Prognostic significance of sustained monomorphic ventricular tachycardia induced by programmed ventricular stimulation using up to triple extrastimuli in survivors of acute myocardial infarction

The prognostic significance of sustained monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation using up to 3 extrastimuli was evaluated in 133 consecutive survivors of acute myocardial infarction (AMI) at a mean interval of 1.8 +/- 1.1 months after onset. This was compared with hemodynamic and angiographic abnormalities shown by cardiac catheterization and ventricular ectopic activity detected by Holter monitoring. Sustained monomorphic VT was induced in 25 (19%) patients, sustained polymorphic VT in 11 (8%) patients, nonsustained monomorphic VT (greater than or equal to 10 beats) in 12 patients (9%) and nonsustained polymorphic VT in 9 patients (7%). Multivariate logistic regression analysis of clinical, angiographic, hemodynamic and electrocardiographic variables showed that the presence of a left ventricular aneurysm (p = 0.005) and Lown grade 4B ventricular ectopic activity (p less than 0.001) were independent predictors of inducibility of sustained monomorphic VT. During a mean follow-up of 21 +/- 13 months, there were 8 (6%) sudden cardiac deaths and 3 (2.3%) spontaneous occurrences of life-threatening sustained VT. The 2-year probability of freedom from sudden cardiac death or sustained ventricular tachyarrhythmias was 53 +/- 13% for patients with inducible sustained monomorphic VT, 70 +/- 10% for those with a left ventricular ejection fraction less than 40% and 58 +/- 13% for those with Lown grade 4B ventricular ectopic activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.     

Risk stratification and prognosis of patients treated with amiodarone for malignant ventricular tachyarrhythmias after myocardial infarction

Summary Seventy-seven consecutive patients (mean age 62 years) with episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) after acute myocardial infarction (AMI) were evaluated to assess the long-term efficacy of first-line amiodarone treatment and to identify clinical and laboratory factors associated with a high risk of death or arrhythmia recurrence. The presenting arrhythmia was VT in 41 cases (53%) and VF in 36 (47%). VT or VF occurred between the 4th and 90th day after AMI in 45 cases (58%) and later (more than 90 days) in the remaining 32 (42%). The mean number of arrhythmic episodes was 4.2. Forty patients (52%) were in New York Heart Association (NYHA) class I or II, and 37 (48%) were in class III or IV. Mean left ventricular ejection fraction was 32%; ventricular aneurysm was present in 41 subjects. Most patients had multivessel coronary artery disease. Amiodarone was administered as a first-choice drug in all patients, in combination with other antiarrhythmic drugs in 14. By ventricular stimulation after loading doses of amiodarone, sustained VT was inducible in 46 (62%) and noninducible in 28 (38%). During a mean follow-up of 28 months the incidence of cardiac mortality at 1, 3, and 5 years was 21%, 37%, and 47%; of sudden death was 7%, 19%, and 23%; of nonfatal VT recurrence was 13%, 13%, and 24%, respectively. The overall incidence of amiodarone side effects was 35%. Factors independently associated with mortality for all causes and cardiac mortality included NYHA class III or IV (p<0,01), ejection fraction -35% (p<0,01), and age -65 years (p=0,03). History of cardiac arrest was a weak predictor only by univariate analysis (p=0.05). No single variable was consistently related to an increased risk of sudden death and nonfatal VT recurrence, not even inducibility of sustained VT during electropharmacologic studies (18% of incidence in responders and 30% in nonresponders, p = ns). In this study, amiodarone treatment of patients with life-threatening ventricular tachyarrhythmias after myocardial infarction confirmed its beneficial, but not uniform, efficacy. Severe left ventricular dysfunction, age, and, less significantly, history of cardiac arrest, were independent predictors of death. Identification of patients at high risk of arrhythmia recurrence and sudden death remains undefined during amiodarone treatment.     

Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy.

