Parenteral Antiarrhythmic Drug Therapy in Ventricular Tachycardia/Ventricular Fibrillation: Evolving Role of Class III Agents—Focus on Amiodarone

Intravenous Amiodarone. More effective intravenous antiarrhythmic agents are required for treatment of patients with refractory malignant ventricular arrhythmias. More recently, a great deal of interest has been focused on use of intravenous amiodarone for these patients. Uncontrolled early studies showed that intravenous amiodarone was effective in 42% to 81% of treated patients. Recent large cooperative trials have documented the efficacy of intravenous amiodarone in these patients and have shown an efficacy comparable to bretylium in patients with refractory sustained ventricular tachycardia or fibrillation.     

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.     

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation.

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.     

Amiodarone: The expanding antiarrhythmic role and how to follow a patient on chronic therapy

Amiodarone was introduced as an antiarrhythmic compound in the early 1970s and was approved in the U.S. for the treatment of refractory ventricular arrhythmias in late 1984. Since that time the drug has become the most widely studied antiarrhythmic compound with expanding potential indications, including maintaining stability of sinus rhythm, secondary prevention in the survivors of myocardial infarction, and prolongation of survival in certain subsets of patients with congestive heart failure. Intravenous amiodarone was introduced in the U.S. in 1995 for the control of recurrent destabilizing ventricular tachycardia or ventricular fibrillation resistant to conventional therapy. The level of comfort in its use has risen considerably in the recent past. This has stemmed from the reasonably decisive evidence that class I agents increase mortality in patients with structural heart disease. In contrast, amiodarone either reduces mortality or its effect is neutral; this is consistent with its low to negligible proarrhyfhmic actions. The drug does not aggravate heart failure and it may even increase left ventricular ejection fraction and improve exercise capacity. Above all, it is becoming increasingly evident from wider experience and from controlled clinical trials that the side-effect profile of the drug is not as compelling an issue as it appeared to be when first used in much higher doses. Therefore, the overall objective of amiodarone therapy is to use the lowest dose that produces a defined therapeutic end point without causing serious side effects. Careful clinical surveillance in conjunction with monitoring of certain laboratory parameters and indices of efficacy at regular intervals permits the drug to be used effectively in a large number of patients who fail to respond to, or are intolerant of other antiarrhythmic compounds. Many experienced clinicians have begun to consider the use of amiodarone as first-line therapy in certain disorders of rhythm, especially in patients with severely compromised ventricular function.     

Therapy with antiarrhythmic agents in cardiac insufficiency]

The antiarrhythmic drugs characteristics are generally inadequate for the treatment of arrhythmics in heart failure. The pharmacokinetics and pharmaco dynamics of these drugs on heart failure are also altered conditioning its clinical use with a need for tayloring of therapeutics doses. Drug interaction and pro arrhythmic effects are also possible cause of difficulties. That must be considered according with the information about the pro arrhythmic effect of each drug. There is no consensus about how choose these drugs. The published therapeutic antiarrhythmic regimens are variable: monotherapy with amiodarone or propafenone and drug association regimens with type 1 drugs sometimes with beta-blockers. The efficacy of invasive or non invasive oriented drug therapy for the suppression of ventricular arrhythmics and reduction of mortality is generally accepted. When there is a great decrease of ejection fraction mexiletine and amiodarone are generally recommended. More recent information considers that treatment of "potentially malignant arrhythmias" are not justifiable.     

High incidence of clinical and subclinical toxicity associated with amiodarone treatment of refractory tachyarrhythmias

Amiodarone has been hailed as the most effective single antiarrhythmic drug for treatment of refractory supraventricular and ventricular arrhythmias. However, questions continue to arise about its long-term potential toxicity and true efficacy rates. We, therefore, reviewed our experience with 78 patients, mean age 59 +/- 14 years, with drug refractory tachyarrhythmias treated with amiodarone. Sixty-two patients were treated for recurrent ventricular tachycardia or ventricular fibrillation, 4 for complex ventricular ectopy and 12 for supraventricular tachyarrhythmias. Patients have been treated for a mean of 9.9 months (range, 1 day to 39.1 months); 34(55%) continued to be successfully treated for ventricular tachycardia/ventricular fibrillation, 2 (50%) for complex ventricular ectopy and 5 (42%) for supraventricular tachyarrhythmias. Amiodarone toxicity was frequent, occurring in 57/72 patients (79%) who were treated for more than one week. Adverse effects led to drug discontinuation in 15 (21%), 3 because of pulmonary toxicity (1 in combination with neuropathy and another with drug-induced hepatitis); 2 because of chemical hepatitis; 1, confusion; 6, neuropathy; 2, arrhythmia exacerbation; 2, symptomatic bradycardia; and 1 because of impotence. Of the 62 ventricular tachycardia/ventricular fibrillation patients who were treated with amiodarone, 8 (13%) expired: 4 died suddenly and 4 from documented ventricular tachycardia during treatment. In contrast, of 16 patients who had discontinued amiodarone because of initial adverse effects or drug failure and were treated with alternative antiarrhythmic medications, 5 (31%) died suddenly. In conclusion, amiodarone appears to be fairly effective in high risk patients with refractory cardiac tachyarrhythmias but results in a rather high incidence of adverse effects in long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

