参松养心胶囊治疗室性早搏的疗效观察

目的 观察参松养心胶囊治疗不同病因室性早搏的疗效与安全性。方法选择心功能NYHAⅠ～Ⅲ级的室性早搏患者136例,采用多中心随机对照为治疗组（76例）和对照组（60例）,治疗组口服参松养心胶囊4粒,3次／d;对照组Ⅵ服心律平150mg,3次／d,疗程4周。观察2组患者室性早搏的总有效率、症状改善率及安全性。结果治疗组总有效率为92．1％,症状改善率为86．8％;对照组总有效率为73．3％,症状改善率63．3％。2组比较差异有统计学意义（P〈0．05）,治疗组室性早搏疗效和临床症状改善优于对照组。结论参松养心胶囊对不同病因的室性早搏有明显疗效,且无严重不良反廊。     

人血浆中普罗帕酮对映体浓度的立体选择性HPLC测定法

 目的：建立血浆中普罗帕酮对映体浓度的立体选择性高效液相色谱测定法。方法：血浆标本经碱化以正己烷 异戊醇(99:1)提取、吹干后与GITC柱前衍生化，形成非对映体。以乙晴-水-冰醋酸(60∶40∶0.01)为流动相，经C₁₈ODS柱分离后在紫外λ208nm处检测。结果：对映体曲线范围25μg·L^-1～800μg·L^-1；最低检出限<20μg·L^-1；批内、批间平均RSD均<6%；平均回收率：102.2%；临床大多数常用药物对本法无干扰。结论：本法为普罗帕酮临床药动 药效学研究提供了一种简便、可行的检测方法。     

普罗帕酮治疗儿童心肌病心律失常疗效观察

目的探讨普罗帕酮治疗小儿心肌病心律失常的疗效,以及普罗帕酮治疗26例心肌病中不同心律失常的疗效差别。方法对26例儿童心肌病心律失常患者进行普罗帕酮治疗前后血浆心钠素(ANP)浓度、心脏指数(CI)变化的观察,并对观察各数据进行分析。结果心律失常发作时心肌病患儿血浆ANP浓度明显高于正常对照组和转复后、CI则明显低于正常对照组和转复后(P<0.05)。心肌病患儿在心律失常发作时血浆ANP和CI之间有良好的相关关系(r1=0.602,r2=0.759,P<0.05)。静脉注射普罗帕酮后室上性心动过速组(含心房扑动)的转复率明显高于室性心动过速组(P<0.05)。心肌病用药过程中无1例病情加重。结论普罗帕酮是治疗小儿心肌病心律失常安全有效的药物,虽然总体疗效稍差。     

普罗帕酮和普鲁卡因胺抗犬缺血性快速室性心律失常的对比研究(英文)

目的　观察普罗帕酮对犬在体心脏缺血性快速室性心律失常的心电生理影响并与普鲁卡因胺对比 ,以探讨其抗缺血性快速室性心律失常的效果及作用机制。方法　用冠状动脉左前降支结扎并部分再灌注法造成犬急性前壁心肌梗死 ,5～ 8d后 ,辅以心室程控电刺激 (PES)技术及冠状动脉内恒定微量直流电刺激技术 ,并诱发与终止持续性室性心动过速和心室纤颤 ,制备成犬急性心肌缺血再灌注后可控性快速室性心律失常的在体心脏心电模型 ,心电图对比观察普罗帕酮及普鲁卡因胺的抗心律失常作用。结果　普罗帕酮及普鲁卡因胺均能显著地延长心肌梗死犬的心电图QTc间期 (P <0 .0 1 )及正常和缺血心肌的有效不应期 (P <0 .0 1 ) ,降低缺血心肌和左室心肌的有效不应期离散度 (P <0 .0 1 ) ,提高正常心肌和缺血心肌的舒张期兴奋阈值 (P <0 .0 1 ) ,抑制PES诱发的持续性室性心动过速和心室纤颤 (P <0 .0 1 ) ,并能预防犬急性心肌梗死后再次缺血所致的自发性室性心动过速和心室纤颤 (P <0 .0 5)。结论　①该犬在体心脏心电药理学实验模型具有较好的重复性、可靠性及临床相关性 ,是一种有价值的心电药理学实验研究模型。②普罗帕酮及普鲁卡因胺均具有抗缺血性快速室性心律失常的心电生理作用 ,是有效的抗颤药物 ,两药效果相似     

Propafenone in Wolff-Parkinson-White syndrome at risk

Summary We present our experience on the efficacy of propafenone in ten symptomatic patients with Wolff-Parkinson-White syndrome. The symptoms were dizziness in seven patients and syncope in three patients. While experiencing the symptoms, three of them presented an episode of atrial fibrillation, the shortest preexcited RR intervals being 140, 190, and 200 ms. In the other seven patients, the ECG was not recorded during the symptoms, but an episode of atrial fibrillation was subsequently induced by transesophageal pacing. The shortest preexcited RR intervals during induced atrial fibrillation were 180, 200, 270, 240, 230, 250, and 200 ms. Seven patients had both atrial fibrillation and supraventricular tachycardia. Propafenone (1–2 mg/kg) administered IV in only the patients with sustained atrial fibrillation (spontaneous in two and induced in one patient) prolonged the shortest preexcited RR intervals from 190, 200, and 180 ms to 340, 335, and 340 ms. In the other seven patients, propafenone was not given IV because atrial fibrillation rapidly deteriorated into ventricular fibrillation (one patient) or spontaneously reverted within 1–2 minutes to sinus rhythm (six patients). After oral propafenone, serial trans-esophageal pacing studies reinduced atrial fibrillation in 4 of 6 patients (the shortest preexcited RR intervals increased from 190, 180, 200, and 270 ms to 420, 320, 340, and 380 ms); only in one patient was it possible after propafenone to induce an atrial flutter without preexcitation. After propafenone therapy in 4 of 7 patients, supraventricular tachycardia was not inducible. All patients were asymptomatic during the follow-up period (3–18 months). The minimum therapeutic dosage was 600 mg/day.     

