Cross talking molecular mechanisms in the failing heart : present and future targets of medical therapy

The old heart failure (HF) treatments that increased contractility have generally increased also mortality, whereas neurohumoral antagonism has successfully improved survival. Nevertheless death rate and disability remains a major social problem, mainly for patients’ undertreatment, either due to late treatment initiation, inappropriate dosages, or lack of persistence for possible side effects. This brief review will address the neurohumoral overdrive that makes heart fail and triggers most, if not all changes in molecular mechanisms recently demonstrated to occur in HF syndrome. This review has also the scope of drawing the attention of cardiologists on the Guidelines suggestions in order to prescribe the drugs that restore a normal adrenergic receptors density thus providing a simultaneous improvement in other interdependent mechanisms. Molecular mechanisms related with the increase in circulating neurohormones and some exciting novel heart failure therapies, such as replacement of the ischemic or failing cells with new cardiomyocytes from stem cells, and the changes of adrenergic signaling by selectively modulating specific molecules will briefly be taken into account.