胺碘酮治疗冠心病室性心律失常效果的临床观察

目的观察并比较胺碘酮与普罗帕酮治疗冠心病室性心律失常效果。方法随机选取90例冠心病室性心律失常患者为研究对象,按照随机化原则分为胺碘酮治疗组和普罗帕酮治疗组各45例,两组常规治疗基础疾病的措施相同,前组给予600 mg/d胺碘酮口服,3次/天,1周后剂量改为200~400 mg/d,分2次服,2周后改为每次维持200 mg或100 mg;后组给予患者150 mg盐酸普罗帕酮片口服,3次/天。4周后观察治疗效果。结果应用胺碘酮治疗45例冠心病室性心律失常患者的显效、有效、无效人数分别为21、19、5例,总有效率为88.89%,应用普罗帕酮治疗45例冠心病室性心律失常患者的显效、有效、无效人数分别为18、14、13例,总有效率为71.11%,碘胺酮的疗效和总有效率均高于普罗帕酮(P均<0.05),不良反应发生率相同(P=0.25)。结论盐酸胺碘酮治疗冠心病室性心律失常效果明显,因其有扩张冠状动脉,改善心肌供血的作用,适用于伴有器质性心脏病者,故值得临床广泛应用。     

胺碘酮治疗心律失常34例疗效观察

目的观察胺碘酮治疗心律失常的临床疗效。方法对34例快速性心律失常患者静脉注射胺碘酮首剂150mg,随后以6～30μg·kg-1·min-1维持静脉滴注1～4d;同时口服胺碘酮600mg/d,1周后减为400mg/d,2周可减至200～300mg/d维持。如仍有室性心律失常,加用胺碘酮200mg口服,每天1次,连用15～30d。结果显效18例占52.9%,有效15例占44.1%,无效1例占2.9%,总有效率为97.1%。其中出现低血压1例,恶心呕吐2例。结论胺碘酮是广谱抗心律失常药,不良反应少,在防治危及生命的室性心律失常患者可列为一线抗心律失常药物。     

胺碘酮治疗心律失常34例疗效观察

目的 观察胺碘酮治疗心律失常的临床疗效.方法 对34例快速性心律失常患者静脉注射胺碘酮首剂150mg,随后以6～30μg·kg-1·min-1维持静脉滴注1～4d;同时口服胺碘酮600mg/d,1周后减为400mg/d,2周可减至200～300mg/d维持.如仍有室性心律失常,加用胺碘酮200mg口服,每天1次,连用15～30d.结果 显效18例占52.9%,有效15例占44.1%,无效1例占2.9%,总有效率为97.1%.其中出现低血压1例,恶心呕吐2例.结论 胺碘酮是广谱抗心律失常药,不良反应少,在防治危及生命的室性心律失常患者可列为一线抗心律失常药物.     

胺碘酮干预治疗恶性室性心律失常及心源性猝死疗效分析

目的观察胺碘酮治疗恶性室性心律失常以及心源性猝死的疗效。方法将165例ICU伴发恶性室性心律失常住院患者采用随机数字表法分为治疗组和对照组。对照组进行针对原发病及症状体征的综合治疗。治疗组在此基础上加用胺碘酮300mg／d口服,连服1周后改为100mg／d,口服,然后将两组患者恶性室性心律失常复发率及心性源猝死发生率进行比较。结果治疗组恶性室性心律失常复发率及心性源猝死发生率分别为18．60％和6．98％,均显低于对照组．P〈0．05,差异有统计学意义。结论胺碘酮可有效控制恶性室性心律失常以及心源性猝死,临床价值较高。     

胺碘酮治疗急性心肌梗死室性心律失常150例临床报告

目的评价胺碘酮治疗急性心肌梗死（acute myocardial infarction,AMI）室性心律失常的疗效和安全性。方法观察150例AMI患者采用胺碘酮治疗室性心律失常的疗效和安全性,随访1年。结果反复发作的持续性室速、室颤患者,首剂3～5mg／kg胺碘酮10min内静脉注射;再以1—1．5mg／min维持,室速均被有效终止。以200mg／d胺碘酮作为长期维持量能有效控制室性期前收缩。结论采用胺碘酮治疗AMI患者室性心律失常效果满意,安全可靠。     

