Cardioprotective Brain Mechanisms

Abstract

Progressive cardiac dysfunction after a myocardial infarction (MI) is a major contributor to the high incidence of heart failure in many parts of the world. The initial myocardial injury and the resulting decrease in left ventricular (LV) function activate a variety of systems to sustain the cardiovascular homeostasis. However, in the long-term their activation contributes to adverse cardiac remodeling and a further decrease in LV function. In recent years it has become apparent that the central nervous system (CNS) plays a pivotal role in this regard. Post-MI, several stimuli can activate CNS-angiotensinergic sympathoexcitatory pathways and as a result not only cause sympathetic hyperactivity but also activate the circulating and cardiac renin-angiotensin-aldosterone system, cytokines, and vasopressin, all contributing to further myocyte loss and decreased myocyte function.1 No braking, that is, balancing mechanisms are apparently being activated, and this is considered the main reason for progressive cardiac dysfunction leading to clinical heart failure and death. Drug therapy involving β-blockers, angiotensin-converting enzyme inhibitors/angiotensin II type 1-receptor blockers, and mineralocorticoid receptor blockers has a marked impact, but heart failure remains a major problem. The study by Okada et al2 in the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology provides a new perspective …