The renin-angiotensin system is activated in the majority of patients with chronic
congestive heart failure. This may be part of the pathophysiology of the disease, a secondary phenomenon, or the result of intense
diuretic therapy. Irrespective of the mechanism of
renin-
angiotensin activation, converting
enzyme inhibitors are an effective form of
therapy as well as a means to evaluate pathophysiologic mechanisms of
congestive heart failure. Because of the activation of the renin-angiotensin system,
angiotensin-mediated vasoconstriction and
aldosterone-mediated
sodium retention can be suppressed and, in some individuals, completely blocked by converting
enzyme inhibitors. Improved forward cardiac flow and reduction of pulmonary congestion occur with reversal of vasoconstriction, so that relief of
edema, due to enhanced
sodium and water excretion, will occur. While it is easy to identify a close correlation between markers of
renin-
angiotensin activity and the initial response to converting
enzyme inhibitors, it is more difficult to identify this response long-term. This may be due to changes in
dietary sodium intake, intensity of
diuretic therapy, or alteration in renal blood flow and function. Clinically, however, the response to converting
enzyme inhibitors is favorable in the majority of people.