OBJECTIVES: The aim of this study was to evaluate the survival of patients with hypertrophic cardiomyopathy (HCM) after resuscitated ventricular fibrillation or syncopal sustained ventricular tachycardia (VT/VF) when treated with low dose amiodarone or implantable cardioverter defibrillators (ICDs). BACKGROUND: Prospective data on clinical outcome in patients with HCM who survive a cardiac arrest are limited, but studies conducted before the widespread use of amiodarone and/or ICD therapy suggest that over a third die within seven years from sudden cardiac death or progressive heart failure. METHODS: Sixteen HCM patients with a history of VT/VF (nine male, age at VT/VF 19 +/- 8 years [range 10 to 36]) were studied. Syncopal sustained ventricular tachycardia/ventricular fibrillation occurred during or immediately after exertion in eight patients and was the initial presentation in eight. One patient had disabling neurologic deficit after VT/VF. Before VT/VF, two patients had angina, four had syncope and six had a family history of premature sudden cardiac death. After VT/VF all patients were in New York Heart Association class I or II, three had nonsustained VT during ambulatory electrocardiography and 11 had an abnormal exercise blood pressure response. After VT/VF eight patients were treated with low dose amiodarone and six received an ICD. Prophylactic therapy was declined by two patients. RESULTS: Mean follow-up was 6.1 +/- 4.0 years (range 0.5 to 14.5). Cumulative survival (death or ICD discharge) for the entire cohort was 59% at five years (95% confidence interval: 33% to 84%). Thirteen (81%) patients were alive at last follow-up. Two patients died suddenly while taking low dose amiodarone, and one died due to neurologic complications of his initial cardiac arrest. Three patients had one or more appropriate ICD discharges during follow-up; the times to first shock after ICD implantation were 23, 197 and 1,124 days. CONCLUSIONS: This study shows that patients with HCM who survive an episode of VT/VF remain at risk for a recurrent event. Implantable cardioverter defibrillator therapy appears to offer the best potential benefit regarding outcome.     

Incidence and timing of recurrences of sudden death and ventricular tachycardia during antiarrhythmic drug treatment after myocardial infarction.

Incidence and timing of recurrences of sustained ventricular tachycardia (VT) or sudden death were studied in 206 patients who survived their first episode of ventricular fibrillation (VF; n = 52) or sustained VT (n = 154) after myocardial infarction. All patients were treated with (empirically selected) antiarrhythmic drugs; 49% received amiodarone. After a mean follow-up of 36 months, 64 patients (41%) in the VT group and 10 (19%) in the VF group had nonfatal VT recurrences. Sudden death occurred in 22 (14%) and 9 (17%) patients in the VT and VF groups, respectively. Incidence of sudden death had 2 peaks at approximately 3 and 12 months. Nonfatal VT recurrences were more frequent (most often occurring in first 6 months) in the VT than in the VF group. Sudden death occurred during the following 3 years in only 10% of patients who survived 1 year. There was a much higher incidence of sudden death in patients with left ventricular ejection fraction (LVEF) less than or equal to 40% than in those with LVEF greater than 40% (28 of 65 vs 3 of 141; p less than 0.0001), but no relation between LVEF and nonfatal VT recurrences.     

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.     

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)     

Management of refractory sustained ventricular tachycardia with amiodarone: a reappraisal

We examined the value of clinical variables, chronic 24-hour ambulatory ECG monitoring, and chronic electrophysiologic (EP) testing in 49 patients with recurrent and refractory sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) treated with chronic oral amiodarone in order to develop a prospective approach to the management of these patients. All patients underwent control EP studies followed by continuous telemetric cardiac monitoring during oral amiodarone administration (mean duration 29 +/- 6 days, mean dose 739 +/- 230 mg). Follow-up 24-hour ambulatory ECG monitoring and EP studies were performed. Thirty VT recurrences occurred in the first 4 weeks of amiodarone therapy (total incidence, 61%), with the majority (55%) in the first 3 weeks of treatment. During long-term follow-up (1 to 42, mean 15 +/- 12 months), there were 12 symptomatic VT/VF recurrences (incidence 24%). There was a higher incidence of VT recurrences if patients had inducible sustained or nonsustained VT at chronic EP study (p less than 0.01), or complex ventricular arrhythmias on ambulatory ECG monitoring (p less than 0.05). The sensitivity, specificity, and predictive accuracy of chronic EP testing and 24-hour ambulatory ECG monitoring were 100%, 35%, and 51%, and 58%, 84%, and 78%, respectively. Chronic EP testing correctly identified all patients who had their arrhythmia suppressed by amiodarone on long-term follow-up, while 42% of all VT recurrences occurred in patients without complex ventricular arrhythmias on 24-hour ambulatory ECG monitor.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Prognostic determinants in hypertrophic cardiomyopathy. Prospective evaluation of a therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings.

