Amiodarone in heart insufficiency]

The purpose of this study was to analyse the effects of amiodarone on the treatment of cardiac failure. The effects of 200 mg/day of amiodarone were assessed in 18 patients with a history of cardiac failure. Functional class, heart rate, blood pressure, left ventricular ejection fraction, heart size, treadmill exercise tolerance and electrocardiogram were assessed before and eight weeks after the use of amiodarone, and the side effects were monitored. In 18 patients receiving amiodarone, the functional class and heart rate decreased significantly (p < 0.05) from 2.7 +/- 0.4 to 1.2 +/- 0.4 and 103 +/- 15 to 69 +/- 8.5 beats/min respectively. The ejection fraction and the exercise tolerance increased significantly (p < 0.05) from 29.2 +/- 5.5% to 41.5% and from 379.8 +/- 271 sec to 897.8 +/- 350.8 sec respectively. The incidence of atrial and ventricular arrhythmias decreased significantly and no side effects were observed. Amiodarone appears to produce benefits in patients with cardiac failure with atrial and ventricular arrhythmias.     

Effectiveness of amiodarone on ventricular arrhythmias during and after acute myocardial infarction

A randomized, placebo-controlled study examined the effect of amiodarone on the incidence of ventricular arrhythmias after acute myocardial infarction (AMI). Two hundred patients with AMI were randomized to receive amiodarone, 200 mg every 8 hours for 1 month, followed by 200 mg/day, or placebo, starting 48 hours after the onset of chest pain. Twenty-four-hour Holter monitoring was performed on day 1, repeated after 8 days and subsequently at 3-month intervals. One hundred seventy-two patients were followed for 6 to 42 months and monitor data were available at 6 to 9 months in 129 patients. Amiodarone was well tolerated, with no serious side effects; 12 patients were withdrawn from therapy. At 6 to 9 months more than 1 ventricular premature complex per hour was present in 3 of the 59 amiodarone-treated patients (5%) and 24 of the 70 placebo-treated patients (34%) (p less than 0.02). Complex arrhythmias (multifocal, early cycle, repetitive, bigeminy, trigeminy or ventricular tachycardia) were present in 5 of 59 of the amiodarone-treated patients (8%) and 20 of 70 placebo-treated patients (28%) (p less than 0.005). Sixteen patients in the amiodarone group and 11 in the placebo group died (difference not significant). Thus, amiodarone can reduce the frequency and complexity of ventricular arrhythmias after AMI, but it is unlikely that this will result in a substantial beneficial effect on post-AMI mortality risk.     

Hemodynamics during chronic amiodarone administration in Japanese patients with idiopathic dilated cardiomyopathy and ventricular arrhythmia: a retrospective study

OBJECTIVES: Nonischemic heart disease, especially idiopathic dilated cardiomyopathy, is relatively common among Japanese patients receiving amiodarone for concomitant ventricular arrhythmia, but the hemodynamic effects of amiodarone in these Japanese patients are unclear. The hemodynamic changes during chronic amiodarone administration were retrospectively studied in patients with idiopathic dilated cardiomyopathy and ventricular arrhythmia. METHODS: Fifty-two patients [42 males, 10 females, 53 +/- 2 years (mean age +/- SE)] with ventricular tachyarrhythmia and idiopathic dilated cardiomyopathy with left ventricular ejection fraction of 27 +/- 1% (mean +/- SE) were treated with 200-400 mg daily of oral amiodarone as the loading dose for the initial 14 days and 100-200 mg daily maintenance dose for a further 6 months. No patients were taking beta-blockers or positive inotropic drugs. Echocardiographic examination was performed before (baseline), at week 2 and at month 6 of amiodarone therapy. Twenty four-hour Holter monitoring during the same time period was also performed in 34 patients. Seventeen patients underwent right heart catheterization before and at week 2. RESULTS: Echocardiographic measurements showed no significant change in left ventricular end-diastolic dimension, although there was a slight increase in fractional shortening from 16 +/- 1% to 19 +/- 1% (p < 0.05) and 18 +/- 1% (mean +/- SE) (p < 0.01) at week 2 and month 6 of amiodarone therapy, respectively. Amiodarone markedly reduced the mean heart rate and the frequency of premature ventricular complexes on ambulatory monitoring. The cardiac index did not change and the pulmonary capillary wedge pressure tended to decrease slightly at week 2 in the 17 patients who underwent catheterization. CONCLUSIONS: This retrospective study showed no worsening of the hemodynamic state during chronic amiodarone administration in Japanese patients with idiopathic dilated cardiomyopathy and ventricular arrhythmia.     

