Pleiotropic effects of cardiac drugs on healing post-MI. The good, bad, and ugly.

Healing after myocardial infarction (MI) is a well-orchestrated time-dependent process that involves inflammation, tissue repair with extracellular collagen matrix (ECCM) deposition and scar formation, and remodeling of myocardial structure, matrix, vasculature, and function. Rapid early ECCM degradation followed by slow ECCM replacement and maturation during post-MI healing results in a prolonged window of enhanced vulnerability to adverse remodeling. Decreased ECCM results in adverse ventricular remodeling, dysfunction, and rupture. Inflammation, a critical factor in normal healing, if impaired results in adverse remodeling and rupture. Several therapeutic drugs prescribed after MI exert pleiotropic effects that suppress ECCM and inflammation during healing and may have good, bad, or ugly consequences. This article reviews the potential impact of pleiotropic effects of some prototypic cardiac drugs such as renin-angiotensin-aldosterone system (RAAS) inhibitors, statins, and thrombolytics during healing post-ST-segment-elevation MI (STEMI), with special focus on inflammation, ECCM and remodeling, and implications in the elderly.