ABSTRACT
One consistent finding in heart failure therapy for the last decade has been the singular utility of the angiotensin converting enzyme (ACE) inhibitors. At least six of these agents currently are approved for use in the U.S., and more than a dozen are in some stage of development. However, despite their well-demonstrated utility in symptom attenuation and, in some studies, mortality reduction, how these drugs achieve their clinical effects still needs to be elucidated. At the biochemical level, they inhibit the action of angiotensin converting enzyme in mediating the conversion of angiotensin I to angiotensin II as well as interfering with the degradation of bradykinin. However, the role of these pharmacological effects in mediating clinical efficacy and toxicity is not clear.