Antiadrenergic effect of chronic amiodarone therapy in human heart failure.

OBJECTIVES: The aim of the present study was to evaluate the influence of amiodarone on neurochemical parameters of sympathetic nervous activity in patients with congestive heart failure. BACKGROUND: Unlike most antiarrhythmic agents, amiodarone has been shown to exert a beneficial effect on survival in some studies of patients with congestive heart failure. The pharmacology of this agent is complex, and as such, the mode of its action is unclear in humans. Some experimental studies suggest that amiodarone exerts a sympatholytic effect. METHODS: To evaluate the effect of amiodarone on sympathetic nervous activity, we measured the total systemic and cardiac norepinephrine (NE) spillover rate by isotope dilution in 58 patients with severe heart failure (left ventricular ejection fraction 20 +/- 1%), 22 of whom were receiving chronic amiodarone treatment. Release rates for dihydroxyphenylalanine (DOPA, a precursor of NE), and endogenous and radiolabeled dihydroxyphenylglycol (DHPG and 3H-DHPG, intraneuronal metabolites of NE and 3H-NE, respectively) were also determined to assess sympathetic neuronal integrity. RESULTS: Amiodarone-treated patients had significantly lower cardiac spillover rates for NE (42%, p = 0.001), DOPA (74%, p < 0.001), DHPG (44%, p < 0.01) and 3H-DHPG (51%, p < 0.01) than those patients not treated with amiodarone. Hemodynamic assessment of amiodarone-treated patients revealed higher cardiac output (4.4 +/- 0.2 vs. 3.7 +/- 0.2 liters/min, p < 0.01), and slightly lower pulmonary capillary wedge pressure (18 +/- 2 vs. 22 +/- 1, p = NS) than in untreated patients. After correction for the potential confounding effect of hemodynamic differences, amiodarone-treated patients continued to demonstrate significantly lower spillover rates of NE, DOPA and DHPG from the heart. CONCLUSIONS: These data indicate that amiodarone may exert beneficial effects on the failing human heart through a sympatholytic process, and this action appears to be relatively cardioselective.     

Amiodarone is safe and highly effective therapy for supraventricular tachycardia in infants

BACKGROUND: The clinical effectiveness of amiodarone must be weighed against the likelihood of adverse effects. Adverse effects are less common in children than in adults, yet there have been no large studies assessing the efficacy and safety of amiodarone in the first 9 months of life. We sought to assess the safety and efficacy of amiodarone as primary therapy for supraventricular tachycardia in infancy. METHODS: We evaluated the clinical course of 50 consecutive infants and neonates (1.0+/-1.5 months, 35 male) treated with amiodarone for supraventricular tachyarrhythmias between July 1994 and July 1999. At presentation, congenital heart disease, congestive heart failure, or ventricular dysfunction were present in 24%, 36%, and 44% of the infants, respectively. Infants received a 7- to 10-day load of amiodarone at either 10 or 20 mg/kg/d. If this failed to control the arrhythmia, oral propranolol (2 mg/kg/d) was added. Patients were followed up for 16.0+/-13.0 months, and antiarrhythmic drugs were discontinued as tolerated. RESULTS: Rhythm control was achieved in all patients. Of the 34 patients who have reached 1 year of age, 23 (68%) have remained free of arrhythmia, despite discontinuation of propranolol and amiodarone. Growth and development remained normal for age. Higher loading doses of amiodarone were associated with an increase in the corrected QT interval, but no proarrhythmia was seen. There were no side effects necessitating drug withdrawal. CONCLUSIONS: Amiodarone is an effective and safe therapy for tachycardia control in infancy.     

