Komajda M, Eugène M, Evans J, Laurenceau J L, Hubermann J P, Thomas D, Drobinski G, Leprince J L, Ganty J, Wajman A, Guedj D, Grosgogeat Y
Arch Mal Coeur Vaiss. 1983 Jan;76(1):29-36.
We studied the hemodynamic, echocardiographic, phonomechanographic and hormonal changes during acute (25 mg) and chronic (6 months--75 to 225 mg/day) treatment of 10 patients with congestive cardiac failure due to cardiomyopathy with dilatation with SQ 14 225 (Captopril). The following changes were observed after the single dose: an increase in cardiac output (p less than 0,001), in stroke volume (p less than 0,01), a reduction in heart rate (p less than 0,01), in peripheral resistance (p less than 0,001) and pulmonary capillary pressure (p less than 0,001). There were no significant changes in end systolic or end diastolic left ventricular internal diameter. Plasma renin activity increased (p less than 0,001); there was a concurrent fall in serum aldosterone (NS): the plasma concentration of converting enzyme decreased (p less than 0,001). There was a correlation between the increase in peripheral resistance under basal conditions and the basal plasma renin activity (R = 0,72, p less than 0,02). The decrease in peripheral resistance after captopril also correlated with basal plasma renin activity (R = 0,89, p less than 0,01). After six months continuous therapy, the hemodynamic effect was sustained and was accompanied by a significant symptomatic improvement. Left ventricular internal end systolic and end diastolic diameters decreased (p less than 0,01 and p less than 0,01 respectively). The pre-ejectional period decreased (p less than 0,05). Serum aldosterone fell significantly (p less than 0,001) as did plasma renin activity (p less than 0,01); the serum level of converting enzyme remained low with respect to its initial value. These results show that captopril may be useful in severe cardiac failure without tolerance during long-term administration. No renal or hematological toxicity was observed in this group of patients.
我们研究了10例因扩张型心肌病导致充血性心力衰竭的患者，在使用SQ 14 225（卡托普利）进行急性（25毫克）和慢性（6个月 - 每天75至225毫克）治疗期间的血流动力学、超声心动图、心音图和激素变化。单次给药后观察到以下变化：心输出量增加（p < 0.001），每搏输出量增加（p < 0.01），心率降低（p < 0.01），外周阻力降低（p < 0.001）和肺毛细血管压力降低（p < 0.001）。左心室收缩末期或舒张末期内径无显著变化。血浆肾素活性增加（p < 0.001）；血清醛固酮同时下降（无显著性差异）：血浆转换酶浓度降低（p < 0.001）。基础状态下外周阻力的增加与基础血浆肾素活性之间存在相关性（R = 0.72，p < 0.02）。卡托普利治疗后外周阻力的降低也与基础血浆肾素活性相关（R = 0.89，p < 0.01）。连续治疗六个月后，血流动力学效应持续存在，并伴有明显的症状改善。左心室内径收缩末期和舒张末期均减小（分别为p < 0.01和p < 0.01）。射血前期缩短（p < 0.05）。血清醛固酮显著下降（p < 0.001），血浆肾素活性也下降（p < 0.01）；转换酶的血清水平相对于初始值仍保持较低。这些结果表明，卡托普利可能对严重心力衰竭患者长期给药时无耐受性有用。在该组患者中未观察到肾脏或血液学毒性。
