胺碘酮和普罗帕酮治疗冠心病并室性心律失常的疗效比较

比较胺碘酮和普罗帕酮治疗冠心病心肌缺血患者室性心律失常的疗效。6 9例冠心病心肌缺血合并室性心律失常患者 ,均接受冠心病正规治疗 ,其中 35例同时口服胺碘酮片 (胺碘酮组 ) ,34例口服普罗帕酮片 (普罗帕酮组 ) ,疗程 4周。疗程开始及结束时均行 2 4h动态心电图及 12导联心电图检查。结果 :两组患者用药后 2 4h室性早搏 ,短阵室性心动过速的发作次数均明显减少 (胺碘酮组用药后与用药前比较分别为 2 70 5± 14 77个vs 6 834± 45 2 8个 ,7.4 2± 3.30次vs 1.2 9± 0 .93次 ;普罗帕酮组则分别为 6 712± 3385个vs 396 2± 1983个 ,8.0 5± 3.37次vs4 .2 2± 2 .5 9次 ,P均 <0 .0 1)。胺碘酮组的疗效高于普罗帕酮组 (P <0 .0 1)。两组未见严重副作用。结论 :胺碘酮对冠心病伴室性心律失常的疗效优于普罗帕酮。     

胺碘酮和美西律治疗冠心病并室性心律失常56例疗效比较

目的比较胺碘酮和美西律治疗冠心病心肌缺血患者室性心律失常的疗效。方法56例冠心病心肌缺血合并室性心律失常患者,均接受冠心病正规治疗,其中30例同时口服胺碘酮片(胺碘酮组),26例口服美西律片(美西律组),疗程4周。疗程开始及结束时均行24h动态心电图及12导联心电图检查。结果两组患者用药后24h室性早搏、短阵室性心动过速的发作次数均明显减少,胺碘酮组用药后与用药前比较分别为(2801±356)个和(6935±1427)个,(1.28±0.92)次和(7.39±3.31)次;美西律组则分别为(3958±966)个和(6726±1395)个,(4.25±2.61)次和(8.10±3.32)次,P均<0.01。胺碘酮组的疗效高于美西律组(P<0.01)。两组均未见严重副作用。结论胺碘酮对冠心病伴室性心律失常的疗效优于美西律。     

胺碘酮联合倍他乐克治疗冠心病频发室性期前收缩的疗效观察

目的探讨胺碘酮联合倍他乐克治疗冠心病室性心律失常的疗效及安全性。方法将60例冠心病频发室性期前收缩患者随机分为观察组(30例)和对照组(30例),观察组给予静脉注射胺碘酮(24h)及口服维持,同时口服倍他乐克治疗;对照组静脉注射利多卡因(24h),同时口服倍他乐克治疗,疗程均为4周。结果观察组总有效率为90.0%,高于对照组的76.7%,差异有统计学意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论胺碘酮联合倍他乐克治疗冠心病室性心律失常安全、有效。     

胺碘酮治疗冠心病室性心律失常的疗效观察

目的 观察胺碘酮治疗冠心病室性心律失常的疗效.方法 选取2011年1月-2013年2月我院收治的冠心病室性心律失常患者86例,将其随机分为对照组和观察组.对照组口服普罗帕酮;观察组口服胺碘酮,根据患者的病情变化逐渐停止用药,至少坚持服药2个月.2个月后,比较两组患者疗效.结果 观察组总有效率为95.3%,高于对照组的79.1%,差异有统计学意义（P＜0.05）.结论 胺碘酮治疗冠心病室性心律失常有显著的疗效,有临床应用推广价值.     

