The loss of myocytes as a consequence of myocardial infarction results
in a prompt reduction in regional wall motion and often leads to more
protracted and progressive changes in ventricular architecture. The r
ecognition that the process of ventricular enlargement following myoca
rdial infarction is modifiable provided the initial rationale for the
use of angiotensin-converting enzyme (ACE) inhibitors as therapy to pr
event deterioration in ventricular size and function following infarct
ion. Experimental and clinical studies have documented the effectivene
ss of this therapy in preventing this late enlargement following infar
ction. Increasing clinical evidence indicates that this new use of ACE
inhibitor therapy in survivors of acute myocardial infarction will le
ad to an improvement in clinical outcome.