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硝苯地平与急性心肌梗死

Nifedipine and acute myocardial infarction.

作者信息

Roberts R, Jaffe A S, Henry P D, Sobel B E

出版信息

Herz. 1981 Apr;6(2):90-7.

PMID:7227967
Abstract

In consideration of the results of experimental studies indicating that nifedipine, a vasodilating calcium antagonist with little inotropic or electrophysiological effects, increases coronary flow to both normal and ischemic zones potentially rendering protection of ischemic myocardium as well as the results of clinical studies in patients with angina pectoris, this pilot study was carried out in patients with acute myocardial infarction to evaluate the clinical, hemodynamic and electrophysiological responses. Nifedipine was administered sublingually in a dosage of 10 mg initially, after an interval of 1 to 1.5 hours and thereafter to maintain the pressure at the level prevailing after three hours. As compared with a control group, the frequency of ventricular dysrhythmia as well as the frequency of complex dysrhythmias in the 17 treated patients were similar (mean 313 vs. 325 PVCs/24 hours; and 5.9 vs. 3.6 episodes respectively in treated and controls). No patient developed evidence of second or third degree AV block. Systemic vascular resistance fell from 1661 to 1283 dyne . s . cm-5 and cardiac index increased from 3.2 to 3.59 l/min/m2 at one hour. Arterial pressure decreased from 146/93 to 131/88 mm Hg. Pulmonary artery pressure remained unchanged in five patients and decreased by more than 3 mm Hg in four. Thus, in patients with acute myocardial infarction nifedipine decreases systemic resistance and, provided preload is not substantially reduced, increases cardiac output. Neither an exacerbation of chest pain nor an increase in ventricular dysrhythmia was observed. Extensive clinical investigation will be needed to definitively characterize effects of nifedipine on infarct size, coronary flow and prognosis of patients with acute myocardial infarction.

摘要

鉴于实验研究结果表明,硝苯地平这种具有微弱变力或电生理效应的血管舒张性钙拮抗剂可增加正常和缺血区域的冠状动脉血流量,从而有可能对缺血心肌起到保护作用,以及心绞痛患者的临床研究结果,本初步研究针对急性心肌梗死患者开展,以评估其临床、血流动力学和电生理反应。硝苯地平初始舌下含服剂量为10mg,1至1.5小时后再次给药,此后维持血压在三小时后的水平。与对照组相比,17例接受治疗患者的室性心律失常频率以及复杂心律失常频率相似(平均每24小时室性早搏分别为313次和325次;治疗组和对照组分别为5.9次和3.6次发作)。无患者出现二度或三度房室传导阻滞证据。一小时时,全身血管阻力从1661降至1283达因·秒·厘米⁻⁵,心脏指数从3.2升至3.59升/分钟/平方米。动脉血压从146/93降至131/88毫米汞柱。五例患者肺动脉压保持不变,四例患者肺动脉压下降超过3毫米汞柱。因此,在急性心肌梗死患者中,硝苯地平可降低全身阻力,且在不显著降低前负荷的情况下增加心输出量。未观察到胸痛加重或室性心律失常增加。需要进行广泛的临床研究以明确硝苯地平对急性心肌梗死患者梗死面积、冠状动脉血流量和预后的影响。

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Nifedipine and acute myocardial infarction.硝苯地平与急性心肌梗死
Herz. 1981 Apr;6(2):90-7.
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[Nifedipine in acute myocardial infarction (author's transl)].硝苯地平用于急性心肌梗死(作者译)
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Comparison of intravenous nifedipine and sodium nitroprusside for treatment of acute hypertension after cardiac surgery.静脉注射硝苯地平与硝普钠治疗心脏手术后急性高血压的比较。
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Beneficial effects of nifedipine on regional myocardial blood flow in patients with coronary artery disease.硝苯地平对冠心病患者局部心肌血流的有益作用。
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