Post-infarction myocardial remodelling: why does it happen?

Abstract

Myocardial remodelling is currently the subject of intense investigative interest. The question "Why does it happen?' is not clearly answerable by today's methods; however, the work of many basic scientists and clinicians has allowed an improved understanding of the process. Multiple mechanisms are probably operative in the cardiac remodelling process, including cell drop-out, myocyte slippage, collagen replacement and growth, and myocyte hypertrophy. The concept of heart failure as primarily a structural problem rather than the result of a specific biochemical "defect' is advanced. There is now direct evidence that cardiac myocytes are enlarged in both experimental and clinical left ventricular remodelling. Possible signal processing cascades are potential pathways to myocyte remodelling. Although not proven, the enlarged and elongated cardiac myocyte may be at a structural disadvantage, thus contributing functionally to the clinical syndrome of heart failure. Reversal of established cardiomegaly--regression of myocardial remodelling--is an unusual but occasional event in patients with cardiomyopathy that can be observed experimentally.