Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)     

小剂量胺碘酮治疗扩张性心肌病伴发心律失常

目的 探讨小剂量胺碘酮治疗扩张性心肌病伴发阵发性室性心动过速和预防心脏性猝死的疗效。方法 扩张性心肌病患者65例,分为小剂量胺碘酮治疗组（n=33）及对照组（n=32）,基础治疗用利尿药、强心苷、血管紧张素转化酶抑制药及硝酸酯,随访12个月,用超声心动图测定心功能指数,动态心电图监测阵发性室性心动过速和猝死率,进行两组病例比较。结果 治疗12个月后,两组心功能指数均较治疗前改善,小剂量胺碘酮治疗组患者阵发性室性心动过速较对照组明显减少。两组猝死率没有明显区别。结论 小剂量胺碘酮对于改善心功能和治疗扩张性心肌病患者恶性室性心律失常有效．可减少新发室性心律失常。     

The effect of spironolactone on ventricular tachyarrhythmias in patients with implantable cardioverter-defibrillators

Background- Previous studies have suggested that aldosterone blockade can reduce the incidence of ventricular tachycardia (VT) or ventricular fibrillation (VF) in patients with heart failure. The SPIronolactone to Reduce ICD Therapy (SPIRIT) trial was designed to test the hypothesis that spironolactone reduces the incidence of VT/VF in patients with implantable cardioverter-defibrillators (ICDs) who are at moderately high risk for recurrent VT/VF. Methods and Results- Ninety patients who had ICDs who were at moderately high risk for recurrent VT/VF and who were not candidates for spironolactone by current heart failure guidelines were randomized to receive spironolactone 25 mg daily or placebo in a double-blind fashion. All patients had previously received ICD therapy (shock or antitachycardia pacing) for VT/VF within 2 years of randomization or an ICD for secondary prevention of VT/VF within 6 months of randomization. The primary end point was time to first recurrence of VT/VF requiring ICD therapy. After a median follow-up of 35 months, the Kaplan-Meier probability estimates for VT/VF requiring ICD therapy were 68.7% in the placebo group and 84.7% in the spironolactone group. Compared with placebo, spironolactone was associated with a similar risk of VT/VF (hazard ratio, 1.01; 95% CI, 0.64-1.83; P=0.71). There was no significant difference between the median times to first VT/VF recurrence requiring ICD therapy in the 2 groups. Conclusions- In patients with ICDs who were at moderately high risk for recurrent VT/VF on account of a recent VT/VF event that was either sustained or treated by the ICD and who were not candidates for spironolactone by current heart failure guidelines, spironolactone did not delay the first recurrence of VT/VF or reduce the risk of recurrent VT/VF.     

Abnormal signal-averaged electrocardiograms in patients with nonischemic congestive cardiomyopathy: relationship to sustained ventricular tachyarrhythmias

We assessed whether signal-averaged electrocardiography could identify patients with sustained ventricular arrhythmias in 41 patients with non-ischemic cardiomyopathy. Twelve of these patients presented with sustained ventricular arrhythmia and 29 patients had no history of sustained ventricular arrhythmias. The mean ejection fractions in the groups were 30 +/- 9% and 24 +/- 9%, respectively. Results were compared with signal-averaged electrocardiograms in 55 normal individuals. The filtered QRS duration was longest in patients with sustained ventricular arrhythmias (130.2 +/- 19.5 vs 105.0 +/- 13.1 msec in the group without sustained ventricular arrhythmia, p less than .001 and 95.9 +/- 9.1 in the normal group, p less than .001). The voltage in the last 40 msec of the filtered QRS was lower in the sustained ventricular arrhythmia group (11.3 +/- 9.3 microV) than the group without sustained ventricular arrhythmia (53.5 +/- 28.3 microV; p less than .001) or the normal group (53.7 +/- 25.2 microV; p less than .001). Eighty-three percent of patients in the sustained ventricular arrhythmia group had an abnormal signal-averaged electrocardiogram characterized by both a long filtered QRS duration and a late potential of low voltage level; only 2% of normal subjects and 14% of patients without sustained ventricular arrhythmias had an abnormal signal-averaged electrocardiogram. The signal-averaged electrocardiogram can identify patients with nonischemic congestive cardiomyopathy and sustained ventricular arrhythmias.     