参附益心颗粒治疗充血性心力衰竭患者室性心律失常的临床观察

目的观察参附益心颗粒治疗充血性心力衰竭(CHF)室性心律失常(VA)的临床疗效和安全性。方法选择心功能Ⅱ级～Ⅳ级的CHF合并VA的住院患者105例,随机分为两组。A组56例,给予参附益心颗粒每次6g～12g,3次/日。B组49例,给予胺碘酮,第一周为每次0.2g,3次/日,之后逐渐减量至每次0.2g,1次/日,观察期4周。在试验开始和第四周末分别检测动态心电图和其他实验室检查,并观察试验期内两组出现的副反应。结果两组控制VA的总有效率分别是83.33%和84.44%(P>0.05);副反应的发生率则分别是7.41%和20.00%(P<0.05)。结论参附益心颗粒可以控制CHF合并VA,其临床疗效初步判断与胺碘酮相仿,但副反应的发生率则显著低于后者。     

Electrophysiologically guided amiodarone therapy versus the implantable cardioverter-defibrillator for sustained ventricular tachyarrhythmias after myocardial infarction: results of long-term follow-up

OBJECTIVES: We sought to compare the long-term survival rates of patients with sustained ventricular tachyarrhythmia after myocardial infarction (MI) who were treated according to the results of electrophysiological (EP) study either with amiodarone or an implantable cardioverter-defibrillator (ICD). BACKGROUND: Patients with sustained ventricular tachyarrhythmias after MI are at high risk of sudden cardiac death (SCD). However, data comparing the long-term survival rates of patients treated with amiodarone or ICD, according to the results of EP testing, are lacking. METHODS: Patients underwent a first EP study at baseline and a second one after a loading dose of amiodarone of 14 +/- 2.9 g. According to the results of the second EP study, patients were classified either as responders or non-responders to amiodarone; non-responders were eventually treated with an ICD. RESULTS: Eighty-four consecutive patients with MI (78 men; 21-77 years old; mean left ventricular (LV) ejection fraction 36 +/- 11%) were consecutively included. Forty-three patients (51%) were responders, and 41 patients (49%) were non-responders to amiodarone therapy. During a mean follow-up period of 63 +/- 30 months, SCD and total mortality rates were significantly higher in the amiodarone-treated patients (p = 0.03 and 0.02, respectively). CONCLUSIONS: The long-term survival of patients with sustained ventricular tachyarrhythmias after MI, with depressed LV function, is significantly better with an ICD than with amiodarone therapy, even when stratified according to the results of the EP study. These patients should benefit from early ICD placement, and any previous amiodarone treatment seems to have no additional value.     

Development of congestive heart failure and alterations in left ventricular function in patients with sustained ventricular tachyarrhythmias treated with amiodarone

The interaction between the efficacy and tolerance of amiodarone and the degree of left ventricular (LV) dysfunction was assessed in 126 patients with sustained ventricular tachyarrhythmias. In all patients radionuclide angiographic LV ejection fraction (EF) was measured before and after 8 to 12 months of amiodarone therapy. At baseline mean EF was 25 +/- 13% and 86 patients had an EF of 30% or less. In patients receiving amiodarone at steady state, there was a small but significant increase in EF (23 to 26%, p less than 0.05). Congestive heart failure (CHF) was present in 43 patients before amiodarone therapy. In 16 patients new (9 patients) or worsened (7 patients) CHF developed during the first year of amiodarone therapy. Development of CHF was not consistently related to a change in EF or heart rate. The clinical efficacy and tolerance of amiodarone were affected by the baseline EF and development of CHF. Efficacy and tolerance was 80% in patients with an EF of more than 30% and 60% in those with an EF of 30% or less. Among the 16 patients in whom new or worsened CHF developed, 6 (38%) died and 9 (56%) had recurrent ventricular tachyarrhythmias. Both baseline EF and development of CHF during amiodarone treatment significantly affect the prognosis in patients with ventricular tachyarrhythmias.     

Cardiac function in patients on chronic amiodarone therapy

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.     