胺碘酮大剂量静脉应用治疗急性心肌梗死后恶性室性心律失常

目的:观察大剂量静脉应用胺碘酮救治经利多卡因等治疗无效的急性心肌梗死并发恶性室性心律失常患者的临床疗效。方法:42例患者急性心肌梗死并发室速、室颤,经利多卡因等药物治疗无效后,改用大剂量胺碘酮静脉给药。结果:40例急性心肌梗死发病1～8小时发生室速、室颤者,经静脉用胺碘酮0.5～1小时内均有效;另2例是急性心肌梗死发病后1～2周出现的持续性室速,24小时内也有效。42例患者住院期间无一例死于心律失常,6例发生静脉炎,2例在口服胺碘酮过程中出现房室传导阻滞,无一例发生肺中毒等其他副作用;亦无一例出现或加重充血性心力衰竭。结论:大剂量静脉应用胺碘酮对治疗急性心肌梗死并发致命性室性心律失常是一种极其有效而且安全的方法。     

稳心颗粒联合美托洛尔治疗冠心病室性心律失常疗效观察

目的观察稳心颗粒联合关托洛尔治疗冠心病室性心律失常的疗效。方法将115例冠心病合并室性心律失常患者随机分为治疗组（A组）40例,口服稳心颗粒和美托洛尔治疗;对照组75例[其中关托洛尔组（B组）37例。口服美托洛尔治疗,胺碘酮组（C组）38例,口服胺碘酮治疗]。结果治疗组在动态心电图疗效上优于单用美托洛尔组（P〈0．05）,与胺碘酮组疗效比较差异无统计学意义（P〉0．05）。在临床症状改善上效果优于单用美托洛尔组和胺碘酮组（P〈0．05）。结论稳心颗粒联合美托洛尔能有效治疗冠心病室性心律失常,不良反应小,患者耐受性良好,具有临床应用价值。     

胺碘酮治疗冠心病室性心律失常37例临床研究

目的观察胺碘酮治疗冠心病室性心律失常的效果。方法选取我院2010年3月~2014年12月收治的冠心病室性心律失常患者74例,随机将其分为观察组和对照组,各37例。在对症治疗的基础上,对照组给予普罗帕酮治疗,观察组给予胺碘酮治疗,两组均以7天为1个疗程,共治疗1个疗程。结果观察组总有效率为97.30%;对照组总有效率为83.78%。两组比较,差异有统计学意义(P0.05)。结论胺碘酮治疗冠心病室性心律失常效果满意,值得临床推广。     

室性心律失常患者治疗中胺碘酮的应用效果分析

目的探讨胺碘酮治疗室性心律失常的临床效果。方法我院2011年1月～2013年1月问收治的冠心痛室性心律失常患者54例,对其临床资料进行回顾性分析。结果服用胺碘酮的观察组患者心电图检查结果优于口服普罗帕酮的对照组患者,临床疗效优于对照组,二者差异有统计学意义（P〈0．05）;两组不良反应发生率无显著差异（P〈0．05）。结论室性心律失常应用小剂量胺碘酮治疗效果颇佳,可作临床推广应用。     

三味檀香胶囊联合胺碘酮治疗冠心病室性心律失常

目的观察三味檀香胶囊联合胺碘酮治疗冠心病室性心律失常的疗效。方法 100例冠心病患者随机分为两组,在常规治疗冠心病基础上,治疗组服用三味檀香胶囊及胺碘酮,对照组只服用胺碘酮,疗程为4周。结果治疗组总有效率及治疗前后室性早搏总数均较对照组有统计学意义(P0.05),治疗后治疗组QT离散度较对照组相对更小(P0.05)。结论三味檀香胶囊联合胺碘酮治疗冠心病室性心律失常疗效优于单用胺碘酮。     

胺碘酮联合普罗帕酮治疗室性期前收缩的临床研究

目的 观察胺碘酮联合普罗帕酮治疗室性期前收缩的疗效及安全性。方法将291例室性期前收缩患者随机分成3组,A组（65例）给予普罗帕酮片150mg口服,1次／8h。B组（68例）给予胺碘酮200mg口服,3次／d,1周后改为200mg口服,2次／d,再1周后改为200mg口服,1次／d。C组（68例）开始给予胺碘酮200mg口服,3次／d,普罗帕酮片150mg口服,1次/8h,治疗1周后,停用普罗帕酮片,同时胺碘酮改成200mg口服,2次／d,再1周后,胺碘酮改为200mg口服,1次／d。治疗周期均为3个月。结果住院期间,c组在控制室性期前收缩的时间上明显短于B组;出院后,c组在停药后的3个月里室性期前收缩复发率远低于A组。结论联合使用胺碘酮及普罗帕酮治疗室性期前收缩是安全有效的。     

European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias

Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.     

