Effect of oral captopril on premature ventricular complexes in patients with preserved left ventricular systolic function: a randomized clinical trial.
Effect of oral captopril on premature ventricular complexes in patients with preserved left ventricular systolic function: a randomized clinical trial.
复制标题
口服卡托普利对保留左心室收缩功能的患者室性早搏的影响：一项随机临床试验。
DOI：
10.1002/clc.4960160205
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发表时间：
1993
影响因子：
2.7
通讯作者：
Lehmann,MH
中科院分区：
文献类型：
--
作者：
Steinman,RT;Gilley,D;Gunther,S;Fromm,BS;Lehmann,MH
一些研究表明，心衰患者的血管紧张素转换酶（ACE）抑制与自发性早衰心室复合体（pvc）发生频率的降低有关。目前尚不清楚这一发现是ACE抑制的主要作用还是治疗心力衰竭的次要结果。对于存在主要药物作用，ACE抑制期间的PVC抑制也应发生在左心室收缩功能保留的患者中。因此，我们进行了一项随机双盲安慰剂对照交叉临床试验，以评估口服卡托普利（50mg . b. d）对11例患者室性心律失常频率的影响，这些患者的血压为30pcs /h（在48小时的动态记录期间），左心室射血分数≥45%（通过放射性核素多门采集扫描测量）。给药药物的药理学活性由血浆肾素活性中位数增加到2来证明。从安慰剂期间的1.1 ng/AI/ml/h下降了4 ng/AI/ml/h (p = 0.001)，卡托普利期间的平均舒张压与安慰剂相比下降了8.5±10.3 （p < 0.03）。卡托普利治疗组的平均室性早搏数为491±378次/小时，而安慰剂组为389±169次/小时，差异无统计学意义。在卡托普利治疗期间，左心室射血分数、血浆儿茶酚胺或血清钾也没有显著变化。因此，在保留左心室收缩功能的患者中，ACE抑制不能抑制心室异位活动。外推到心力衰竭患者，我们的观察结果反对ACE抑制剂的原发性PVC抑制作用，但不排除这些药物可能的继发性抗心律失常作用。
Some studies have suggested that angiotensin‐converting enzyme (ACE) inhibition in patients with heart failure is associated with a decrease in frequency of spontaneous premature ventricular complexes (PVCs). It is not clear whether such a finding represents a primary effect of ACE inhibition or, instead, a secondary result of treatment of heart failure. For a primary drug effect to be present, PVC suppression during ACE inhibition should also occur in patients with preserved left ventricular systolic function. We therefore undertook a randomized double‐blind placebo‐controlled crossover clinical trial to assess the effect of oral captopril (50 mg. b. i. d.) on ventricular arrhythmia frequency in 11 patients with > 30 PVCs/h (during a 48‐h ambulatory recording) and a left ventricular ejection fraction of ≥ 45% (measured by radionuclide multigated acquisition scan). Pharmacologic activity of the administered drug was evidenced by an increase in median plasma renin activity to 2. 4 ng/AI/ml/h from a value of 1.1 ng/AI/ml/h during placebo (p = 0.001) and an 8.5 ± 10.3 drop in mean diastolic blood pressure during captopril versus placebo (p < 0.03).During captopril treatment, a mean of 491 ± 378 PVCs/h were observed compared with 389 ± 169 PVCs/h during placebo, a nonsignificant difference. There was also no significant change in left ventricular ejection fraction, plasma catecholamines, or serum potassium during captopril treatment. Thus, ACE inhibition in patients with preserved left ventricular systolic function fails to suppress ventricular ectopic activity. Extrapolated to patients with heart failure, our observations argue against a primary PVC suppressive action of ACE inhibitors but do not rule out possible secondary antiarrhythmic effects of these agents.