BACKGROUND. Patients with hypertrophic cardiomyopathy (HCM) frequently have arrhythmias and hemodynamic abnormalities and are prone to sudden death and syncope. An important need exists for improved risk stratification and definition of appropriate investigation and therapy. METHODS AND RESULTS. The relation of 31 clinical, Holter, cardiac catheterization, and electrophysiological (EP) variables to subsequent cardiac events in 230 HCM patients was examined by multivariate analysis. Studies were for cardiac arrest (n = 32), syncope (n = 80), presyncope (n = 52), ventricular tachycardia (VT) on Holter (n = 36), a strong family history of sudden death (n = 9), and palpitations (n = 21). Nonsustained VT on Holter was present in 115 patients (50%). Sustained ventricular arrhythmia was induced in 82 patients (36%). Seventeen cardiac events (eight sudden deaths, one cardiac arrest, and eight syncope with defibrillator discharges) occurred during a follow-up of 28 +/- 19 months. The 1-year and 5-year event-free rates were 99% and 79%, respectively. Two variables were significant independent predictors of subsequent events: sustained ventricular arrhythmia induced at EP study (beta, 3.5; p = 0.002) and a history of cardiac arrest or syncope (beta, 2.9; p less than 0.05). Only two of 66 patients without symptoms of impaired consciousness had a cardiac event (3-year event-free rate, 97%). In contrast, nonsustained VT on Holter was associated with a worse prognosis only in patients with symptoms of impaired consciousness: 11 of 79 symptomatic patients with VT on Holter (14%) had events versus only four of 85 symptomatic patients without VT on Holter (5%) (p = 0.057). Notably, none of 51 patients without symptoms of impaired consciousness in whom VT was not induced at EP study had a cardiac event. CONCLUSIONS. In HCM, VT on Holter is of benign prognostic significance in the absence of symptoms of impaired consciousness and inducible VT, and sustained VT induced at EP study, especially when associated with cardiac arrest or syncope, identifies a subgroup at high risk for subsequent cardiac events.     

Prognostic factors in nonsustained ventricular tachycardia

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction ≤0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction ≤0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction > 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction ?0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.     

Long-term results of amiodarone therapy in patients with recurrent sustained ventricular tachycardia or ventricular fibrillation

Four hundred sixty-two patients, all with either documented spontaneous sustained ventricular tachycardia or cardiac arrest unresponsive to other antiarrhythmic drugs (2.6/patient), were treated with amiodarone. Thirty-five patients (7.6%) failed to respond or died during the initial oral or intravenous loading phase. The remaining 427 patients were discharged on treatment with oral amiodarone and followed up for up to 98 months. Recurrence of ventricular tachycardia or sudden cardiac death at 1, 3 and 5 years by life-table analysis was 19%, 33% and 43%, respectively, for patients discharged on amiodarone therapy. The sudden cardiac death rate was 9%, 15% and 21%, respectively, at 1, 3 and 5 years. Side effects were reported by 45% of patients after 1 year, by 61% after 2 years and by 86% after 5 years. Amiodarone was discontinued because of side effects in 14%, 26% and 37% of patients after 1, 3 and 5 years, respectively. Incidence rates of recurrence of arrhythmia, sudden cardiac death and side effects were highest in the early months and then decreased. By multivariate analysis, advanced age, low ejection fraction and a history of cardiac arrest were independent risk factors for sudden cardiac death during amiodarone therapy.     