Mexiletine: long-term efficacy and hemodynamic actions in patients with ventricular arrhythmia

Fifty-one patients with symptomatic ventricular tachycardia who failed control on current anti-arrhythmics were studied. Seventy-four percent had ischemic heart disease and 81% had congestive heart failure. Patients underwent serial 24 Holter recordings and radionuclide ventriculography before, during dose titration and during long-term mexiletine therapy. Twenty-eight patients (55%) were successfully controlled. Of these, 17 (33%) remained controlled greater than or equal to 1 year. Early and late side effects were common but benign and included mostly gastric pain and nausea. Twenty-eight patients underwent radionuclide ventriculography before and during mexiletine therapy: there was no significant difference in heart rate, blood pressure, left ventricular ejection fraction, stroke volume and end-diastolic volumes before and during mexiletine. Left ventricular ejection fraction was 21.4 +/- 2.2%, (SD) and 21.3 +/- 2.2% (SD) before and during mexiletine respectively. Digoxin blood levels measured in 15 patients were not significantly changed by mexiletine. In conclusion, mexiletine is effective and safe in many patients with intractable ventricular tachycardia. It has no significant hemodynamic effects even in patients with congestive heart failure nor does it affect digoxin blood levels. Its usefulness is limited by a high incidence of gastric intolerance.     

Mexiletine: double-blind comparison with procainamide in PVC suppression and open-label sequential comparison with amiodarone in life-threatening ventricular arrhythmias

The antiarrhythmic effects of mexiletine (n = 14) were compared to procainamide (n = 16) by a double-blind parallel protocol in 30 patients (group I) with frequent premature ventricular contractions (PVCs) (greater than 20/hr), and to amiodarone by an open-label sequential approach in 25 patients (mean left ventricular ejection fraction of 32.6 +/- 13.4%) with life-threatening ventricular arrhythmias (group II) resistant to two or more conventional agents. The predetermined end point of therapy in group I patients was met in 6 of 14 (43%) given mexiletine, with 7 (50%) requiring drug discontinuation for severe gastrointestinal or central nervous system side effects and only 3 of 16 patients (19%) given procainamide, with 5 (31%) developing limiting side effects. Increases in dose led to a higher efficacy rate for PVC suppression with a corresponding increase in side effects with mexiletine; with procainamide, the higher dose was not associated with greater PVC suppression. In group II patients, mexiletine was effective in 4 (16%), with one patient discontinuing the drug during long-term therapy; mexiletine was ineffective in 16 (64%) and early side effects developed in 5 (20%). Patients not responding to or not tolerating mexiletine were given amiodarone; 20 of 21 (95%) responded with arrhythmia control after the loading dose. During a mean follow-up period of 2 years, sudden death occurred in two patients, death from heart failure in two, and death from subarachnoid hemorrhage in one patient; 15 (75%) patients are alive and free of arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias

Efficacy, side effects and predictors of response for intravenous amiodarone were evaluated in 46 patients with recurrent drug-refractory sustained ventricular tachycardia or ventricular fibrillation, or both, who were treated with intravenous amiodarone. Of the 46 patients, 27 (58.5%) responded early to intravenous amiodarone and 6 (13%) showed a late response to amiodarone. The majority of patients who responded to intravenous amiodarone did so within the first 2 h of therapy, and all responded within 84 h. Patients with an ejection fraction greater than 25% were more likely to respond (p less than 0.05). Major side effects occurred in 13% of patients. The cumulative 2 year mortality rate due to arrhythmia recurrence or sudden death for responders discharged from the hospital was 23% and the cumulative overall 2 year mortality rate was 46%. In conclusion, intravenous amiodarone is rapidly effective in the majority of patients with recurrent ventricular tachycardia or ventricular fibrillation refractory to other drugs. The poor long-term outcome of patients who require this therapy, respond to it and are discharged on long-term oral amiodarone therapy warrants consideration of other long-term treatment of these patients. Use of intravenous amiodarone is an important new modality in the treatment of drug-refractory malignant ventricular arrhythmias.     

Short- and long-term antiarrhythmic and hemodynamic effects of d,l-sotalol in patients with symptomatic ventricular arrhythmias.

