Liebau G, Riegger A J, Schanzenbächer P, Steilner H, Oehrlein S
Br J Clin Pharmacol. 1982;14 Suppl 2(Suppl 2):193S-199S. doi: 10.1111/j.1365-2125.1982.tb02077.x.
Vasodilator therapy is used widely for the treatment of congestive heart failure irrespective of its origin. The acute and long-term effects of captopril were studied in 50 patients with congestive heart failure due to valvular incompetence, hypertension, cardiomyopathy, and ischaemic heart disease. Haemodynamic studies were performed in all patients. In those with valvular incompetence, regurgitation fractions were measured cineangiographically. In patients with ischaemic heart disease coronary sinus blood flow was assessed by a thermodilution technique. During clinical follow-up patients were studied by non-invasive techniques including electrocardiography, echocardiography and chest radiography. In the short-term studies, left ventricular filling pressure, total peripheral resistance, and end-diastolic and end-systolic volumes decreased after captopril, while cardiac output, stroke volume, and ejection fraction increased. Valvular regurgitation fraction was assessed in 10 patients with aortic or mitral insufficiency. In every patient the regurgitation fraction decreased. Coronary blood flow was measured in eight patients with severe ischaemic heart disease. In three patients it remained constant and in the other five patients it decreased. At the same time a highly significant decrease of myocardial oxygen consumption was measured. During long-term treatment clinical improvement occurred in most of the patients. This was documented by a reduction of ventricular diameters in hypertensive heart disease as well as in valvular incompetence. These values remained constant in congestive cardiomyopathy despite clinical improvement. Serious hypotensive episodes were observed in eight patients with valvular stenosis or complex congenital cardiac abnormalities. Captopril is therefore an effective vasodilator for the treatment of congestive heart failure. In patients with intact left ventricular function captopril should not be given because severe hypotensive episodes may occur. Ischaemic heart disease with congestive heart failure is no contraindication for treatment with captopril because the reduction in myocardial blood flow is balanced by the reduced myocardial oxygen consumption.
血管扩张剂疗法广泛用于治疗各种原因引起的充血性心力衰竭。对50例因瓣膜功能不全、高血压、心肌病和缺血性心脏病导致充血性心力衰竭的患者进行了卡托普利的急性和长期疗效研究。对所有患者进行了血流动力学研究。对于瓣膜功能不全的患者，通过心血管造影测量反流分数。对于缺血性心脏病患者，采用热稀释技术评估冠状窦血流量。在临床随访期间，通过包括心电图、超声心动图和胸部X线摄影在内的非侵入性技术对患者进行研究。在短期研究中，卡托普利治疗后左心室充盈压、总外周阻力、舒张末期和收缩末期容积降低，而心输出量、每搏量和射血分数增加。对10例主动脉或二尖瓣关闭不全患者评估了瓣膜反流分数。每位患者的反流分数均降低。对8例严重缺血性心脏病患者测量了冠状动脉血流量。3例患者血流量保持不变，另外5例患者血流量降低。同时测量到心肌耗氧量显著降低。在长期治疗期间，大多数患者临床症状改善。这在高血压性心脏病以及瓣膜功能不全患者中通过心室直径的减小得到证实。尽管临床症状改善，但充血性心肌病患者的这些数值保持不变。在8例瓣膜狭窄或复杂先天性心脏异常患者中观察到严重的低血压发作。因此，卡托普利是治疗充血性心力衰竭的有效血管扩张剂。对于左心室功能正常的患者，不应给予卡托普利，因为可能会发生严重的低血压发作。伴有充血性心力衰竭的缺血性心脏病不是卡托普利治疗的禁忌症，因为心肌血流量的减少被心肌耗氧量的降低所平衡。
