Cellular Cardiac Reinforcement

Abstract

Because they are terminally differentiated cells, adult cardiomyocytes cannot regenerate and there is no myocardial pool of stem cells to replace those which have suffered irreversible ischemic injury. In fact, this dogma has been recently challenged by some experimental (for a review, see1])and clinico-pathological studies [2[3]] suggesting that cardiomyocytes of infarcted or failing human hearts had actually retained a capacity of reentering a cell cycle. Whereas these observations are interesting from a cognitive standpoint, their clinical relevance is probably limited because the number of “new” cells that can be generated through this mechanism is by far too low to compensate for the loss of cardiomyocytes resulting from an infarct (or at least an infarct large enough to cause heart failure).Thus, in clinical practice, the usual responses to myocardial infarction involve evolution of the infarct zone toward a fibrous noncontractile scar and hypertrophy of cells harboured in the still viable segments of the heart. At best, these compensatory responses can temporarily maintain an adequate contractile function. At worst, the combination of interstitial fibrosis and inappropriate remodelling promote deterioration of systolic and diastolic functions and lead to heart failure.