静脉胺碘酮在危及生命的室性心律失常中的应用

介绍静脉应用胺碘酮对危及生命的室性心律失常的临床应用经验。 5 6例合并器质性心脏病的反复发作持续性室性心动过速 (VT) /心室颤动 (VF)患者 ,男 42例、女 14例 ,年龄 49.6± 13.8岁 ,其中冠心病心肌梗死 42例、心肌病13例、先天性心脏病 1例。静脉注射胺碘酮首剂 3～ 5mg/kg,10min注入 ,继之以 1.0～ 1.5mg/min维持静脉点滴 ,以后依病情渐减。静脉应用同时加用口服 6 0 0～ 12 0 0mg/2 4h。第 1次负荷量后 ,若心律失常控制不理想 ,可每隔 15～30min再给 1.5～ 3.0mg/kg的追加负荷量。以VT、VF消失为有效。第 1个 2 4h静脉用量 15 86 .5± 316 .8mg。维持静脉点滴 4.5± 2 .6天。总有效率 85 .7%。对持续性VT终止率 2 6 .9%。静脉用药早期对PR、QTc间期、QRS波时限无影响。静脉用药期间 ,3例出现窦性心动过缓 ,经减量后恢复 ;1例出现一过性Ⅱ度房室阻滞 ;12例出现静脉炎。静脉胺碘酮治疗危及生命的室性心律失常安全有效。 2 4h 10 0 0～ 15 0 0mg为较合适的初始静脉用量。     

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.     

Current approaches to drug treatment of ventricular arrhythmias

Ventricular arrhythmias are common and cause serious problems, ranging from symptom aggravation to sudden cardiac death. New knowledge about arrhythmias and new antiarrhythmic drugs provide greater opportunities for treatment choice and evaluations. A prognostic classification of ventricular arrhythmias helps to focus management. For benign ventricular arrhythmias, the objective of drug treatment is alleviation. The best management approach to potentially malignant ventricular arrhythmias, however, is not yet known, and data from ongoing clinical studies continue to accrue, developing the knowledge base needed to devise better regimens. Symptomatic patients can be managed either by symptom alleviation, as in benign arrhythmia, or more aggressively, as in malignant ventricular arrhythmia. Treatment is not mandatory for asymptomatic patients with potentially malignant ventricular arrhythmias, because there is no evidence that reducing arrhythmia prolongs life or effectively prevents symptomatic disease. Also, antiarrhythmic drugs have the potential for causing adverse effects, even lethal ones. For malignant ventricular arrhythmia, the objective of treatment is prevention of symptomatic ventricular arrhythmia and sudden cardiac death. Effective new methods predictive of successful drug treatment in individual patients are available; these methods remove much of the empiricism from management of patients with malignant ventricular arrhythmia. Treatment deemed effective by rigorous noninvasive evaluation or by electrophysiologic studies has a high probability of success in the long term. Drug management of malignant ventricular arrhythmia should become more effective in the future as a result of newly developing approaches to drug evaluation.     

Suppression of ventricular arrhythmias with intravenous disopyramide and lidocaine: efficacy comparison in a randomized trial.

