Ventricular dilatation and remodeling after myocardial infarction

Abstract

Objective: To discuss the important predictors of ventricular enlargement after myocardial infarction and the appropriate time frame for the initiation of medical and pharmacologic therapy.

Design: A review of the important contributions relative to the process known as "postinfarction ventricular remodeling" is provided; current clinical implications and areas for future investigation are discussed.

Material and methods: Ventricular dilatation is an important factor in the prognosis after infarction. Stretching and thinning of the myocardium within the infarct region can be seen within hours after the acute event and may be accompanied by delayed but potentially progressive stretching and thinning in the noninfarct regions. Development of left ventricular hypertrophy in the nonischemic myocardium, in response to increased wall stress, can be observed but may be insufficient for proper compensation. This process is referred to as postinfarction remodeling and can result in progressive and long-term changes in ventricular architecture and function in the absence of additional ischemic injury.

Results: The most effective way to limit the extent of postinfarction ventricular remodeling is to limit infarct size by prompt medical intervention within the first few hours. In addition to traditional post-infarction medications such as beta-blockers, nitrates, and aspirin, long-term benefit may be derived by use of adjunctive pharmacologic therapy such as angiotensin converting enzyme inhibitors, which have been shown to be valuable in limiting the extent of ventricular chamber dilatation after infarction. Studies in animal models and conclusions from clinical trials have shown that angiotensin converting enzyme inhibitors also decrease late mortality and cardiac morbidity after infarction, likely through favorable effects on both hemodynamic and neurohumoral factors specific to this class of medication.

Conclusion: These investigations notwithstanding, further studies are necessary for a complete understanding of the pathogenesis of postinfarction ventricular remodeling and the appropriate timing of specific pharmacologic therapy intended to limit ventricular dilatation. The hemodynamic and neurohumoral interactions on and within the heart must be thoroughly understood relative to microscopic and macroscopic changes in cardiac size, shape, and function after myocardial infarction.