{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T19:37:22Z","timestamp":1757705842324},"reference-count":75,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,2,4]],"date-time":"2009-02-04T00:00:00Z","timestamp":1233705600000},"content-version":"vor","delay-in-days":5847,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Cardiology"],"published-print":{"date-parts":[[1993,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The concept of \u201ccardioprotection\u201d with ACE inhibitors has evolved over the last decade. In the 1980s, protective benefits of ACE inhibitors in hypertension were established, regression of left ventricular hypertrophy was demonstrated, and improved ventricular function and survival in mild\u2010to\u2010moderate and severe congestive heart failure was documented. A further \u201cprotective\u201d role of ACE inhibitors in coronary artery disease is emerging as more attention is focused on the concept of local tissue reninangiotensin systems. Recent contributions to the literature describe significant benefits of ACE\u2010inhibitor therapy in acute myocardial infarction, including suppression of ventricular arrhythmias and reduction of both early and late ventricular dilation, preservation of left ventricular function, and improved survival. All of the above effects can be considered \u201ccardioprotective.\u201d However, as new benefits are reported in the 1990s, a broadened view of \u201ccardiovascular protection\u201d emerges from investigative studies in the literature. ACE inhibitors may reduce tolerance to nitrates, reduce angina in some but not all studies, and limit smooth muscle cell proliferation (and perhaps restenosis) induced by experimental balloon angioplasty. Local vascular effects may attenuate atherosclerotic changes in the arterial wall in experimental animals and may decrease the incidence of aneurysm formation in hypertensive animals. The effectiveness of ACE inhibitors in acute myocarditis, suggested by reports that captopril may reduce lesions of murine myocarditis when administered early after infection with coxsackievirus B3, requires clinical confirmation. Despite these apparently diverse \u201ccardiovascular protective\u201d consequences of ACE inhibitor therapy, the mechanism(s) of action of these agents remain to be elucidated. These agents affect not only the systemic renin\u2010angiotensin systems, but local tissue systems as well. Debate continues as to the significance of the sulfhydryl group in certain ACE inhibitors: at the present time it is not clear whether the thiol group provides a treatment benefit. Finally, stimulation of other vasodilator systems by ACE inhibitors (bradykinin, prostacyclin) may play an important role in the \u201ccardiovascular protective\u201d effects of these agents.<\/jats:p>","DOI":"10.1002\/clc.4960160204","type":"journal-article","created":{"date-parts":[[2009,2,4]],"date-time":"2009-02-04T09:24:00Z","timestamp":1233739440000},"page":"95-103","source":"Crossref","is-referenced-by-count":11,"title":["Cardioprotection with angiotensin\u2010converting enzyme inhibitors: Redefined for the 1990s"],"prefix":"10.1002","volume":"16","author":[{"given":"Robert 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