Clinical relevance of apoptosis in early and late post-infarction left ventricular remodeling.
Apoptosis may represent an important pathophysiological mechanism causing progressive myocardiocyte loss and left ventricular dilation, even late after acute myocardial infarction (AMI). This review discusses the role of myocardial apoptosis on the basis of findings from experimental studies in animals and from observational studies in humans with the purpose of assessing the clinical relevance, determinants and mechanisms of myocardial apoptosis and the potential therapeutic implications. A more profound understanding of the impact of myocardiocyte loss on prognosis and of the mechanisms involved may lead to an improved understanding of cardiac remodeling and possibly to an improved patient care. In fact, among the potential modulators of myocardial apoptosis, angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers have already been shown to improve the prognosis and symptoms in patients with post-infarction heart failure, and a reduction in myocardial apoptosis could partly contribute to such a beneficial effect. Several other putative factors could also modulate myocardial apoptosis after AMI, and many are currently under intense investigation. In particular, the infarct-related artery patency late after AMI may be a major clinical determinant of myocardial apoptosis and clinical benefits deriving from an open artery (the "open-artery hypothesis"), such as a slowing down of the remodeling process and a reduced arrhythmic risk, could be due, at least in part, to a reduced apoptotic myocardiocyte loss.
Abbate
Antonio
A
Institute of Cardiology, Catholic University, Rome, Italy.
Biondi-Zoccai
Giuseppe
G
Petrolini
Alessandro
A
Biasucci
Luigi M
LM
Baldi
Alfonso
A
D000818:Animals; D017209:Apoptosis; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D020257:Ventricular Remodeling / Q000502:physiology*