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Updated: Sep 27, 2026
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Clinical relevance of apoptosis in early and late post-infarction left ventricular remodeling
Antonio Abbate1, Giuseppe Biondi-Zoccai, Alessandro Petrolini
1Institute of Cardiology, Catholic University, Rome, Italy.
Insights
Apoptosis, programmed cell death, contributes to heart muscle cell loss after acute myocardial infarction (AMI). Reducing this cell loss may improve outcomes and guide new heart failure therapies.
Area of Science:
- Cardiology
- Pathophysiology
- Molecular Biology
Background:
- Apoptosis (programmed cell death) is implicated in progressive myocyte loss and left ventricular dilation post-acute myocardial infarction (AMI).
- Understanding myocyte loss mechanisms is crucial for improving cardiac remodeling insights and patient care.
Purpose of the Study:
- To review the role of myocardial apoptosis in the context of AMI.
- To assess the clinical relevance, determinants, mechanisms, and therapeutic implications of myocardial apoptosis.
Main Methods:
- Review of experimental animal studies.
- Review of observational human studies.
Main Results:
- Myocardial apoptosis contributes to myocyte loss and cardiac remodeling after AMI.
- Angiotensin-converting enzyme inhibitors and beta-blockers may reduce myocardial apoptosis, contributing to improved prognosis.
- Infarct-related artery patency is a key determinant of myocardial apoptosis and clinical benefits, potentially via reduced cell loss.
Conclusions:
- Myocardial apoptosis is a significant factor in post-AMI cardiac dysfunction.
- Therapeutic strategies targeting apoptosis, alongside maintaining infarct artery patency, hold promise for managing heart failure post-AMI.
Abstract:
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.