冠心病慢性心力衰竭患者室性心律失常的临床治疗分析

目的探讨冠心病慢性心力衰竭患者室性心律失常的临床治疗效果。方法选取2011年1月至2012年8月我院收治的冠心病慢性心力衰竭合并室性心律失常患者共120例,随机分为实验组和对照组,其中对照组患者采用常规治疗,而实验组患者在此基础上加用胺碘酮治疗。结果实验组患者临床疗效显效、有效、无效分别为31例（51．67％）、22例（36．67％）、7例（11．67％）,总有效率达88．33％;而对照组患者临床疗效显效、有效、无效分别为13例（21．67％）、25例（41．67％）、22例（36．67％）,总有效率为63．33％。两组患者总有效率差异存在统计学意义（P〈0．05）,说明实验纽患者的总有效率明显高于对照组患者。结论胺碘酮配合常规治疗冠心病慢性心力衰竭合并室性心律失常具有较佳的临床效果。     

口服胺碘酮联合静脉注射利多卡因治疗急性心肌梗死室性心律失常的疗效观察

目的探讨口服胺碘酮联合静脉注射利多卡因治疗急性心肌梗死室性心律失常的临床疗效。方法收集我院2011年7月至2012年8月治疗的80例急性心肌梗死室性心律失常患者,随机分成对照组和观察组各40例,对照组给与口服胺碘酮进行治疗,观察组在对照组的基础上给予静脉推注利多卡因1mg/kg,然后每10min给0.5mg/kg,至早搏消失。结果观察组显效32例,显效率为80.0%,有效7例,有效率为17.5%,无效1例,总有效率为97.5%;对照组显效20例,显效率为50.0%,有效10例,无效10例,总有效率为75.0%,两组比较有显著性差异(P<0.05)。结论口服胺碘酮联合静脉注射利多卡因治疗急性心肌梗死室性心律失常疗效显著,值得推广。     

胺碘酮治疗顽固性心律失常疗效分析

目的本文旨在探索采用胺碘酮治疗室性心律失常患者的临床有效性和安全性。方法采用lf缶床资料回顾分析法进行回顾分析自2008年11月一2011年3月这一时期来本院就诊的120例冠心病并伴有室性心律失常的患者的临床资料,前7d给予患者1：3服胺碘酮0．2e,／次,3次／d后改为0．2∥次,2次／d,也连续用7d,后减为0．2g,1次／d进行维持治疗。采用动态心电图、超声心动图等来评价治疗效果以及患者心率、Q-T间期变化以及不良反应等。结果研究结果显示本次120例患者采用胺碘酮治疗室性心律失常的总有效率为95％,其中显效78例（65％）,有效36例（30％）,所有患者都没有出现严重的不良反应。结论采用胺碘酮治疗室性心律失常患者的临床疗效比较满意,且不良反应少安全性比较高。     

步长稳心颗粒联合胺碘酮治疗老年人室性早搏的疗效观察

目的观察步长稳心颗粒联合胺碘酮治疗老年室性早搏的疗效。方法将64例老年室性早搏患者随机分为治疗组34例和对照组30例。治疗组服用步长稳心颗粒1包（9g）,每天3次;胺碘酮200mg,每天3次,7d后减为200mg,每天2次,维持量为0．1—0．2mg／d;对照组仅口服胺碘酮,用法同治疗组。治疗后比较2组疗效。结果治疗组总有效率为82．35％高于对照组的66．67％,差异有统计学意义（P〈0．05）。结论步长稳心颗粒联合胺碘酮治疗老年室性心律失常临床疗效较满意,不良反应轻微,值得推广应用。     

胺碘酮治疗老年室性心律失常的临床疗效及安全性

目的 分析胺碘酮治疗老年室性心律失常患者的临床疗效及安全性.方法 将136例年龄≥65岁室性心律失常患者随机分为观察组和对照组各68例,两组患者在试验前10 d均停用其他抗心律失常药物.对照组患者给予相关病因综合治疗,观察组在对照组治疗基础上应用胺碘酮200 mg,口服,3次/d.根据患者情况,7d后改为200 mg,2次/d.7d后,再改为200 mg,1次/d,维持到患者心律失常控制,而后给予每天50 mg维持,两组患者均治疗4周.结果 治疗后观察组显效率、总有效率分别为51.47％、92.65％,均显著高于对照组的51.47％、92.65％ （P ＜0.05）,两组不良反应发生率差异无统计学意义（P＞0.05）.结论 胺碘酮能够显著控制老年患者室性心律失常,临床效果显著,不良反应少,是一种能有效抑制心律失常,又不会促发心律失常的药物.     

