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卡托普利对急性心肌梗死患者压力反射敏感性的急性影响。

Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction.

作者信息

Marakas S A, Kyriakidis M K, Vourlioti A N, Petropoulakis P N, Toutouzas P K

机构信息

Department of Cardiology, Hippokration Hospital, Athens University, Greece.

出版信息

Eur Heart J. 1995 Jul;16(7):914-21. doi: 10.1093/oxfordjournals.eurheartj.a061025.

Abstract

Depressed baroreflex sensitivity (BRS) after acute myocardial infarction (AMI) is considered an indication of decreased vagal and/or increased sympathetic tone. To determine the effect of angiotensin converting enzyme inhibitors (ACEI) on BRS after AMI we studied 27 patients with a first Q wave AMI, no signs of heart failure and no history of arterial hypertension or diabetes mellitus. An additional group of 10 patients with the same clinical characteristics served as controls. On the 5th day after the onset of AMI, three consecutive boluses of phenylephrine were given intravenously and baseline BRS was taken as the mean slope of the linear regression lines of RR intervals over systolic blood pressure. QT interval was also measured and corrected according to Bazett's formula (QTc). Consequently, a single oral dose of captopril 50 mg or placebo was given to treatment or control group patients, respectively; BRS and QTc were reassessed 1 h later. One hour after captopril administration BRS increased from 5.95 +/- 2.80 to 9.14 +/- 3.46 ms.mmHg-1 (P < 0.0001); QTc increased from 414 +/- 46 to 425 +/- 46 ms (P < 0.0001), systolic blood pressure decreased from 125 +/- 19 to 115 +/- 15 mmHg (P = 0.0002), while heart rate did not change significantly. Baseline BRS was correlated only with age (r = -0.74, P < 0.0001). In the control group, 1 h after placebo, no difference was observed in any variable compared to baseline. Captopril appears to improve BRS immediately in the early phase of AMI.

摘要

急性心肌梗死(AMI)后压力反射敏感性(BRS)降低被认为是迷走神经张力降低和/或交感神经张力增加的表现。为了确定血管紧张素转换酶抑制剂(ACEI)对AMI后BRS的影响,我们研究了27例首次发生Q波型AMI、无心力衰竭体征且无动脉高血压或糖尿病病史的患者。另外10例具有相同临床特征的患者作为对照组。在AMI发作后第5天,静脉内连续给予三次去氧肾上腺素推注,并将基线BRS作为RR间期对收缩压的线性回归线的平均斜率。还测量了QT间期并根据Bazett公式(QTc)进行校正。随后,分别给予治疗组或对照组患者单次口服50mg卡托普利或安慰剂;1小时后重新评估BRS和QTc。给予卡托普利1小时后,BRS从5.95±2.80增加至9.14±3.46ms·mmHg-1(P<0.0001);QTc从414±46增加至425±46ms(P<0.0001),收缩压从125±19降至115±15mmHg(P=0.0002),而心率无显著变化。基线BRS仅与年龄相关(r=-0.74,P<0.0001)。在对照组中,给予安慰剂1小时后,与基线相比,任何变量均未观察到差异。卡托普利似乎在AMI早期可立即改善BRS。

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