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.     

Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease.

AIM: To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias. METHODS: Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia. RESULTS: At 36 months. 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0.05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5.9 times higher (P=0.008) than that for patients on sotalol. CONCLUSION: Sotalol is superior to amiodarone for long-term treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly.     

Clinical usefulness of electrophysiologic testing in patients with ventricular tachycardia and chronic chagasic cardiomyopathy treated with amiodarone or sotalol

INTRODUCTION: This study assessed the role of electrophysiologic testing to identify therapeutic strategies for the treatment of patients with sustained ventricular tachycardia (VT) and chronic chagasic cardiomyopathy treated with amiodarone or sotalol. METHODS AND RESULTS: One hundred fifteen patients [69 men (60%); mean age 52 +/- 10 years] with chagasic cardiomyopathy presenting with symptomatic VT were studied after loading with Class III antiarrhythmic drugs; 78 had a history of sustained VT, and 37 with symptomatic nonsustained VT had sustained VT induced at baseline electrophysiologic study. All but 12 patients also underwent baseline electrophysiologic study. Mean left ventricular ejection fraction was 0.49 +/- 0.14. Based on results of electrophysiologic study after loading with Class III drugs, patients were divided into three groups: group 1 (n = 23) had no sustained VT induced; group 2 (n = 45) had only tolerated sustained VT induced; and group 3 (n = 47) had hemodynamically unstable sustained VT induced. After a mean follow-up of 52 +/- 32 months, total mortality rate was 39.1%; it was significantly higher in group 3 than in groups 2 and 1 [69%, 22.2%, and 26%, respectively, P < 0.0001, hazard ratio (HR) 10.4, 95% confidence interval (CI) 3.8, 21.8]. There was no significant difference in total mortality rate between groups 1 and 2 (P = 0.40, HR 1.5, 95% CI 0.75, 4.58). Cardiac mortality and sudden cardiac death rates also were higher in group 3 patients. CONCLUSION: In patients with chagasic cardiomyopathy and sustained VT, electrophysiologic testing can predict long-term efficacy of Class III antiarrhythmic drugs. This may help in the selection of patients for implantable cardioverter defibrillator therapy.     

Low-dose oral sotalol for monomorphic ventricular tachycardia: effects during programmed electrical stimulation and follow-up

The effects of oral sotalol were compared with the findings obtained in the baseline study of a group of 26 consecutive patients with sustained monomorphic ventricular tachycardia or ventricular fibrillation and inducible ventricular tachycardia. The mean age was 62 years and the mean ejection fraction 33%. The number of non-inducible patients after sotalol administration (mean dose of 251 +/- 81 mg day-1) was 13 out of 21 (62%). The cycle length of the induced tachycardia changed from 293 +/- 32 to 303 +/- 41 ms (non-significant (NS]. The coupling interval of the first extrastimulus did not lengthen for the subgroup with persistent inducibility. The number of patients requiring defibrillation during the induction study did not decrease on (2/8) or off drugs (6/22). After the first administration of oral sotalol, two patients developed polymorphic ventricular tachycardia or torsade de pointes and one suffered from left ventricular failure. Long-term treatment with sotalol was given to 15 non-inducible patients, and two inducible patients, combined with an AICD or a pacemaker. Over a mean follow-up period of 13 months, three recurrences were observed in these 17 patients, including the patient with the AICD. This represents an efficacy of 82% for patients chronically treated with a low dose of oral sotalol.     

