Antianginal, hemodynamic and coronary vascular effects of captopril in stable angina pectoris

A pilot study was performed to assess the short-term effects of intravenous captopril on anginal threshold and systemic and coronary hemodynamics in patients with stable angina pectoris. Twelve patients with documented coronary artery disease, stable angina pectoris and normal left ventricular function were studied by an incremental atrial pacing stress test before and after intravenous captopril (n = 8) or placebo (n = 4). There were no significant differences in the extent of coronary disease or left ventricular function between the 2 groups and resting plasma-renin levels were normal. Captopril increased the time to angina (14 ± 4 to 19 ± 5 minutes, p <0.05), increased heart rate at development of angina (126 ± 7 to 142 ±7 beats/min, p <0.05) and tended to increase coronary blood flow (229 ± 154 to 296 ± 259 ml/min, p = 0.11) and decrease coronary vascular resistance (53 ± 10 to 47 ± 3 dynes s cm−5/1,000, p = 0.11) at peak stress without alteration in systemic hemodynamics. No significant changes were seen after placebo administration. Therefore, intravenous captopril appears to cause a short-term increase of coronary vascular reserve, and anginal threshold in patients with chronic stable angina. This effect appears to be independent of inhibition of the systemic renin-angiotensin system or systemic hemodynamic changes.