Beta-blocker therapy in patients with ventricular tachyarrhythmias in the setting of left ventricular dysfunction

Although several studies suggest beta blockers (BB) are effective in suppressing ventricular arrhythmias, less is known about their role in the treatment of patients with ventricular tachyarrhythmias associated with impaired left ventricular function. To assess the tolerance and efficacy of these agents, 32 patients presenting with either ventricular fibrillation (18) or sustained ventricular tachycardia (14) were studied during BB therapy. Left ventricular dysfunction (mean ejection fraction 29%) was present as a consequence of coronary artery disease (26) or cardiomyopathy (6). Baseline arrhythmia assessment revealed recurrent ventricular tachycardia in all patients. Antiarrhythmic drug therapy including BB was guided by programmed stimulation (10), exercise testing (8), ambulatory monitoring (12), or was given empirically (2). Beta blockers were well tolerated, as measured by exercise duration, which improved significantly, and by long-term maintenance, which continued in 23 of 32 (72%) patients. Over a mean follow-up of 668 days, patients treated with BB had a relatively low incidence of both sudden (3%) and nonsudden (9%) death. Thus, BB can be effective and well tolerated adjunct therapy in patients with a history of ventricular tachyarrhythmias in the setting of impaired left ventricular function.     

Long-term low-dose amiodarone therapy in the management of ventricular and supraventricular tachyarrhythmias: Efficacy and safety

Background: Amiodarone hydrochloride has been in use for two decades for the control of ventricular and supraventricular arrhythmias. Established and emerging evidence indicates that amiodarone has an antiarrhythmic efficacy superior to that of most other drugs. Hypothesis: The study was undertaken to evaluate the efficacy and acceptability of low-dose amiodarone therapy in the long-term management of supraventricular and ventricular tachyarrhythmias. Methods: A total of 124 patients with symptomatic drug-refractory or life-threatening arrhythmias managed with low-dose oral amiodarone therapy over a 10-year period was analyzed retrospectively. Of these, 45 patients (36%) had ventricular arrhythmias, 52 (42%) had atrial arrhythmias, and 27 (22%) had atrioventricular reentry tachycardia. Loading doses of amiodarone 600 mg daily for 1 week were administered for supraventricular arrhythmias and 600–1200 mg daily for 2 weeks for ventricular arrhythmias. Maintenance daily doses were 194 ± 48 and 206 ± 55 mg, respectively. Mean treatment duration was 32 ± 28 months, with 326.3 patient years of therapy. Results: Of 39 patients with sustained ventricular tachyarrhythmias, the actuarial incidence of satisfactory arrhythmia control (absence of sudden cardiac death or nonfatal arrhythmia recurrence) was 78% at 1 year and 71 % at 2 years. Satisfactory control of supraventricular arrhythmias (mean ventricular rate < 100/min with significant symptomatic improvement for sustained atrial arrhythmias and < 1 attack per year for paroxysmal atrial or atrioventricular arrhythmias) was achieved in 73, 65, and 62% of patients at 1, 2, and 3 years, respectively. The cumulative incidence of amiodarone-related adverse effects was 5.8 per 100 patient years, with drug withdrawal required in 12 patients (9.7%). Fifteen patients had thyroid dysfunction, 2 had hepatic toxicity, and 1 developed nonfatal pulmonary fibrosis. Overall, the incidence of successful use of amiodarone (satisfactory arrhythmia control and freedom from side effects) was 67, 59, and 53% at 1, 2, and 3 years, respectively. Conclusions: The results of this study suggest that the efficacy of low-dose amiodarone therapy in the management of serious ventricular and supraventricular arrhythmias would be similar to those achieved with higher doses, but with a much more acceptable side effect profile.     

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.     