Transmural dispersion of repolarization and ventricular tachyarrhythmias

BACKGROUND: Myocardial transmural dispersion of repolarization (TDR) has been associated with reentrant arrhythmias in animal studies but a clinical association has not yet to been demonstrated. The present study examines the relationship between TDR and ventricular tachyarrhythmias in human subjects. METHODS: This study consisted of 65 patients with non-sustained ventricular tachycardia, sustained ventricular tachycardia, ventricular fibrillation or unexplained syncope with organic heart disease. The control group included 65 patients with paroxysmal supraventricular tachycardia. The 12 ECG was recorded at a recording rate of 100 mm/sec. The interval from the peak to the end of the T wave in the precordial (ECG), referred to as TpTe was assumed to be representative of TDR. RESULTS: Patients were divided into three groups based on the ability to induce VT at the time of electrophysiologic study: VT inducible group (n=37), VT non-inducible group (n=25) and control group (n=65). V4 TpTe/ radical RR was significantly prolonged in the VT inducible group, as compared to the VT non-inducible group (n=25) and the control group (118.9 +/- 26.1 vs. 103.9 +/- 25.7, 104.1 +/- 22.6 ms, P<.05). Patients who develop VT spontaneously (n=13) during a mean follow-up period of 25 months, displayed significantly prolonged V3 TpTe/ radical RR, compared to patients who did not develop VT spontaneously or the control group (132.5 +/- 37.4 vs. 109.8 +/- 26.3, 107.1 +/- 24.1 ms, P <.05). CONCLUSION: Prolonged TDR is associated with inducibility as well as spontaneous development of VT in higher risk patients. TDR may be a useful index for predicting ventricular tachyarrhythmias.     

Randomized controlled trial of prophylactic antiarrhythmic theraphy in patients with inducible ventricular tachyarrhythmias after recent myocardial infarction

Survivors of acute myocardial infarction who had inducible sustainedventricular tachyarrhythmias at programmed stimulation 1–4weeks after infarction were recruited to a randomized pilottrial of Class 1 antiarrhythmic drugs, in an attempt to determinewhether their mortality and risk of spontaneous ventriculartachycardia and fibrillation could be reduced by treatment. Of 136 eligible patients, 96 (71%) joined the trial and 47 wererandonized to ‘no treatment’ and 49 were randomizedto ‘treatment’ (quinidine, disopyramide or mexiletinegiven to attain ‘therapeutic’ serum levels). Duringfollow-up, the two groups fared similarly. For the ‘treatment’and ‘no treatment’ groups, the respective 3-yearprobabilities of remaining incident-free were:cardiac death,0.91 vs 0.89; instantaneous death + non-fatal ventricular tachyarrhythmias,0.87 vs 0.87; cardiac death+non-fatal ventricular tachyarrhythmias,083 vs 0.85. The highest risk patients with inducible ventricular tachycardiafared similarly in the ‘treatment’ and ’notreatment’ groups. The respective probabilities of remainingincident-free were: cardiac death, 0.89 vs 0.88; instantaneousdeath+non-fatal ventricular tachyarrhythmias, 0.79 vs 0.84 cardiacdeath+non-fatal ventricular tachyarrhythmias,0.76 vs 0.77. We conclude that prophylactic Class I antiarrhythmic drug therapywith quinidine, disopyramide or mexiletine given to achievea ‘therapeutic’ serum level does not appear to alterthe prognosis with inducible ventricular tachyarrhythmias aftermyocardial infarction.     

Incidence of nonsustained and sustained ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) is a frequent phenomenon in some patients with heart disease, but its association with sustained ventricular tachycardias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) is still not clear. The aim of this study was to determine whether NSVT incidence was associated with sustained VT/VF in patients with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Retrospective data analysis was conducted in 923 ICD patients with a mean follow-up of 4 months. NSVT and sustained VT/VF were defined as device-detected tachycardias. The incidence rates of NSVT and sustained VT/VF as well as ICD therapies were determined as episodes per patient. The NSVT index was defined as the product of NSVT episodes/day times the mean number of beats per episode, i.e., total beats/day. The NSVT index peak was defined as the highest value on or prior to the day with sustained VT/VF episodes. Patients (n = 393) with NSVT experienced a higher incidence of sustained VT/VF (17.2 +/- 63.0 episodes/patient) and ICD therapies (15.2 +/- 61.4 episodes/patient) than patients (n = 530) without NSVT (sustained VT/VF: 0.5 +/- 6.6 and therapies: 0.5 +/- 5.6; P < 0.0001). Approximately 74% of NSVT index peaks occurred on the same day or <3 days prior to sustained VT/VF episodes. The index was higher for peaks < or =3 days prior to the day with sustained VT/VF (94.3 +/- 140.1 total beats/day) than for peaks >3 days prior to the day with sustained VT/VF (32.7 +/- 55.9 total beats/day; P < 0.0001). CONCLUSION: ICD patients with NSVT represent a population more likely to experience sustained VT/VF episodes with a temporal association between an NSVT surge and sustained VT/VF occurrence.     