Prognosis of patients with sustained ventricular tachycardia and of survivors of cardiac arrest not inducible by programmed stimulation.

The aim of this study was to analyze the long-term clinical outcome of 60 prospectively studied patients with documented sustained ventricular tachyarrhythmia that was not inducible during baseline programmed ventricular stimulation: 39 with cardiac arrest due to noninfarction ventricular fibrillation (VF) and 21 with mild hemodynamically compromising sustained ventricular tachycardia (VT). Left ventricular ejection fraction was 55 +/- 14% in the VF group and 50 +/- 13% in the VT group (difference not significant). Patients were discharged without conventional antiarrhythmic drugs and received only empirical beta-blocker therapy. During a mean follow-up period of 21 +/- 16 months (mean +/- SD), 10 of 60 patients (17%) died suddenly. The actuarial incidence of sudden death at 1 and 4 years was similar in both groups (VF group, 10 and 20%; VT group, 16 and 16%) (p = 0.48). The actuarial incidence of sudden cardiac death was significantly higher in patients with left ventricular ejection fraction < or = 40% than in those with > 40% (1-year incidence in VF group, 40 vs 0%; VT group, 50 vs 0%) (p = 0.005 and p = 0.01, respectively). Multivariate regression analysis identified left ventricular ejection fraction < or = 40% and previous myocardial infarction as the only independent predictor of sudden cardiac death. The occurrence of frequent ventricular pairs during Holter monitoring was the only independent predictor of sustained VT recurrences. It is concluded that patients with sustained ventricular tachyarrhythmia in whom arrhythmia was non-inducible during baseline ventricular stimulation and not treated with antiarrhythmic therapy have a favorable outcome if left ventricular ejection fraction is high.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic assessment of survivors of ventricular tachycardia and ventricular fibrillation with ambulatory monitoring

The ability to assess prognosis in patients with serious ventricular arrhythmias treated with antiarrhythmic drugs by the degree of complexity on the 24-hour ambulatory electrocardiogram was evaluated in 59 survivors of ventricular tachycardia (VT) and ventricular fibrillation. After conventional therapy had failed, patients were treated with investigational drugs until symptomatic VT was abolished. A Holter monitor recording, obtained once the therapeutic regimen was established, was graded for the presence or absence of asymptomatic VT. Fifty-two patients were asymptomatic at discharge and were followed for 700 days. Of 44 patients followed for 1 year, none had recurrent syncope or died if asymptomatic VT was absent at 1 month (p <0.002). After 700 days, 27 patients (82%) without asymptomatic VT at 1 month were doing well, compared with 11 patients (58%) with asymptomatic VT at 1 month (p <0.002). In patients at risk for sudden cardiac arrest, early abolition of asymptomatic VT on ambulatory monitoring can be used to predict a good long-term clinical response.     

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.     

Implantable defibrillator event rates in patients with idiopathic dilated cardiomyopathy, nonsustained ventricular tachycardia on Holter and a left ventricular ejection fraction below 30%

OBJECTIVES: This study investigated the incidence of appropriate implantable cardioverter defibrillator (ICD) interventions for ventricular tachycardia (VT) or ventricular fibrillation (VF) in patients with idiopathic dilated cardiomyopathy (IDC) and nonsustained VT in the presence of a left ventricular ejection fraction below 30%, versus in patients with syncope and patients with a history of VT or VF. BACKGROUND: To date, only limited information is available about the prophylactic use of ICDs in patients with IDC. METHODS: From January 1993 to July 2000, 101 patients with IDC underwent implantation of ICDs with electrogram storage capability at our institution. Patients were placed into one of three groups according to their clinical presentation: asymptomatic or mildly symptomatic nonsustained VT in the presence of a left ventricular ejection fraction < or = 30% (49 patients, prophylactic group), unexplained syncope or near syncope (26 patients, syncope group) and a history of sustained VT or VF (26 patients, VT/VF group). RESULTS: During 36 +/- 22 months follow-up, 18 of 49 patients (37%) in the prophylactic group received appropriate shocks for VT or VF, compared with 8 of 26 patients (31%) in the syncope group and with 9 of 26 patients (35%) of the VT/VF group. Multivariate Cox analysis of baseline clinical variables identified left ventricular ejection fraction, atrial fibrillation and a history of sustained VT or VF as predictors for appropriate ICD interventions during follow-up. CONCLUSIONS: Patients with IDC and prophylactic ICD implantation for nonsustained VT in the presence of a left ventricular ejection fraction < or = 30% had an incidence of appropriate ICD interventions similar to that of patients with a history of syncope or sustained VT or VF. These findings indicate that ICDs may have a role in not only secondary but also primary prevention of sudden death in IDC.     

