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[依诺昔酮与慢性心力衰竭中的室性心律失常]

[Enoximone and ventricular arrhythmia in chronic heart failure].

作者信息

Treese N, Rhein S, Werneyer A, Erbel R, Meyer J

机构信息

II Medizinische Klinik, Johannes Gutenberg-Universitat Mainz.

出版信息

Z Kardiol. 1991;80 Suppl 4:85-91.

PMID:1833903
Abstract

Potentially malignant ventricular arrhythmias are common in chronic heart failure. The aggravation of such arrhythmias has many causes in these patients and cannot be predicted. Therefore, proarrhythmia due to PDE-inhibitors which increase cytosolic calcium levels by specific inhibition of the degradation of cyclo-AMP may be difficult to recognize. A retrospective analysis of 24-h Holter ECG was performed in 31 patients (NYHA classes III and IV) under long-term enoximone therapy. At baseline, 68% of the patients had ventricular couplets and nonsustained ventricular tachycardia. After a mean treatment period of 7 months, 10% of the patients showed a significant increase, 16% a significant decrease (greater than 90%) of ventricular couplets and salvos, and an additional 32% of the patients showed a significant decrease (greater than 70%) of single PVCs. The change of the arrhythmia profile was not related to the clinical course in these patients. Furthermore, 24-h Holter recordings were analyzed in a randomized long-term trial with captopril and enoximone that included 20 patients of NYHA class II. Despite comparable baseline findings, a reduction of cardiopulmonary exercise capacity was observed in patients treated with enoximone, but not with captopril. However, the arrhythmia profile was similar in both treatment groups. These findings suggest that, in most patients with advanced chronic heart failure, long-term enoximone therapy is not associated with an important increase of ventricular arrhythmias. According to the 24-h Holter findings of the European Enoximone Data Bank, proarrhythmia can be expected in 12% of all patients. Control of the arrhythmia profile, however, is mandatory, because the incidence of proarrhythmia cannot be predicted in the individual patient.

摘要

潜在恶性室性心律失常在慢性心力衰竭患者中很常见。这类心律失常的加重在这些患者中有多种原因且无法预测。因此,磷酸二酯酶抑制剂通过特异性抑制环磷酸腺苷降解来增加胞浆钙水平所导致的致心律失常作用可能难以识别。对31例(纽约心脏协会心功能Ⅲ级和Ⅳ级)接受长期依诺昔酮治疗的患者进行了24小时动态心电图回顾性分析。基线时,68%的患者有室性早搏二联律和非持续性室性心动过速。平均治疗7个月后,10%的患者室性早搏二联律和短阵室性心动过速显著增加,16%显著减少(超过90%),另有32%的患者单个室性早搏显著减少(超过70%)。这些患者心律失常情况的变化与临床病程无关。此外,在一项包括20例纽约心脏协会心功能Ⅱ级患者的卡托普利和依诺昔酮随机长期试验中,对24小时动态心电图记录进行了分析。尽管基线结果相似,但接受依诺昔酮治疗的患者心肺运动能力下降,而接受卡托普利治疗的患者未出现这种情况。然而,两个治疗组的心律失常情况相似。这些发现表明,在大多数晚期慢性心力衰竭患者中,长期依诺昔酮治疗与室性心律失常的重要增加无关。根据欧洲依诺昔酮数据库的24小时动态心电图结果,预计所有患者中有12%会出现致心律失常作用。然而,必须对心律失常情况进行监测,因为无法在个体患者中预测致心律失常作用的发生率。

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