Twenty-six patients with clinically significant ventricular arrhythmias were randomly assigned to treatment with either intravenous disopyramide or lidocaine; crossover to the other agent was permitted in nine cases of primary drug failure. In addition, disopyramide was administered nonrandomly to seven patients with ventricular arrhythmias not controlled by lidocaine in standard doses. Arrhythmia control (greater than 50 percent reduction of premature ventricular complexes) was achieved in all 22 trials with disopyramide and in 9 of 13 trails with lidocaine in the random study, whereas clinical efficacy (arrhythmia control with absence of side effects) occurred respectively in 15 of 22, and 8 of 13 trials. In all 11 patients (7 nonrandom, 4 random) whose arrhythmia was not controlled with lidocaine the arrhythmia was controlled with disopyramide. Thus, the clinical efficacy of intravenous disopyramide ran parallel to that of lidocaine in patients with ventricular arrhythmias. Furthermore, intravenous disopyramide was an effective alternative agent for patients with arrhythmia not controlled by lidocaine.     

胺碘酮联合美托洛尔治疗心律失常的临床疗效分析

目的探讨胺碘酮联合美托洛尔治疗心律失常的临床疗效。方法选取我院在2009年01月到2012年12月收治的90例心律失常患者随机分为对照组和观察组,对照组患者单独给予胺碘酮治疗,观察组患者给予胺碘酮联合美托洛尔治疗,对比观察两组治疗方法的临床疗效。结果两组患者在临床疗效总有效率、治疗前后期前收缩、血压情况上存在的差异性具有统计学意义（P〈0．05）;两组患者在不良反应发生率上无明显差异性（P〉0．05）。结论胺碘酮联合美托洛尔治疗心律失常取得的临床疗效显著,具有安全、可靠性。     

胺碘酮不同给药方法治疗恶性心律失常

目的对胺碘酮不同给药方法治疗恶性心律失常的临床疗效进行观察和探讨。方法选择50例于2012年1月至2013年7月间在我院进行恶性心律失常治疗的患者资料进行研究和分析,将患者分为对照组和治疗组两组,每组各有25例患者,对对照组患者进行胺碘酮治疗,对治疗组患者进行胺碘酮联合门冬氨酸钾镁治疗,比较和分析两组患者的治疗效果。结果对照组8例患者治疗显效,9例患者治疗有效,8例患者治疗无效,治疗总有效率为68％,治疗组15例患者治疗显效,9例患者治疗有效,1例患者治疗无效,治疗总有效率为96％,两组患者治疗效果差异具有统计学意义（P〈0．05）。对照组患者药物起效时间为明显长于治疗组患者,两组患者药物起效时间差异具有统计学意义（P〈0．05）。两组患者不良反应发生情况差异不具有统计学意义（P〉0．05）。结论对恶性心律失常患者进行胺碘酮联合门冬氨酸钾镁治疗能够取得更加理想的治疗效果,值得推广和应用。     

静脉注射免疫球蛋白在暴发性心肌炎中的应用价值

摘要 静脉注射免疫球蛋白(IVIG)是临床上推荐治疗暴发性心肌炎（FM）的一种药物治疗方案，其可通过抗病毒、抗炎、免疫调节等相关机制减少心肌细胞损伤，可能改善左室功能、降低恶性心律失常发生率，降低FM患者死亡率，在FM的治疗中具有一定的应用价值。但IVIG治疗FM的最佳时机、剂量和用法，以及对FM患者预后的影响仍有待进一步开展更多的前瞻性临床研究来明确。     

Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.

AIMS: Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. METHODS AND RESULTS: The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. CONCLUSION: Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.     

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.     

Oral and Intravenous Amiodarone for Atrial Fibrillation-Flutter

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.     

Contemporary Clinical Trials in Ventricular Tachycardia and Fibrillation: Implications of ESVEM, CASCADE, and CASH for Clinical Management

Trials in Ventricular Tachycardias. Recent clinical trials in patients with ventricular tachycardia (VT) or fibrillation (VF) have occurred in the setting of the disappointing results of postinfarction secondary prevention studies using Class I antiarrhythmics (e.g., CAST). ESVEM addressed in a randomized trial whether electrophysiologic study (EPS) or Hotter monitoring (HM) is a more accurate predictor of long-term antiarrhythmic drug efficacy in VT/VF patients (N = 486) and what the relative efficacy of various antiarrhythmic agents is for VT/VF. Surprisingly, arrhythmia recurrence rates were not significantly different by the method of determining an efficacy prediction. However, arrhythmia recurrence and mortality were lower (by about 50% at 1 year) in patients treated with sotalol (a mixed Class II/III agent) than with other drugs (Class I). CASCADE evaluated empiric amiodarone versus guided (EPS or HM) standard (Class I) therapy in survivors of out-of-hospital cardiac arrest due to VF. The primary endpoint of cardiac death, resuscitated VF, or syncopal shock (in ICD patients) was reduced by amiodarone compared with conventional therapy (9% vs 23% at 1 year). An interim report of the ongoing CASH study suggested in 230 survivors of cardiac arrest that propafenone (Class IC) provided less effective prophylaxis (approximately 20% 1-year mortality) compared with randomly assigned therapies with amiodarone, metoprolol, or an ICD (approximately 14% mortality rates) and was excluded from further study. These studies have led to a paradigm shift in the approach to antiarrhythmic therapy of VT/VF: drugs with antisympathetic plus Class III (refractoriness prolonging) action (i.e., sotalol, amiodarone) are superior to traditional drugs with Class I (conduction slowing) effects, even when guided by EPS or HM.     