稳心颗粒治疗冠心病室性期前收缩的临床研究

目的研究稳心颗粒治疗冠心病室性期前收缩的临床疗效。方法将70例病人随机分为稳心颗粒组(治疗组)36例和心律平组(对照组)34例,两组均以4周为1个疗程,观察两组治疗前后综合临床疗效、心电图疗效、伴随症状改善情况、心功能改善情况及不良反应。结果治疗组总有效率为88.89%,明显优于对照组的61.76%(P<0.05),两组治疗后临床症状积分、心功能均较治疗前明显改善(P<0.05或P<0.01),且治疗组优于对照组(P<0.05或P<0.01)。结论稳心颗粒能改善冠心病室性期前收缩病人的症状及心功能,疗效显著,且不良反应发生率低。     

Management of patients with life-threatening sustained ventricular tachyarrhythmias—The role of guided antiarrhythmic drug therapy

Two recent studies have evaluated the utility of electrophysiologic (EP) testing in the treatment of patients with serious ventricular arrhythmias. The first study compared electrophysiologically guided antiarrhythmic drug therapy with nonguided β-blocker therapy. Patients without inducible arrhythmias were assigned to oral metoprolol; patients with inducible arrhythmias were randomly assigned to receive either oral metoprolol or EP-guided drug therapy with propafenone, flecainide, disopyramide, sotalol, or amiodarone. Antiarrhythmic drugs were tested in a random order, but amiodarone was always tested last. A total of 170 patients were evaluated; 115 patients had inducible arrhythmias, and 61 patients were randomly assigned to serial drug testing, 54 to metoprolol without invasive testing, and the remainder who were noninducible to empiric metoprolol. The best outcome was observed in patients without inducible arrhythmias, all of whom received metoprolol. There was no difference in outcome between the two groups with inducible arrhythmias, either treated with metoprolol or with EP-guided serial antiarrhythmic drug testing. The second study evaluated survivors of out-of-hospital ventricular fibrillation (VF) without new myocardial infarction. Patients received assessment of left ventricular ejection fraction, Holter monitoring (HM), and EP testing. Only patients with inducible sustained ventricular arrhythmias or with sufficient ambulatory ventricular ectopy were included in the study. Therapy was randomized either to empiric amiodarone or conventional drug therapy guide by EP testing and/or HM. A total of 228 patients were treated, 113 with amiodarone and 115 with conventional antiarrhythmic drug therapy. The composite primary end points were total mortality, documented out-of-hospital resuscitation from recurrent VF, or syncopal implantable cardioverter/defibrillator shock followed by return of consciousness. Patients treated with empiric amiodarone had a better outcome than did patients treated with guided conventional drug therapy. In those patients in whom an implantable cardioverter/defibrillator was used, patients treated with amiodarone had fewer total shocks and fewer syncopal shocks than did patients treated with conventional therapy. Patients with a history of out-of-hospital VF or sustained ventricular tachycardia without inducible ventricular arrhythmias at EP study have the best outcome. Empiric metoprolol is equivalent to conventional antiarrhythmic drug therapy guided by EP testing. Empiric amiodarone is superior to conventional antiarrhythmic drug therapy guided by HM and/or EP testing.     

Differences in amiodarone efficacy in relation to ejection fraction and basal rhythm in patients with implantable cardioverter defibrillators

Background

Atrial fibrillation (AF) and ventricular arrhythmias (VAs) are associated with increased morbidity and mortality. However, data are lacking concerning the association of AF and VAs. This study aimed to clarify the association between AF and VAs and to investigate the effect of amiodarone on the incidence of VAs in patients with implantable cardioverter defibrillators (ICDs).