Antiarrhythmic properties of a prior oral loading of amiodarone in in vivo canine coronary ligation/reperfusion-induced arrhythmia model: comparison with other class III antiarrhythmic drugs

Amiodarone, which is generally classified as class III antiarrhythmic drug in the Vaughan Williams classification, is widely used for the treatments of refractory arrhythmias. However, we previously reported that intravenous infusion of amiodarone (6.67 mg/kg per hour) did not suppress arrhythmias induced by coronary ligation/reperfusion in dogs. In this study, we examined effects of a prior oral loading of amiodarone on arrhythmias induced by coronary ligation/reperfusion. Sixteen female beagle dogs (8.5 - 12.5 kg) were divided into two groups; one group was given amiodarone (40 mg/kg, orally, n = 8), and the other was given empty gelatin capsules (n = 8) 2 h before the operation. Dogs were anesthetized with pentobarbital and artificially ventilated. The left chest was opened, and the left anterior descending coronary artery was ligated for 30 min and then reperfused. The mean plasma concentration of amiodarone was over 1.3 mug/ml. Although the prior oral loading of amiodarone did not change the QT interval, amiodarone suppressed the number of ectopic beats during coronary ligation and the incidence of ventricular fibrillation during coronary ligation and reperfusion periods (P<0.05 vs control group). In conclusion, a prior oral loading of amiodarone suppressed arrhythmias induced by coronary ligation/reperfusion with a dose that did not prolong the QT interval. This antiarrhythmic property of amiodarone is different from those of the other class III drugs in that antiarrhythmic effects were accompanied by QT prolongation in our all previous studies.     

胺碘酮治疗老年室性心律失常的疗效观察

目的:观察胺碘酮治疗老年室性心律失常的临床疗效。方法:将我院2009年6月-2010年6月收治的94例室性心律失常患者随机均分为2组,对照组采用强心、利尿、扩血管、心肌细胞营养剂等综合治疗,观察组在对照组基础上加用胺碘酮治疗,观察2组的临床疗效及对心率和PR间期的影响。结果:观察组的室性心律失常改善总有效率(83.0%)和心功能改善总有效率(76.6%)均明显高于对照组(63.8%,55.3%)(P<0.05)。观察组治疗后心率明显下降,与治疗前比较差异有统计学意义(P<0.05),但对照组治疗前、后心率比较,差异无统计学意义(P>0.05),并且观察组治疗后心率明显低于同期对照组,2组比较差异有统计学意义(P<0.05)。2组治疗后PR间期均有所延长,但差异无统计学意义(P>0.05)。2组均未见严重不良反应发生。结论:胺碘酮治疗老年室性心律失常能够明显提高心律失常改善率和心功能改善率,并且能够显著降低心率。     

急性冠状动脉综合征合并严重心律失常112例疗效和安全性分析

目的评价胺碘酮治疗ACS合并快速型心房纤颤、心房扑动或室性心律失常的疗效及安全性。方法对112例ACS合并快速型心房纤颤、心房扑动或室性心律失常的患者,先用胺碘酮150mg静脉注射后,必要时追加150mg,续以1.0mg/min滴注,维持6h,后以0.5mg/min速度维持、总量为1050～1500mg。以后口服胺碘酮,第1周600mg/d,第2周400mg/d,第3周200mg/d维持。疗程共4周。结果100例患者有效,起效时间为0.5～24h。结论静脉加口服胺碘酮治疗ACS合并快速型心房纤颤、心房扑动或室性心律失常安全有效。     

Role of antiarrhythmic therapy in patients at risk for sudden cardiac death: an evidence-based review