Comparison of individual and combined effects of procainamide and amiodarone in patients with sustained ventricular tachyarrhythmias

To compare the individual and combined electrophysiological effects of amiodarone and procainamide, 35 patients with sustained ventricular arrhythmias underwent programmed stimulation in the control state, after procainamide (mean concentration, 8.7 +/- 2.8 micrograms/ml), after 13 +/- 2 days of amiodarone (1,400 mg/day x 7 days, then 400 mg/day), and after amiodarone with procainamide (mean procainamide concentration, 7.8 +/- 2.2 micrograms/ml). Sustained ventricular tachycardia (VT) was inducible in all 35 patients during treatment with procainamide alone and with amiodarone alone. Procainamide and amiodarone similarly increased the VT cycle length (+68 vs. +61 msec), the corrected QT interval (+63 vs. +49 msec), and the ventricular effective refractory period measured at paced cycle lengths of 600-550 msec (+23 vs. +21 msec) and 400 msec (+25 vs. +23 msec). Procainamide had a more pronounced effect on QRS duration than amiodarone during sinus rhythm (+18 vs. +8 msec, p less than 0.01) and during paced cycle lengths of 600-550 msec (+32 vs. +23 msec, p less than 0.01) and 400 msec (+37 vs. +28 msec, p less than 0.1) but a similar effect on the QRS duration during VT (+32 vs. +29 msec). During combination therapy, VT initiation was prevented in only two (6%) patients. The combination therapy produced a greater increase (p less than 0.001) than individual therapy in all the electrophysiological intervals assessed, with the exception of the sinus cycle length. On each drug regimen, a cycle length-dependent increase (p less than 0.05) in paced QRS duration was noted (400 more than 600-550 msec).(ABSTRACT TRUNCATED AT 250 WORDS)     

胺碘酮对恶性室性心律失常QT离散度的影响

目的观察胺碘酮对恶性室性心律失常QT离散度的影响。方法观察60例恶性室性心律失常患者服用胺碘酮治疗前后校正的QT离散度（QTcd）的变化。结果应用胺碘酮治疗恶性室性心律失常（LownⅢ级以上）后与治疗前相比较，显著减少（P〈0．05），QTcd亦有显著性下降（P〈0．01），并未发现该药具有严重毒副作用。结论胺碘酮治疗恶性室性心律失常安全有效，能缩小QT离散度，从而减少室颤的发生，可降低恶性严重室性心律失常和心源性猝死。     

胺碘酮对合并于充血性心力衰竭的室性心律失常疗效观察

充血性心力衰竭 (ＣＨＦ)患者合并室性心律失常 ,尤其是复杂性室性心律失常 ,其病死率明显增加 ,因此 ,在纠正心力衰竭的同时 ,能否有效地治疗室性心律失常很重要。本文报道小剂量胺碘酮对ＣＨＦ合并的室性心律失常治疗的有效性、安全性及对其生存率的影响。资料和方法　选择ＣＨＦ心功能Ⅲ Ⅳ级 (ＮＹＨＡ分级 ) ,射血分数 <0 40。室性心律失常 (室性早搏≥ 30个 /ｈ ,成对室性早搏及非持续性室性心动过速和持续性室性心动过速 )。年龄 40～ 75岁。原发病为缺血性心脏病 70例 ,扩张性心肌病 36例、心脏瓣膜病 6 0例 (除重度二尖瓣狭窄、主…     

大剂量胺碘酮对持续性室性心动过速的纠治

目的 :观察大剂量胺碘酮治疗持续性室性心动过速 ( SVT)的临床疗效及副作用。方法 :初始以胺碘酮 15 0 m g静脉注射 (静注 ) ,5～ 10 min注射完毕 ,必要时重复 1～ 2个初始量 ,继以 0 .5～ 5 m g/ min静脉维持 3～ 8d。结果 :6例 SVT均在静脉用药 2 h内得到控制 ,2 h内静脉胺碘酮用量 3 90～ 5 4 0 ( 4 68.4± 5 4 .7) m g;2 4 h内静脉平均用量 10 0 0～ 180 0 ( 14 10 .3± 3 5 6.5 ) m g,除注射局部均发生不同程度的静脉炎外 ,未见低血压、心功能恶化及致心律失常作用。结论 :短期内经静脉大剂量应用胺碘酮安全有效     

Induction of ventricular fibrillation predicts sudden death in patients treated with amiodarone because of ventricular tachyarrhythmias after a myocardial infarction.