Objective features of the surface electrocardiogram during ventricular tachyarrhythmias

The aim of this study was to quantify the electrocardiographicsignal characteristics of three types of ventricular arrhythmia;monomorphic ventricular tachycardia, polymorphic ventriculartachycardia and ventricular fibrillation. Patients in a coronarycare unit were monitored using a single bipolar ECG lead. Thirtyepisodes of ventricular tachyarrhythmia (ten from each group)were recorded automatically by computer. Frequency analysisof ten consecutive 1 s epochs from each recording gave 100 spectrafor each tachyarrhythmia group. Each spectrum was characterisedby the frequency, width and proportional size of the dominantpeak. Despite a qualitative similarity in spectral appearance,there were significant differrences in all characteristics betweenthe tachyarrhythmia groups (P<0·025). Ventricularfibrillation had a higher mean dominant frequency (4·8Hz) than polymorphic ventricular tachycardia (3·7 Hz)and monomorphic ventricular tachycardia (3·8 Hz). Thedominant frequency of ventricular fibrillation was also morevariable than that of monomorphic ventricular tachycardia (P<0·01).Mean peak size was largest for monomorphic ventricular tachycardia(0·78) and smallest for ventricular fibrillation (0·64).The single spectral peaks seen throughout this study indicatethat all three tachyarrhythmias have an underlying periodicmechanism. The difference in spectral characteristics show thatvarying degrees of myocardial electrical organisation can bequantified from surface ECG features.     

Effects of chronic amiodarone on the electrical restitution in the human ventricle with reference to its antiarrhythmic efficacy

Modulation of Electrical Restitution with Amiodarone. Introduction: Dynamic instability of ventricular refractoriness represented by electrical restitution operates synergistically with tissue heterogeneity to increase the propensity for functional reentry leading to ventricular tachycardia/fibrillation (VT/VF). Little is known about the effect of chronic amiodarone on the electrical restitution in the human ventricle. Methods and Results: Restitution kinetics of monophasic action potential duration (MAPD₉₀) in the right ventricular outflow tract (RVOT) and apex (RVA), and of inverse of conduction time from RVOT to RVA (CT^?1), were estimated by an S1–S2 protocol in 22 patients treated with amiodarone (180 ± 33 mg/day for 7 ± 9 months) and in 30 without treatment. In the untreated patients, the restitution kinetics of CT^?1 was steeper in the group with structural heart disease (SHD) (UNT_SHD+, n = 18) than without SHD (UNT_SHD‐, n = 12), whereas MAPD₉₀ restitution parameters were comparable. In the amiodarone‐treated patients (all with SHD), the shortest diastolic interval to produce a ventricular response (DI_min) was increased, the maximum slope of MAPD₉₀ was flattened, and the magnitude of CT^?1 restitution was reduced as compared with UNT_SHD+. Sustained VT/VF was induced in 7 of 18 UNT_SHD+ (38.9%) and in 4 of 22 amiodarone‐treated patients (18.2%, P = 0.07). Concomitant presence of increased CT^?1 restitution and dispersion of MAPD₉₀ restitution was required for the VT/VF induction. The suppression of VT/VF in the amiodarone‐treated patients was associated with a smaller magnitude of CT^?1 restitution in the presence of limited dispersion of MAPD₉₀ restitution. Conclusion: Chronic amiodarone flattens restitution kinetics of MAPD₉₀ and CT^?1 in the human ventricle, which could be antiarrhythmic in patients with limited tissue heterogeneity . (J Cardiovasc Electrophysiol, Vol. 22, pp. 669‐676, June 2011)     

