Bussmann W D, Micke G, Hildenbrand R, Klepzig H
Department of Cardiology, Frankfurt am Main University Hospital, Germany.
Clin Cardiol. 1995 Aug;18(8):465-70. doi: 10.1002/clc.4960180809.
It is known from experiments that angiotensin-converting enzyme inhibitors can limit infarct size. In a prospective, randomized, placebo-controlled double-blind study, 22 patients were given 1.5-2.0 mg captopril/h i.v., while 24 patients were given placebo. Medication was started between 2 and 18 h from the onset of infarction. The two groups were matched for age, infarct location, and time of intervention. With the exception of one patient in either group, all were concurrently given nitroglycerin. The necrosis parameters were provided by the quantitative measurement of the QRS complex. The Q wave decreased with captopril treatment (-0.003 mV), but increased with placebo (+0.14 mV, p < 0.05). The number of ventricular premature beats at 24 h from the start of treatment was 25/h with placebo, and 9/h with captopril (p < 0.02). Ventricular fibrillation occurred seven times in the placebo group, but did not occur in the captopril group. The creatine kinase infarct weight was 59 gram-equivalents (gEq) with placebo, and 45 gEq with captopril (p = NS). Mean arterial pressure was reduced by 12 mmHg with captopril treatment. The results show a beneficial effect of captopril on infarct size and electrical instability, over and above the effect of standard management with nitroglycerin and thrombolysis.
实验表明，血管紧张素转换酶抑制剂可限制梗死面积。在一项前瞻性、随机、安慰剂对照双盲研究中，22例患者静脉注射卡托普利1.5 - 2.0毫克/小时，24例患者给予安慰剂。在梗死发作后2至18小时开始用药。两组在年龄、梗死部位和干预时间方面进行了匹配。除每组各有1例患者外，所有患者均同时给予硝酸甘油。坏死参数通过QRS波群的定量测量提供。卡托普利治疗使Q波减小（-0.003毫伏），而安慰剂使Q波增大（+0.14毫伏，p < 0.05）。治疗开始后24小时，安慰剂组室性早搏次数为25次/小时，卡托普利组为9次/小时（p < 0.02）。安慰剂组发生心室颤动7次，卡托普利组未发生。安慰剂组肌酸激酶梗死重量为59克当量（gEq），卡托普利组为45克当量（p = 无显著性差异）。卡托普利治疗使平均动脉压降低12毫米汞柱。结果表明，卡托普利对梗死面积和电不稳定性具有有益作用，超过了硝酸甘油和溶栓标准治疗的效果。
