Left Ventricular Remodeling after Myocardial Infarction: From Physiopathology to Treatment
Sabina Andreea Leancă1, Daniela Crișu1, Antoniu Octavian Petriș1,2
1Department of Cardiology, Emergency Clinical Hospital "Sf. Spiridon", Bd. Independentei nr. 1, 700111 Iasi, Romania.
Insights
Myocardial infarction (MI) causes heart damage leading to heart failure. This review details the mechanisms of cardiac remodeling after MI and therapies to improve heart structure and function.
Area of Science:
- Cardiology
- Pathophysiology
- Pharmacology
Background:
- Myocardial infarction (MI) is a major global cause of death.
- Atherosclerotic plaque rupture and coronary thrombosis are common causes of MI.
- MI leads to cardiomyocyte death, inflammation, and fibrosis, potentially causing heart failure (HF).
Purpose of the Study:
- To describe the pathophysiological mechanisms of cardiac remodeling post-MI.
- To review therapeutic strategies for mitigating cardiac remodeling and improving cardiac function.
Main Methods:
- Literature review of pathophysiological mechanisms.
- Analysis of current therapeutic strategies for MI and HF.
Main Results:
- Cardiac remodeling involves changes in left ventricular geometry, dimension, and function post-MI.
- Therapies focus on restoring coronary flow and counteracting neurohormonal activation.
- Despite treatments, remodeling can progress to heart failure.
Conclusions:
- Understanding cardiac remodeling mechanisms is crucial for developing effective treatments.
- Therapeutic strategies aim to slow remodeling progression and enhance cardiac recovery.
- Further research is needed to optimize interventions for post-MI patients.
Abstract:
Myocardial infarction (MI) is the leading cause of death and morbidity worldwide, with an incidence relatively high in developed countries and rapidly growing in developing countries. The most common cause of MI is the rupture of an atherosclerotic plaque with subsequent thrombotic occlusion in the coronary circulation. This causes cardiomyocyte death and myocardial necrosis, with subsequent inflammation and fibrosis. Current therapies aim to restore coronary flow by thrombus dissolution with pharmaceutical treatment and/or intravascular stent implantation and to counteract neurohormonal activation. Despite these therapies, the injury caused by myocardial ischemia leads to left ventricular remodeling; this process involves changes in cardiac geometry, dimension and function and eventually progression to heart failure (HF). This review describes the pathophysiological mechanism that leads to cardiac remodeling and the therapeutic strategies with a role in slowing the progression of remodeling and improving cardiac structure and function.
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