Ventricular enlargement following infarction is a modifiable process.

The dilation and distortion of the left ventricle that may occur as a consequence of myocardial infarction are associated with a heightened risk for adverse cardiovascular events. Infarcts that are extensive, transmural, and involve the apex as well as persistently occluded, infarct-related coronary arteries are predisposing factors for ventricular enlargement. Infarct expansion is an early component of the overall process of volume enlargement, which later continues as a volume overload hypertrophy of the remaining myocardium. Therapy to limit myocardial necrosis has been associated with the preservation of a more normal ventricular architecture. The late phase of ventricular remodeling has also been shown to be amendable to therapy, as chronic administration of angiotensin-converting enzyme (ACE) inhibitors has been associated with a reduction in the extent of ventricular dilation. There is currently a great deal of clinical investigative interest not only in whether ACE inhibition therapy following acute myocardial infarction will result in preservation of ventricular volume and topography, but, more importantly, whether it will lead to an improvement in clinical outcome.