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Angiotensin converting enzyme inhibitors in acute myocardial infarction: Mechanisms of action

Guy S Reeder, MD
Section Editor
Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
Deputy Editor
Gordon M Saperia, MD, FACC


A number of modalities may be beneficial in the management of the patient with acute myocardial infarction (MI), including direct angioplasty or fibrinolysis, aspirin, angiotensin converting enzyme (ACE) inhibitors, beta blockers, and nitrates. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST elevation acute coronary syndromes".)

A meta-analysis concluded that administration of an ACE inhibitor within 3 to 16 days of infarction can slow the progression of cardiovascular disease and improve the survival rate (figure 1) [1]. The mechanisms by which ACE inhibitors improve survival after MI will be reviewed here, beginning with a discussion of infarct expansion. The clinical data supporting the use of ACE inhibitors in this setting are presented elsewhere. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials".)


Survivors of acute myocardial infarction (MI) have a significant risk of future cardiovascular events. Infarct expansion, due to thinning and stretching of the infarct zone, occurs within hours to days of a transmural MI and is an important prognostic determinant. Significant left ventricular dilation can begin within three hours from the onset of a first myocardial infarction, particularly among patients with anterior wall damage [2]. Patients who develop infarct expansion have a high risk of developing heart failure and sudden death. Pathologic evidence of infarct expansion has been found in up to 60 percent of patients dying from complications of an MI [3].

Ventricular dilatation itself may be deleterious, independent of the reduction in overall myocardial contractility induced by the infarct. Consistent with this hypothesis is the observation in an animal study that preventing left ventricular dilatation with a restraining mesh placed over the anticipated area of infarction preserved left ventricular geometry and function [4].

Following the initial insult in the area of infarction, ventricular remodeling can lead to progressive regional myocardial dysfunction [5-8]. The remodeling process begins with myocyte necrosis and the formation of fibrotic scar; it is followed by elongation of the infarcted segment and then dilatation and hypertrophy of the border zone ventricular myocardium (figure 2). The extent of microvascular obstruction within the infarcted area during the early healing phase after an infarction is indicative of absent blood flow and predicts left ventricular remodeling and dilatation, independent of infarct size [9]. There is no increase in interstitial fibrosis in the noninfarcted tissue remote from the scar [10]; this tissue retains normal contractility even though it is involved in the remodeling process. (See "Cardiac remodeling: Clinical assessment and therapy".)

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Literature review current through: Nov 2017. | This topic last updated: May 10, 2017.
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