Sudden cardiac death (SCD) accounts for more than half of all cardiac deaths occurring each year in the United States. Although it has several causes, patients at greatest risk are those with coronary artery disease and impaired left ventricular function, heart failure secondary to ischemia or idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy, documented sustained ventricular tachycardia or ventricular fibrillation, and survivors of cardiac arrest. The presence of asymptomatic ventricular arrhythmias, positive signal-averaged electrocardiogram (ECG), low heart rate variability index, or inducible ventricular tachycardia or ventricular fibrillation increases the risk. In primary prevention trials in patients with ischemic heart disease, beta-blockers reduced both total mortality and SCD, whereas class I antiarrhythmic drugs, especially class IC, increased mortality. Among class III agents, d,l-sotalol and dofetilide have a neutral effect on mortality, whereas d-sotalol increases mortality. Amiodarone has a neutral effect on total and cardiac mortality but does reduce the risk of arrhythmic death and cardiac arrest. Three primary prevention trials in patients with ischemic heart disease were conducted with implantable cardioverter-defibrillators (ICDs). Patients with low ejection fractions (EFs), asymptomatic ventricular arrhythmias, and inducible ventricular tachycardia or ventricular fibrillation had significant reductions in total, cardiac, and arrhythmic death with ICDs compared with either no drug therapy or conventional antiarrhythmic agents. The ICDs did not reduce mortality in patients with low EFs and a positive signal-averaged ECG undergoing coronary bypass graft. In those with heart failure, beta-blockers reduced total and SCD mortality, but dofetilide and amiodarone had a neutral effect on mortality. In the secondary prevention of SCD, antiarrhythmic drugs alone generally are not thought to improve survival. In three trials in patients with documented sustained ventricular tachycardia or ventricular fibrillation, or survivors of SCD, ICDs reduced cardiac and arrhythmic mortality. Total mortality, however, was significantly reduced in only one of these trials. The role of antiarrhythmic drugs in secondary prevention of SCD is limited to patients in whom ICD is inappropriate or in combination with ICD. Antiarrhythmics can be given selectively with ICDs to decrease episodes of ventricular tachycardia or fibrillation to reduce ICD discharges, to suppress episodes of nonsustained ventricular tachycardia that trigger ICD discharges, to slow the rate of ventricular tachycardia to increase hemodynamic stability, to allow effective antitachycardia pacing, or to suppress supraventricular arrhythmias.     

In vivo and in vitro antiarrhythmic effects of SSR149744C in animal models of atrial fibrillation and ventricular arrhythmias

SSR149744C (2-butyl-3-{4-[3-(dibutylamino)propyl]benzoyl}-1-benzofuran-5-carboxylate isopropyl fumarate) is a new noniodinated benzofuran derivative structurally related to amiodarone and dronedarone that is currently undergoing clinical trials as an antiarrhythmic agent. As SSR149744C exhibits electrophysiological and hemodynamic properties of class I, II, III, and IV antiarrhythmic agents, the aim of this study was to evaluate its acute intravenous (IV) or oral (PO) antiarrhythmic activities in in vitro and in vivo animal models of atrial and ventricular arrhythmias. In vagally induced atrial fibrillation (AF) in anesthetized dogs, SSR149744C (3 and 10 mg/kg IV) terminated AF in all 7 dogs and prevented reinduction in 4 out of 7 dogs; effective refractory periods of right atrium were dose-dependently and frequency-independently lengthened. In low-K+ medium-induced AF models, SSR149744C (0.1 to 1 microM) prevented AF in isolated guinea pig hearts in a concentration-dependent manner. At the ventricular level, SSR149744C (0.1 to 10 mg/kg IV and 3 to 90 mg/kg PO) prevented reperfusion-induced arrhythmias in anesthetized rats with a dose-effect relationship, and, at doses of 30 to 90 mg/kg PO, it reduced early (0-24 hours) mortality following permanent left coronary artery ligature in conscious rats. The present results show that SSR149744C is an effective antiarrhythmic agent in atrial fibrillation and in ventricular arrhythmias. Like amiodarone and dronedarone, its efficiency in these animal models of arrhythmias is likely be related to its multifactorial mechanism of action.     

Antiarrhythmic and antifibrillatory properties of McN-4130 in several animal models

McN-4130 is an experimental compound having antiarrhythmic and antifibrillatory activity in several animal models. In anesthetized, open-chest pigs subjected to total occlusion and subsequent reperfusion of the left anterior descending coronary artery, McN-4130 dose-dependently (2.5-10.0 mg/kg i.v.) protected against fibrillation and death. Mean arterial pressure was not significantly affected, but heart rate was dose-dependently reduced. In anesthetized normal dogs, McN-4130 increased ventricular fibrillation threshold for up to 45 min. This increase in fibrillation threshold was associated with concurrent increases in ventricular conduction time and ventricular effective refractory period. In conscious dogs subjected to occlusion of the left anterior descending coronary artery 24 h previously, McN-4130, 2.5 and 5.0 mg/kg i.v., significantly reduced the rate of ventricular arrhythmias for up to 45 min. McN-4130 was more effective and had a longer duration of action than comparable doses of lidocaine and disopyramide. McN-4130 was orally effective in this model at 10 mg/kg. These results indicate that McN-4130, a structurally unique experimental antiarrhythmic compound, may be useful as a ventricular antiarrhythmic agent with antifibrillatory properties.     