The antiarrhythmic and hemodynamic effects of sotalol (160 to 480 mg/day), a beta-blocking agent that prolongs ventricular repolarization, were examined in 38 patients with complex symptomatic ventricular ectopic activity. During ambulatory monitoring, 24 patients (63%) exhibited a reduction of greater than 75% in single ventricular premature beats (VPBs) and greater than 90% reduction in repetitive arrhythmia. In contrast to the effects of other agents, left ventricular ejection fraction as determined by radionuclide angiography was not impaired, increasing slightly from 45 +/- 14% to 47 +/- 14% during therapy (p less than 0.05). Antiarrhythmic drug efficacy did not correlate with baseline ejection fraction or sotalol-induced changes in ventricular function. Late follow-up studies disclosed that antiarrhythmic efficacy and tolerance were maintained in the majority of patients. Repeat radionuclide angiography at 6 months revealed no late drug-induced depression of left ventricular function. Sotalol appears to be an effective and well tolerated agent for treatment of complex ventricular ectopic activity, even in the setting of compromised cardiac function.     

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.     

Amiodarone and sustained ventricular arrhythmias: statistical evidence of drug effectiveness

Previous studies have shown that amiodarone prevents sustained ventricular arrhythmias in 77% to 93% of patients. To date, a study using statistical analysis to verify the drug's effectiveness has not been reported. Amiodarone was given to 17 patients with drug refractory sustained ventricular arrhythmias. All patients had serious underlying heart disease including coronary artery disease (15 patients) or cardiomyopathy (two patients). Ten patients had angiographic evidence of a left ventricular aneurysm. All patients had left ventricular dysfunction. The mean left ventricular ejection fraction was 33%. In the 5.5 +/- 8.3 months prior to amiodarone, these 17 patients had documented sustained ventricular arrhythmias requiring countershock (41 episodes), overdrive pacing (four episodes), or intravenous drugs (three episodes). Amiodarone was given as a loading dose (1 gm/day for 10 days) and a maintenance dose (200 to 600 mg/day). During a follow-up period of 8.9 +/- 5.7 months, only eight episodes occurred requiring countershock (5) or overdrive pacing (2); one patient died suddenly. A statistical test constructed for this problem showed a significant (p greater than 0.001) reduced risk of experiencing a sustained ventricular arrhythmia after amiodarone. This statistical model confirms previous studies showing that amiodarone prevents sustained ventricular arrhythmias and prevents sudden cardiac death.     

Amiodarone for control of sustained ventricular tachyarrhythmia: clinical and electrophysiologic effects in 51 patients

We evaluated the electrophysiologic effects of amiodarone and its ability to control ventricular arrhythmia in a selected group of 51 patients with refractory sustained ventricular arrhythmia. Amiodarone in doses of 400 to 800 mg/day prolonged refractoriness in the atria, atrioventricular (AV) node, and ventricle as well as conduction through the AV node and His-Purkinje system. Although it had no effect on measurements of sinus nodal function (sinus nodal recovery time and sinoatrial conduction time), it prolonged the sinus cycle length and 2 patients required a permanent pacemaker for symptomatic sinus bradycardia. Amiodarone did not alter the ease of inducibility in any consistent manner, and only 5 of 43 patients (12%) who had inducible ventricular tachycardia before amiodarone therapy had none induced during amiodarone treatment. The clinical effectiveness of amiodarone could be evaluated in 46 patients followed up for 8.6 +/- 6 months (range 0.5 to 22). It provided effective therapy in 23 patients (50%), partly effective therapy in 13 (28%), and was ineffective in 10 (22%). Adverse effects were noted in 28 of 51 patients (55%), and in 11 of these (22%) the drug had to be discontinued because of adverse effects. We conclude that amiodarone is a useful agent for the treatment of refractory sustained ventricular arrhythmia. Its use should be reserved for patients with life-threatening sustained arrhythmia because of the significant incidence of adverse effects. Furthermore, good clinical response can be observed in patients receiving amiodarone in spite of continued inducibility.     

