Ventricular remodeling after infarction and the extracellular collagen matrix: When is enough enough?

Abstract

Prevention of adverse remodeling after MI remains a therapeutic challenge. Current antiremodeling therapy is clearly not ideal, as many ventricles continue to enlarge after MI, and mortality and morbidity remain significant despite therapy. Collective evidence indicates that the ECCM plays a major role in healing and remodeling after MI. Antifibrotic agents targeting excessive ECCM might be beneficial in selected patients without MI. After MI. however, the situation is complicated by the development of an IZ and a NIZ with differential pathophysiological responses. Because one aim of therapy is to maximize benefits and minimize unwanted, often delayed adverse effects, failure to address protection of the ECCM in the IZ as well as the NIZ in the long term seems to deal with only half the problem. Protecting the ECCM in post-MI survivors should be a future priority.