The effect of antiarrhythmic agents on myocardial contractility and arrhythmia frequency

Most patients requiring antiarrhythmic therapy for ventricular arrhythmias have underlying organic heart disease which causes left ventricular dysfunction. Treatment of these patients' arrhythmias requires knowledge of the hemodynamic as well as antiarrhythmic effects of the available agents. These effects may differ during acute and chronic oral therapy. Several of the newer agents and quinidine are very effective in suppressing ventricular ectopic activity, allowing demonstration of drug effect during ambulatory monitoring. The clinical significance of this for prevention of sudden death has yet to be shown. However, prevention of ventricular tachycardia or fibrillation in the electrophysiology laboratory and suppression of ambient ectopy may generally be separate phenomena, as has been demonstrated for amiodarone.     

胺碘酮联合稳心颗粒治疗不稳定型心绞痛合并室性心律失常疗效及安全性对比

目的探究胺碘酮联合稳心颗粒治疗不稳定型心绞痛合并室性心律失常的疗效及安全性。方法以2009年1月—2012年5月该院收治的76例不稳定性心绞痛合并室性心律失常患者为研究对象,随机分成观察组和对照组,各38例。观察组和对照组均接受常规扩血管抗凝抗血小板治疗。观察组在常规治疗基础上加用胺碘酮和稳心颗粒,对照组在常规治疗基础上加用胺碘酮。观察对比两种治疗方案的疗效及安全性。结果治疗1个疗程后,观察组患者期间心绞痛发生次数、平均24 h内心肌缺血次数少于对照组,且累积硝酸甘油用量明显低于对照组,差异具有统计学意义(t=-8.497、-9.791、-7.836,P<0.05);观察组疗程以及随访期间室性早搏、室颤发生率明显低于对照组(χ2=4.145、5.029,P<0.05);观察组患者疗程以及随访期间部分不良反应发生率明显低于对照组(χ2=4.547、3.934,P<0.05)。结论相比于单纯使用胺碘酮,胺碘酮联合稳心颗粒的治疗方案可以显著降低患者心绞痛和部分室性心律失常发生次数,疗效优于单纯使用胺碘酮,不良反应少,具有更高的安全性,值得在临床实践中加以推广应用。     

Antiarrhythmic effects of pilsicainide hydrochloride and effects on cardiac function and ECG in dogs: comparison with disopyramide

Antiarrhythmic effects and cardiovascular effects of pilsicainide hydrochloride were compared with those of disopyramide in a canine model of coronary ligation-induced ventricular arrhythmias and anesthetized dogs. Pilsicainide (1.25, 2.5 and 5 mg/kg) and disopyramide (2.5 and 5 mg/kg) decreased the arrhythmic ratio ?(ventricular arrhythmias/total heart rate) x 100? dose-dependently. Pilsicainide at 2.5 and 5 mg/kg and disopyramide at 5 mg/kg suppressed ventricular arrhythmias more than 50%. The effective dose of pilsicainide was lower than that of disopyramide, but the effective plasma concentration of pilsicainide was between 3 and 8 micrograms/ml, which was almost the same as that of disopyramide. In anesthetized dogs, both drugs decreased LV dP/dt max in almost the same concentration-dependent manner. PQ-interval was prolonged by pilsicainide, but not by disopyramide. QRS and QTc were prolonged by both drugs in a concentration-dependent manner. However, the prolongation of QTc by disopyramide was provoked at lower plasma concentrations than by pilsicainide. Because the excessive prolongation of QTc lead to the lethal arrhythmias such as torsades de pointes, pilsicainide may be useful as an injectable antiarrhythmic agent superior to disopyramide.     

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。方法将120例冠心病室性心律失常患者随机分为治疗组及对照组,对照组口服普罗帕酮,治疗组口服胺碘酮片,比较两组的疗效及不良反应。结果经过治疗,两组患者的室早数、短阵室速数、QTc间期均有显著改善,差异有统计学意义（P〈0.05）;治疗组的改善情况优于对照组,差异有统计学意义（P〈0.05）。两组均未出现严重的不良反应。结论胺碘酮是相对安全的药物,是治疗冠心病合并快速心律失常的首选,尤其患者有器质性心脏病心力衰竭时,可以获得满意的疗效,值得临床推广应用。