索他洛尔与地高辛联用控制持续性心房颤动心室率的研究

目的 :评估联合应用索他洛尔与地高辛控制持续性心房颤动 (房颤 )心室率的疗效和安全性。方法 :2 2例持续性房颤患者 ,应用地高辛 0 .2 5mg /d治疗 1周后 ,随机分为两组 ,一组维持原治疗 1周 ,另一组联合应用索他洛尔 80～ 16 0mg/d治疗 1～ 2周 ,观察两组治疗前后静息心室率、运动耐量以及不良反应。结果 :索他洛尔联用地高辛组治疗前及治疗 1周以后静息的心室率分别为 (95 .6± 17.6 )次 /min及 (75 .3± 8.3)次 /min ,降低幅度 2 1.2 %(P <0 .0 5 )。治疗后运动耐量活动时间由治疗前的 (2 .9± 1.2 )min延长到 (4.1± 1.8)min ;负荷功率由 (81.8± 2 3.6 )W增加至 (114.5± 2 9.4 )W ,前后比较差异具有非常显著性意义 (P <0 .0 1) ;同时运动负荷后的心室率亦有所下降 ,由用药前的 (171.1± 2 2 .4 )次 /min降至 (15 4 .0± 2 1.5 )次 /min ,降低幅度 17.1%。未见不良反应。单用地高辛治疗者的静息心室率有所下降 ,但运动后的快速心室率无改变。结论 :索他洛尔与地高辛合用可更有效地控制房颤的心室率 ,提高运动耐量。     

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.     

Torsade de pointes during loading with amiodarone

Torsade de pointes represents a potential complication of chronicamiodarone therapy. Several reports have emphasized the needfor a loading dose in order to achieve therapeutic blood levelsrapidly. We report a case of torsade de pointes following asingle oral dose of amiodarone (1400 mg or 30 mg kg^–1)administered after short intravenous loading for preventionof paroxysmal atrial flutter. Torsades de pointes were precededand associated with marked QT prolongation and bradycardia.This report suggests that careful monitoring of patients undergoingoral amiodarone loading is necessary.     

Comparison of the long-term efficacy of implantable defibrillators and sotalol for documented spontaneous sustained ventricular tachyarrhythmias secondary to coronary artery disease

Background: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. Aim: To compare the mortality in patients treated with ATPICD and sotalol for documented spontaneous sustained ventricular tachyarrhythmias occurring late after previous myocardial infarction. Methods: In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol. Results: The two groups were well-matched for age, type of presenting arrhythmia, severity of coronary artery disease and ventricular function. At 36 months Kaplan-Meier estimates of mortality from ventricular tachyarrhythmia were 0% with ATPICD and 15% with sotalol (p=0.03). Kaplan-Meier estimates of total mortality at 36 months were 12% with ATPICD and 25% with sotalol (p=0.09). Multivariate analysis showed hazard ratio of 7.9 (p=0.06) for death from ventricular tachyarrhythmia in patients treated with sotalol compared to ATPICD. Conclusions: While no difference in total mortality was demonstrated, treatment with ATPICD is probably superior to sotalol for preventing deaths due to ventricular tachyarrhythmia. (Aust NZ J Med 1999; 29: 331–341.)     

Comparison of the results of programmed ventricular stimulation from the right ventricular apex and outflow tract: a randomized, prospective study

Objective: The aim of this prospective study was to analysethe yield of programmed ventricular stimulation at the rightventricular apex compared with the outflow tract. Methods: A stepwise randomized cross-over protocol of programmedventricular stimulation with alternating stimulation at bothsites was used in 66 patients who were studied because of sustainedventricular tachycardia (n = 30), ventricular fibrillation (n= 7), or non-sustained ventricular tachycardia and/or syncope(n = 29). Results: There were no significant differences between the resultsof stimulation from either right ventricular site with regardto the presence or absence of structural heart disease, spontaneousarrhythmia, ejection fraction or effective refractory periods.Overall, monomorphic ventricular tachycardia was inducible in33 patients (50%); in 25 patients (75.8%), this arrhythmia wasinduced from both sites. However, in only 17 of these 25 patients(68%) did the induced monomorphic ventricular tachycardias havethe same morphologies and similar (± 50 ms) cycle lengths.Ventricular fibrillation was inducible in 11 patients (17%),mostly by three extrastimuli (n=8; 73%). Conclusions: (1) stimulation from at least two right ventricularsites is desirable because of their independent contributionto the induction of ventricular tachyarrythmias, (2) the non-inducibilityor inducibility at one ventricular site does not predict theeffect at another stimulation site, (3) the effective refractoryperiod at the right ventricular apex and outflow tract do notdiffer, (4) the inducibility of multiple ventricular tachycardiamorphologies emphasizes the importance of documenting the causeof spontaneous arrhythmias with multiple electrocardiographicleads to ensure the correct interpretation of arrhythmias inducedby programmed stimulation, (5) clinical or haemodynamic featurescannot predict whether one or more stimulation sites will berequired for induction of ventricular tachycardia. These resultsare important for the diagnostic evaluation and assessment ofpharmacological or non-pharmacological interventions.     