The use of associated propafenone in patients with amiodarone-resistant ventricular tachycardia

To clarify the risk-benefit ratio involved in association of antiarrhythmic drugs, a combined therapy of amiodarone and propafenone was tested by means of continuous electrocardiographic monitoring, analysis of levels of the drug in the plasma and programmed electrical stimulation in a selected group of 10 patients who had left ventricular dysfunction and spontaneous relapses of sustained ventricular tachycardia despite treatment with amiodarone. Induction of sustained ventricular tachycardia, possible in each case during treatment with amiodarone, was suppressed after addition of propafenone in 2 patients (responders), who had the best ejection fractions of the entire group (greater than 45%). Worsening of spontaneous tachycardias developed in 4 cases during the combined therapy. These ventricular arrhythmias, although generally at a low rate, sometimes had the potential to degenerate into ventricular fibrillation and disappeared after both discontinuation of propafenone or increase of its dosage (1 patient). Of the six cases undergoing chronic combined treatment, only the responders to premature electrical stimulation were completely protected from recurrences of arrhythmia. Three cases, on the other hand, needed permanent endocardial pacing for symptomatic bradyarrhythmias. The combination of treatment with amiodarone and propafenone, although potentially useful in limiting dosages of and toxicity from amiodarone, is frequently associated with undesirable, and occasionally has severe, side-effects. The best candidates for this pharmacological association seem to be patients without severely depressed left ventricular function who have a greater probability of not presenting the inducibility of ventricular tachycardia after the addition of propafenone to the regimen for treatment.     

盐酸关附甲素注射液治疗室性心律失常的多中心随机双盲试验

目的 评价国家一类新药盐酸关附甲素注射液（GFA）治疗室性心律失常的疗效和安全性.方法 随机双盲多中心阳性药对照试验,由全国8家临床药理基地完成.入选不伴严重器质性心脏病的频发室性早搏（室早）患者,室早平均每小时≥150次（用Holter评价）,伴或不伴短阵室性心动过速.采用1∶1随机对照使用GFA或盐酸普罗帕酮.采用静脉负荷加维持量的方法维持6 h.用药前一天和用药日均进行24 h Holter及心电监测进行疗效评价.监测生命体征、心电图及观察不良事件.结果 共入选201例患者,用药前两组在病史、体检、实验室检查、室早数量、短阵室性心动过速数量差异均无统计学意义.GFA组与盐酸普罗帕酮组室早减少百分数和总有效率差异无统计学意义.室早减少百分数分层分析,GFA有优于盐酸普罗帕酮的趋势,达到统计学差异临界值（P=0.0609）.GFA抑制室早的程度以及控制室早的作用出现时间与盐酸普罗帕酮差异无统计学意义.GFA静脉应用耐受性较好,发生不良事件的严重程度明显轻于盐酸普罗帕酮,差异有统计学意义.结论 GFA控制室性心律失常安全有效,其疗效相当于盐酸普罗帕酮,发生的不良事件较盐酸普罗帕酮为轻,今后应对其抗心律失常作用进行进一步的研究.     

Anti-arrhythmia efficacy of propafenone in children. Apropos of 30 cases

Thirty children aged from 3 months to 20 years were treated with propafenone 250 to 650 mg/m2 divided into 2 to 4 daily doses, for a mean period of 14 months (range: 4 days to 5 years); 8 had chronic atrial tachycardia, 9 had junctional arrhythmia and 13 had ventricular arrhythmia. There were 17 good results (suppression of the arrhythmia), 7 fair results (good clinical effect but partial persistence of the arrhythmia) and 6 failures, either because the drug proved ineffective (3 cases) or on account of side-effects (3 cases). In the treatment of chronic atrial tachycardia propafenone seemed to be more effective than amiodarone in 3 cases and as effective as that drug in 2 cases. In junctional arrhythmia propafenone was certainly effective but unpredictably so (3 good results, 2 fair results, 4 failures). Among ventricular arrhythmias, ventricular tachycardia in bursts was the one which benefited most regularly from treatment with propafenone: the results in 8 patients were better than those obtained with other antiarrhythmic agents (class I drugs, beta-blockers, calcium antagonists); only amiodarone proved superior to propafenone in this type of arrhythmia. Despite a 27% incidence of side-effects, propafenone was generally well tolerated by the children, with no significant gastrointestinal disorders. No depressive effect on the myocardium was noted in 6 children with moderate heart failure well controlled by digitalis and diuretics. However, since overdosage may cause severe disorders of conduction with widened ventriculogram, we recommend regular ECG monitoring during the first 3 days of treatment at least: although there is little slowing down of sinus rate (12%) and little modification of the slow phase under treatment, serious toxicity is possible. Thus, propafenone is a drug that should be handled with caution, but it constitutes a major addition to the range of antiarrhythmic agents which can be used in paediatrics.