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.     

Prognostic value of early electrophysiologic studies for ventricular tachycardia recurrence in patients with coronary artery disease treated with amiodarone

Amiodarone was used in 86 patients with ventricular tachycardia (VT) (67 patients) or ventricular fibrillation (19 patients) secondary to coronary artery disease. The mean +/- standard deviation left ventricular ejection fraction was 30 +/- 12% (range 8 to 65%). Prior trials with 4 +/- 1.2 alternate antiarrhythmic agents had been unsuccessful. Amiodarone was loaded at dosages of 1,200 to 1,800 mg/day, with maintenance dosages of 400 to 600 mg/day. Drug efficacy was evaluated by programmed stimulation at 10 to 14 days in 68 patients. In 38 patients sustained VT or ventricular fibrillation was inducible (group I), whereas 30 patients (group II) had either no inducible VT (8) or had nonsustained VT induced (22). Holter monitoring was used to assess drug efficacy in 18 patients (group III). All patients were evaluated at 3- to 6-month intervals with Holter monitors for efficacy and a standard protocol for toxicity. During a long-term follow-up of 18 +/- 16 months, sudden death occurred in 5 patients and nonfatal arrhythmia recurrences were detected in 16. The actuarial probability of freedom from fatal and nonfatal arrhythmia recurrences at 24 months was 0.52 for group I, 0.97 for group II and 0.68 for group III. The mode of induction, rate change or hemodynamic tolerance of the induced ventricular tachycardia did not predict arrhythmia recurrence. Among the clinical variables analyzed, only an ejection fraction of less than or equal to 30% was identified as a significant predictor of arrhythmia recurrence. Nonsudden cardiac death occurred in 21 patients, including 19 from heart failure and 2 from myocardial infarction. Noncardiac death occurred in 7 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of a serial electropharmacologic study in survivors of a cardiac arrest secondary to ventricular tachycardia or ventricular fibrillation

Electrophysiologic studies were performed in 10 patients (8 M, 2 F, mean age: 60.2 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. The cardiac arrest had always been sudden and unexpected. It occurred outside the hospital in 7 cases and in the hospital in 3 cases. Patients in whom cardiac arrest was associated with evidence of acute myocardial infarction were excluded from the study. Nine of the patients were suffering from chronic ischemic heart disease with 1 or more previous myocardial infarctions while 1 had no evidence of organic heart disease. A ventricular aneurysm was present in 4 of them. During control electrophysiologic study a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths + bursts of rapid ventricular pacing) in 9 of the 10 patients (90%) and a non sustained VT was induced in 1 of them (10%). In 3 patients (30%) VT could be initiated only by right ventricular stimulation at a site different from the apex (outflow tract). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in 6 of the 9 patients (66.7%) who underwent this procedure and a partially effective drug regimen (sustained VT no longer inducible, easier to interrupt and considerably slower) was found in 2 patients (22.2%). None of the patients who received a chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14.8 months (range: 3-29) and only 1 had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of the follow-up. It is also noteworthy that amiodarone, alone or in combination, was given chronically to 6 of our patients (60%). These results 1) indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest, and 2) suggest that amiodarone may be effective in preventing sudden death in these patients.