OBJECTIVE--To examine the value of programmed electrical stimulation of the heart in predicting sudden death in patients receiving amiodarone to treat ventricular tachyarrhythmias after myocardial infarction. DESIGN--Consecutive patients; retrospective study. SETTING--Referral centre for cardiology, academic hospital. PATIENTS--106 patients with ventricular tachycardia (n = 77) or ventricular fibrillation (n = 29) late after myocardial infarction. INTERVENTIONS--Programmed electrical stimulation was performed while on amiodarone treatment for at least one month. MEASUREMENTS AND MAIN RESULTS--In 80/106 patients either ventricular fibrillation (n = 15) or sustained monomorphic ventricular tachycardia (n = 65) was induced. After a mean follow up of 50 (SD 40) months (1-144), 11 patients died suddenly and two used their implantable cardioverter debfibrillator. By multivariate analysis two predictors for sudden death were found: (1) inducibility of ventricular fibrillation under amiodarone treatment (P << 0.001), and (2) a left ventricular ejection fraction of < 40% (P < 0.05). The survival rate at one, two, three, and five years was 70%, 62%, 62%, and 40% respectively for patients in whom ventricular fibrillation was induced, and 98%, 96%, 94%, 94% for patients with induced sustained monomorphic ventricular tachycardia. Where there was no sustained arrhythmia, five year survival was 100%. CONCLUSIONS--In patients receiving amiodarone because of life threatening ventricular arrhythmias after myocardial infarction, inducibility of ventricular fibrillation, but not of sustained monomorphic ventricular tachycardia, indicates a high risk of sudden death.     

Impact of accelerated ventricular tachyarrhythmias on mortality in patients with implantable cardioverter-defibrillator therapy

Background

Anti-tachycardia pacing (ATP) and shock delivery may induce or accelerate tachyarrhythmias in patients with implantable cardioverter-defibrillator (ICD). We investigated the incidence, triggers and impact on mortality of accelerated ventricular tachyarrhythmias.

Methods

Database analysis concerning ventricular tachyarrhythmias accelerated by ATP or shock in 1275 ICD patients (age at implantation 59.7 ± 14.0 years; 81% male).

Results

Within a mean follow-up period of 5.3 ± 4.0 years, intracardiac electrograms were available in 1170 patients (91.8%). Overall 157 episodes of accelerated ventricular tachyarrhythmias were found in 100 of 1170 patients (8.5%). Termination of tachyarrhythmias was achieved by shock delivery in 153 episodes (96.8%). Triggers of accelerated tachyarrhythmias were appropriate ATP in 139 (88.5%) and inappropriate ATP in 14 (8.9%), as well as appropriate and inappropriate shocks in 2 (1.3%) episodes, respectively. Chronic heart failure was significantly correlated with the occurrence and recurrence of acceleration (p < 0.001). Patients with accelerated ventricular tachyarrhythmia and subsequent shock therapy revealed higher all-cause mortality (HR 1.760; 95% CI 1.286–2.410; p < 0.001) as well as higher cardiac mortality (HR 2.555; 95% CI 1.446–4.513; p = 0.001). The correlation between acceleration and all-cause mortality was independent of left ventricular function (HR 2.076; 95% CI 1.633–2.639; p < 0.001).

Conclusions

Ventricular ATP with arrhythmia acceleration and subsequent shock delivery is a frequent and serious complication of ICD therapy that predominantly occurs in patients with reduced left ventricular function. Finally, occurrence of accelerated ventricular tachyarrhythmias was associated with increased all-cause mortality.     

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.     