参仙升脉口服液对频率依赖性早搏疗效观察

目的:探讨参仙升脉口服液对频率依赖性早搏的治疗效果。方法:5例频发室性早搏患者先常规给予胺碘酮或心律平口服2~4周,复查动态心电图,总心率减慢,早搏次数增加,患者症状加重,考虑为频率依赖性早搏后,给予参仙升脉口服液治疗2~4周,并进行动态心电图检查分析及患者自觉症状,不良反应观察。结果:动态心电图提示参仙升脉口服液可明显减少早搏次数,改善患者症状,未见明显不良反应。结论:参仙升脉口服液对治疗频率依赖性早搏有较好的疗效。     

A method for evaluating different modes of action of an antiarrhythmic drug in man. The effects of propafenone on sinus nodal functions

In vitro experiments have shown that the antiarrhythmic effects of propafenone are due to a direct depressant action and to a beta-blocking activity. In this study a method was used to evaluate the direct effect and the autonomically mediated actions of an antiarrhythmic agent in a clinical setting. An electrophysiological study was performed twice, at an interval of 24 hr, in 17 patients (age: 52 +/- 17 years) with normal resting and intrinsic heart rate. In the first study the overall effect of intravenous propafenone (1.5-2 mg/kg) was evaluated by comparing the sinus node parameters obtained during the basal state and after drug administration. In the second study the direct depressant effect of the drug was evaluated by comparing the electrophysiological variables obtained following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg) and after propafenone. In the first study there was no significant change in the sinus cycle length and corrected sinus node recovery time and only a small (9.1%) increase in sinuatrial conduction time, whereas in the second study these variables increased significantly. The degree of increase in sinus cycle length and corrected sinus node recovery time was significantly higher in the second study than in the first one. These data suggest that: (1) propafenone has direct depressant effect on sinus automaticity but this effect is counteracted by autonomically mediated actions (most likely of vagolytic type); (2) the beta-blocking effect of the drug demonstrated in isolated atria is not seen in a clinical setting.     

Transient Intraventricular Conduction Delay Associated with Concurrent Intake of Propafenone and Antineoplastic Agents

An 82-year old man was admitted with acute pulmonary edema. Myocardial ischemia and electrolyte abnormalities were excluded and he responded promptly to frusemide, nitrates and morphine. On admission, the duration of the QRS interval was markedly abnormal at 240 ms with a nonspecific intraventricular conduction defect pattern, of left bundle branch block type. This finding was not present three weeks prior to his admission, and was felt to be the result of drug interaction between propafenone and antineoplastic agents, as evidenced by resolution of the clinical and electrocardiographic picture after discontinuation of these agents.     

Intravenous propafenone: Efficacy and safety in the conversion to sinus rhythm of recent onset atrial fibrillation—A single-blind placebo-controlled study

Summary The effectiveness of intravenous propafenone for conversion to sinus rhythm (SR) of paroxysmal atrial fibrillation (AF), lasting less than 7 days, was evaluated with a single-blind, randomized, placebo-controlled study, given the possible spontaneous conversion of this arrhythmia. Group 1 (98 patients) received intravenous propafenone (2 mg/kg iv over 10 minutes followed by 0.007 mg/kg/min); and group 2 (84 patients) received intravenous placebo (0.9% saline solution). The infusion was continued until restoration of SR but no longer than 24 hours. Eight-nine patients (90.8%) received propafenone and 27 patients (32%) receiving placebo were converted to SR (p<0.005). The mean conversion time was 2.46±2.59 hours in group 1 and 17.15±5.78 hours in group 2 (p<0.005). In patients treated with propafenone, conversion of SR mostly occurred in the first 4 hours (86.5%), considered to be the optimal infusion time in our experience. In both groups, the left atrial size was significantly larger in nonconverted than in converted patients. Similarly, the duration of the arrhythmia was significantly longer in nonconverted patients. In nonconverted patients, the mean ventricular rate decreased from 143±beats/min to 101±18 beats/min after propafenone and from 135±19 beats/min to 199 ±16 beats/min after placebo (group 1 vs. group 2: p<0.005). Two episodes of sinus standstill (3.4 and 3.8, seconds, respectively) occurred at SR restoration obtained with propafenone. Intravenous propafenone is an effective, safe, and usually rapid drug for AF treatment. Moreover, it produces a real and significant reduction in the mean ventricular rate in nonconverted patients.     

Failure of Intracardiac Pacing After Fatal Propafenone Overdose: A Case Report

Background

Propafenone is a sodium-channel blocker, class IC antiarrhythmic drug, frequently used to manage supraventricular dysrhythmias, especially atrial fibrillation. We report a self mono-intoxication with propafenone.