Captopril therapy in heart failure

When congestive heart failure occurs, cardiac output decreases and left ventricular end-diastolic pressure increases. These physiologic events cause the heart to stimulate compensatory mechanisms in order to maintain a normal blood pressure and perfusion of the vital organs. These mechanisms stimulate the sympathetic, prostaglandin, vasopressin, and renin-angiotensin-aldosterone (RAA) systems, which work to improve perfusion and blood pressure on a short-term basis. Left uninterrupted, however, these systems increase systemic vascular resistance, which eventually progresses to left ventricular (LV) dysfunction. Captopril, which blocks the RAA system at the conversion of angiotensin I to angiotensin II, has been proved on both a short-term and a long-term basis to be highly suitable for the treatment of congestive heart failure. Its benefits include improvements in LV function parameters, including increases in cardiac output, renal perfusion, exercise tolerance, and ejection fraction, as well as a more favorable Killip's classification.