A synopsis of research in cardiac apoptosis and its application to congestive heart failure.
Cardiac apoptosis diminishes the contractile mass, which leads to heart failure. Apoptosis of cardiac non-myocytes also contributes to maladaptive remodeling and the transition to decompensated congestive heart failure. New antiapoptotic interventions and medications will be available within the next decade. The aim of this study is to provide a critical synopsis of research projects on cardiocyte apoptosis that have implications for current and future practice and to identify methods to prevent or attenuate apoptosis in patients who have poor ventricular function. A retrospective literature review reveals a great many important publications. However, very few investigators discuss the clinical ramifications of cardiocyte apoptosis, nor do they address the clinician who sees poor ventricular contractility daily. Most studies are still investigational and involve antiapoptotic agents such as broad-spectrum caspase inhibitors, antioxidants, calcium channel blockers, insulin-like growth-factor 1, and poly(adenosine diphosphate ribose) synthetase inhibitors. some options have already been incorporated into the clinical practices of cardiologists and cardiac surgeons: repairing or replacing diseased or damaged valves before ventricular function deteriorates; reducing afterload with medication or intra-aortic balloon pulsation in patients who display acute increases in afterload; decreasing catecholamine-induced cardiotoxicity in hemodynamically compromised patients, by using beta-blockers and phosphodiesterase inhibitors; and inserting intra-aortic balloon pumps or ventricular assist devices early in cases of failing myocardium. Coronary revascularization early in myocardial infarction is effective antiapoptotic therapy. Other therapeutic targets are cardiopulmonary bypass and aortic cross-clamping, both of which require reductions in associated myocardial apoptosis.
Khoynezhad
Ali
A
Section of Cardiothoracic Surgery, University of Nebraska Medical Center, Omaha, Nebraska 68198-2315, USA. akhoynezhad@unmc.edu
Jalali
Ziba
Z
Tortolani
Anthony J
AJ
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D009203:Myocardial Infarction / Q000503:physiopathology; D012106:Research; D015398:Signal Transduction / Q000502:physiology