Amiodarone and propafenone: evaluation using serial Holter recordings in patients with ventricular arrhythmia]

OBJECTIVE: To review the experience of the Arrhythmology Department in evaluating antiarrhythmic therapy for ventricular arrhythmias with serial Holter electrocardiographic recordings (ECG-H). To compare the results obtained with the most used drugs in this Department: amiodarone and propafenone (groups AMIO and PROP). DESIGN: Retrospective study. No statistically significant differences between the two groups were found in respect to age, sex, underlying disease, functional class, left ventricular function and associated therapy. SETTING: Arrythmology Department at a Cardiology Service. PATIENTS: 105 sequential patients with ventricular arrhythmias in a basal ECG-H recording, that were evaluated within 1 year with a new recording on amiodarone or propafenone, without major clinical events or therapeutic changes between the two recordings. INTERVENTIONS (daily oral doses): Amiodarone 200-600 (mean 270) mg or propafenone 300-900 (mean 602) mg. RESULTS: No statistically significant differences were found between the two groups, in either the basal ECG-H or that recorded on therapy. The two drugs were similar in the degree of suppression of ventricular premature complexes per hour (VPCH): equal or superior to 75% in 64.3% of the patients on amiodarone and in 63.9% of those on propafenone. The following reductions on therapy were statistically significant (p less than 0.001 if not specified): VPCH, from 346 +/- 480 to 86 +/- 158 on amiodarone and from 418 +/- 524 to 110 +/- 215 on propafenone; most complex arrhythmia recorded, on both drugs; number of patients with pairs, from 72.1 to 34.9% on amiodarone and from 69.4 to 33.9% on propafenone; number of patients with runs of nonsustained ventricular tachycardia (VT), from 27.9 to 2.3% on amiodarone (p less than 0.01); number of runs of VT per recording, from 3 +/- 5 to 1 on amiodarone (p less than 0.06); and maximum number of complexes per run of VT, from 8 +/- 8 to 4 on amiodarone and from 7 +/- 4 to 5 +/- 1 on propafenone (both with p less than 0.06). CONCLUSIONS: Holter recordings were useful in evaluating antiarrhythmic therapy. The effectiveness of amiodarone and propafenone in treating ventricular arrhythmias was not significantly different. The choice between one of these drugs must rely on their collateral effects profile.     

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.     

Long-term reproducibility of electrophysiologically guided therapy with sotalol in patients with ventricular tachyarrhythmias

OBJECTIVES

Goal of this study was to assess the long-term reproducibility of electrophysiologic drug testing in patients with ventricular tachyarrhythmias (VT/VF).

BACKGROUND

Programmed ventricular stimulation (PVS) is still widely used to guide antiarrhythmic therapy in patients with sustained ventricular tachycardia/fibrillation (VT/VF). Sotalol is considered as one of the most effective drugs for VT/VF. Because there is no proof of long-term reproducibility of a successful drug test with sotalol, we investigated the long-term reproducibility of drug testing with sotalol.

METHODS

Thirty patients with VT/VF (age: 57 ± 11 years, 20 patients with coronary heart disease, 7 patients with no structural heart disease, 3 with others) and reproducible induction of VT/VF (28 patients VT, two patients VF) in a baseline PVS, were suppressible with sotalol (mean dosage 395 ± 137 mg) in a subsequent PVS. After a mean follow-up of 13 ± 10 months a PVS was again performed in patients, who had no evidence of progressive cardiac disease, who did not experience any arrhythmia recurrences or who were drug compliant. Irrespective of the inducibility after long-term therapy with sotalol, all patients were kept on the initial sotalol regimen. All 30 patients had a stable cardiac condition, were free of VT/VF recurrences and were drug compliant.

RESULTS

Despite the clinical efficacy of sotalol, in 12 patients (40%) VT/VF could again be induced after 13 ± 10.2 months. Inducibility was independent of age, heart disease, ejection fraction and follow-up time. During a further follow-up of 22.1 ± 10.9 months, five patients experienced nonfatal VT recurrences independently of the prior inducibility.

CONCLUSIONS

This study shows a lacking long-term reproducibility of an initial effective PVS with sotalol. Despite an uneventful clinical follow-up, late electrophysiologic testing showed a VT/VF inducibility in a high portion of patients. Hence, electrophysiologic testing performed late after the initial drug test may no longer be predictive of outcome.