Left ventricular dysfunction and cytoprotection.

Abstract

With the projections of increasing aging of the population, heart failure is expected to become a major health problem for most Western societies. Therefore, the study of the pathophysiological mechanisms involved in heart failure should be one of the main priorities of cardiovascular research. A substantial amount of knowledge has been gathered in the recent years on the mechanisms involved in the development of heart failure. One such mechanism is the development of myocyte's apoptosis. This apoptotic mechanism is responsible for a substantial decrease in the number of cardiac myocytes, and therefore for the worsening of heart failure. This apoptotic mechanism can be triggered by a number of mechanisms such as the adrenergic stimulation, the angiotensin II production, changes in calcium homeostasis, and changes in cellular metabolism. At least in theory, the development of therapies (such as beta blockers, ACE inhibitors, calcium channel blockers and trimetazidine) that can inhibit these mechanisms can have a cytoprotective role and therefore reduce the development of heart failure. Because of its main role in the production of energy for the cell, the mitochondrion is one of the mainframes of cell viability. If the mitochondrial function is decreased the myocyte will be in jeopardy. Therefore, drugs that can prevent mitochondrial dysfunction will obviously have a cytoprotective role in heart failure.