomly assigned to oral treatment with d,l-sotalol (ICD/sotalol group, n = 46) or no antiarrhythmic medication (n = 47, ICD-only group).Results. During follow-up, 25 patients (53.2%) in the ICD-only group had a VT/VF recurrence in comparison to 15 patients (28.3%) in the sotalol group and 15 patients (32.6%) in the ICD/sotalol group (p = 0.0013). Therapy with d,l-sotalol, amiodarone or metoprolol was instituted in 12 patients (25.5%) of the ICD-only group due to frequent VT/VF recurrences or symptomatic supraventricular tachyarrhythmias. In nine patients, 17% of the sotalol group, an ICD was implanted after VT/VF recurrence, three patients (5.7%) received amiodarone. Total mortality was not different between the three groups.Conclusions. D,l-sotalol significantly reduces the incidence of recurrences of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.