Amiodarone in patients with previous drug-mediated torsade de pointes. Long-term safety and efficacy

The safety and efficacy of long-term amiodarone therapy were examined in 12 patients who had previously developed torsade de pointes as a complication of previous antiarrhythmic therapy. The QTc intervals were determined at the time of torsade de pointes (570 +/- 40 ms), after 7 days of amiodarone loading (490 +/- 70 ms), and after 3 months of chronic amiodarone administration (580 +/- 80 ms). Compared to a drug-free control period, QTc was significantly prolonged (P less than 0.05) at the time of torsade de pointes, after amiodarone loading, and after 3 months of amiodarone therapy. The QTc intervals at the time of torsade de pointes and after chronic amiodarone treatment were not significantly different. At 16 +/- 7 months of follow-up, all patients remained free of subsequent torsade de pointes, syncope, or sudden death. In addition, 5 of 6 patients with a history of sustained ventricular tachycardia remained free from arrhythmic recurrence despite persistence of inducible ventricular tachycardia during programmed stimulation studies done before discharge. We conclude that amiodarone can often be used safely and effectively in patients who have previously had an episode of drug-mediated torsade de pointes. Amiodarone-induced QTc prolongation, even when marked, does not predict recurrent torsade de pointes. These observations also suggest that the propensity for a drug to produce this arrhythmia is dependent on other electrophysiologic effects in addition to its ability to simply lengthen repolarization.     

Propafenone: noninvasive evaluation of efficacy

Propafenone, a new antiarrhythmic drug, was administered to 60 patients with a history of refractory ventricular tachyarrhythmias, including ventricular fibrillation in 16 and ventricular tachycardia (VT) in 44. A noninvasive protocol was followed utilizing ambulatory monitoring and exercise testing for evaluation of drug effect. The protocol involved acute drug testing with 450 mg of propafenone followed by maintenance therapy with 150 to 300 mg t.i.d. for 4 days. The protocol was completed by 57 patients; in 3 patients side effects developed that necessitated discontinuation of the drug before evaluation. When evaluated by monitoring, 34 patients (60%) responded to the drug, with total elimination of runs of VT, a greater than 90% reduction in couplets and a greater than 50% decrease in the frequency of ventricular premature beats. Based on exercise testing, 36 patients (63%) were deemed responders. When both exercise and monitoring were considered, 30 of 57 patients (53%) responded to propafenone. The acute drug test predicted the response to maintenance therapy in 84% of patients. Propafenone did not change left ventricular function in patients with normal ejection fractions (greater than 50%). However, in those with an ejection fraction less than 50%, propafenone significantly reduced this value (34% vs 29%, p less than 0.01). Side effects occurred in 20 patients (33%) and included nausea, congestive heart failure, aggravation of arrhythmia and conduction abnormalities. Eleven patients have continued on propafenone for an average of 16 months with continued efficacy and freedom from side effects.     

Hemodynamic effects of encainide in patients with ventricular arrhythmia and poor ventricular function

Gated cardiac scanning was used to evaluate the hemodynamic effects of encainide in 19 patients (1 woman) with complex ventricular arrhythmia and depressed left ventricular (LV) function (ejection fraction less than 45%). Patients were 36 to 80 years old (average 61). All were candidates for long-term encainide therapy after having failed with currently available antiarrhythmics. Sixty-three percent had congestive heart failure before they received encainide. All were evaluated in the hospital before encainide therapy by a gated cardiac scan performed at least 3 days after discontinuing all antiarrhythmic drugs. Patients received oral encainide in doses of 75 to 200 mg. Gated cardiac scans were repeated 1 to 2 weeks later when an 80% reduction in frequency of premature ventricular complexes was observed on a 24-hour Holter recording. No patient had worsening of congestive heart failure during encainide therapy. Encainide did not significantly affect ejection fraction, which averaged 22 +/- 10% before and 25 +/- 14% (SD) after encainide (difference not significant [NS]). Other hemodynamic variables, including heart rate, blood pressure, stroke volume and end-diastolic volume, remained unchanged during encainide therapy. Digoxin blood levels in 10 patients averaged 1.04 +/- 0.43 before and 1.22 +/- 0.47 mg/ml (NS) during encainide therapy. Thus, encainide given orally in clinically effective doses does not appear to have significant hemodynamic effects in patients with ventricular arrhythmia and depressed LV function.     

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

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