索他洛尔联合胺碘酮对心律失常的疗效观察

目的探讨索他洛尔联合胺碘酮治疗心律失常的临床效果。 方法选取2016年1—12月荣成市人民医院收治的100例心律失常患者,按随机数表法将所有患者分为对照组和研究组,各50例。对照组患者接受胺碘酮治疗,研究组在对照组的基础上联合索他洛尔治疗。 结果对照组治疗12个月后转复率为42.0%(21/50),观察组治疗12个月后转复率为54.0%(27/50),差异有统计学意义(P<0.05)。治疗后,两组患者心率、舒张压和收缩压均较治疗前降低,差异有统计学意义(P<0.05),观察组患者心率、舒张压和收缩压优于对照组,差异有统计学意义(P<0.05)。两组患者均未出现严重不良反应。 结论索他洛尔联合胺碘酮治疗心律失常效果显著,值得临床推广应用。     

Effects of hypothyroidism on the Vulnerability to ventricular fibrillation in dogs: A comparative study with amiodarone

Summary It has been shown that thyroid hormone has a significant effect on the heart and that suppression of thyroid function may contribute to the antiarrhythmic effect of amiodarone. The study was aimed at investigating the effects of hypothyroidism, compared with those of amiodarone, on vulnerability to ventricular fibrillation in dogs. In this study, 25 adult dogs were randomly divided into three groups: a hypothyroid group following total thyroidectomy (n=9), an amiodarone group (n=8, 400 mg per day, 4 weeks), and a control group (n=8). Both amiodarone and control groups were subjected to sham surgery. Five to 8 weeks after surgery, ventricular fibrillation threshold and other electrophys-iological parameters were determined. Right ventricular effective refractory period, monophasic action potential duration, and ventricular fibrillation threshold were significantly increased in both the thyroidectomized and amiodarone-treated animals. There was no significant change in monophasic action potential duration dispersion. The incidence of ventricular fibrillation during ischemia and reperfusion was significantly reduced in both treated groups compared with the sham-operated euthyroid controls. These observations suggest that hypothyroidism has a significant antifibrillatory effect in dogs. Homogeneous prolongation of repolarization and refractoriness may contribute to the antifibrillatory action of hypothyroidism.     

生理性起搏联合索他洛尔预防病窦综合征患者的房性快速心律失常

目的观察生理性起搏联合索他洛尔对病窦综合征（SSS）患者房性快速心律失常的预防作用.方法52例伴严重房性快速心律失常的SSS患者,在植入DDD起搏器1个月后,分为70次/分单纯起搏（A组）、60次/分起搏＋索他洛尔80mg/d（B组）和70次/分起搏＋索他洛尔80mg/d（C组）三组,随访治疗8周时自动模式转换（AMS）、高频心房事件（HARE）和连发房早（PACR）的发生次数.结果三组患者的房性快速心律失常均显著下降,AMS、HARE分别下降42%、56%、87%和45%、56%、87%,起搏＋药物治疗组（B组或C组）与单纯起搏组（A组）比较差异均有显著性（P＜0.05）,以C组更明显.结论生理性起搏联合索他洛尔对预防SSS患者的房性快速心律失常有显著作用.     

Sudden cardiac death while taking amiodarone therapy: the role of abnormal repolarization

Torsade depointes may occur as a complication of amiodaronetherapy. We report a patient receiving amiodarone who was resuscitatedfrom cardiovascular collapse and documented ventricular fibrillation.At subsequent electrophysiology study, while the patient wastaking amiodarone therapy, monophasic action potentials withearly after depolarisations were recorded which were not presentwhen the patient was restudied 6 weeks after discontinuationof amiodarone. Early after-depolarisations may be importantin the genesis of polymorphic ventricular tachycardia complicatingamiodarone therapy.