ABSTRACT
Cardiac remodeling describes the adaptive response of the myocardium to pathophysiological changes. The remodeling process can be measured at different levels. Cardiac remodeling is defined by the structural and concomitant functional alterations in the heart following an ischemic event. The ischemia-induced architectural remodeling encompasses ventricular dilatation, myocardial hypertrophy, deposition of collagen, and apoptosis in the area-at-risk and the remote myocardium. Myocardial ischemia will lead to the loss of viable cardiomyocytes by three different mechanisms: necrosis, apoptosis, and autophagic cell death. Necrosis is well characterized by cell swelling, disruption of cell organelles and cell membranes, and an inflammatory tissue reaction. The hypertrophic response of cardiomyocytes has been studied extensively in the past decade using genetically modified mouse models and in vitro models. Cardiomyocyte hypertrophic growth in vivo is triggered by various stimuli such as ventricular pressure-or volume-overload, IR, or drug induced.
