[Remodeling after myocardial infarction--left ventricular dilation as potential therapeutic target]

Abstract

Acute myocardial infarction triggers post-infarction left ventricular remodeling and proceeds concurrently on several levels: macroscopic, involving modification of left ventricular geometry (size, shape and wall thickness), microscopic, involving change of the number of cardiomyocytes and structure of cardiac connective tissue and submicroscopic, involving changes within cardiomyocytes. This phenomenon is triggered on one side by mechanical increase of cardiomyocyte load and on the other side by activation of neurohumoral systems. The most important element of the remodeling process--left ventricular dilation--is an adverse phenomenon, underlying progression to heart failure. Since more and more arguments indicates that this phenomenon is reversible, it is possible that in future interventions will be developed aimed at decreasing or at least halting post-infarction left ventricular dilation.