Intravenous Procainamide for Predicting the Response of Sustained Ventricular Tachycardia to Type III Antiarrhythmic Drugs

The use of serial electrophysiology studies to guide antiarrhythmic drug therapy in patients with ventricular tachycardia is both costly and time consuming. Intravenous procainamide administered during of the initial electrophysiology study has previously been shown to be useful in predicting the efficacy of oral antiarrhythmic medications (type I and III). The purpose of this study is to confirm that ventricular tachycardia suppression after intravenous procainamide correlates with suppression on oral class III antiarrhythmic medications (amiodarone and sotalol). This study included all patients with sustained ventricular tachycardia who underwent an initial electrophysiology study including an acute suppression trial with intravenous procainamide and a subsequent restudy on oral amiodarone or sotalol. The response to intravenous procainamide was then compared with these type III antiarrhythmic medications. Between January 1993 and May 1995, 360 patients underwent electrophysiology studies for suspected or documented ventricular arrhythmias. One hundred patients (28%) had an inducible sustained ventricular tachycardia, and 26 patients received both intravenous procainamide and subsequently oral amiodarone or sotalol. Acute infusion of procainamide provided a highly specific method for predicting suppression of oral amiodarone and sotalol (82% and 100% respectively). However, several patients who were not suppressed by intravenous procainamide were suppressed by oral sotalol resulting in lower overall predictive accuracy 12/15 (80%) for amiodarone vs. 5/11 (45%) for sotalol treated group. We conclude that the acute infusion of procainamide may help to predict ventricular tachycardia suppression after oral amiodarone and sotalol. A larger prospective trial is warranted to confirm this finding.     

静脉艾司洛尔治疗快速性室性心律失常的临床观察简

目的 探讨艾司洛尔治疗快速性室性心律失常的临床疗效及安全性.方法 2011年1月至2012年12月在解放军252医院心内科住院的49例患者,在住院期间发生快速室性心律失常,年龄（61.72±3.32）岁.分为两组：单纯艾司洛尔组为电复律或电除颤＋艾司洛尔（26例）;联合艾司洛尔组为电复律或电除颤＋盐酸胺碘酮＋艾司洛尔（23例）.结果 联合电复律或电除颤治疗,单纯艾司洛尔组有效率96％ （25/26）,在胺碘酮无效的基础上或同时加用静脉艾司洛尔,有效率69.5％ （16/23）,单纯艾司洛尔组终止交感风暴的成功率显著高于胺碘酮组,差异有统计学意义（P＜0.05）.艾司洛尔给药后室性心动过速或心室颤动复发次数明显减少,相应除颤次数较常规组少;未发生不能维持的低血压状态和严重缓慢性心律失常.结论 及时的电复律或电除颤和使用β受体阻断药艾司洛尔,可有效控制快速性室性心律失常的发作.     

胺碘酮治疗维吾尔族器质性心脏病人室性心律失常的疗效和安全性

目的：评价胺碘酮治疗维吾尔族器质性心脏病人室性心律失常的疗效和安全性。方法：观察47例维吾尔族器质性心脏病人采用胺碘酮治疗室性心律失常的疗效和安全性，随访1～3年。结果：6例反复发作的持续性室速、室颤病人，首剂3～5mg／kg胺碘酮10min内静脉注射，再以1～1．5mg／min缓慢滴注，室速均被有效终止。以200mg／d胺碘酮作为长期维持量能有效的控制室性早搏(92．7％)。6例静脉注射胺碘酮病人中窦性心动过缓5例、PR间期延长1例；在41例长期口服维持量的病人中甲状腺功能低下者1例、窦性心动过缓18例、QT间期延长22例，但无肺损害发生。结论：采用胺碘酮治疗维吾尔族器质性心脏病人室性心律失常效果满意，安全可靠。