Left Ventricular Remodeling after Myocardial Infarction: From Physiopathology to Treatment

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.

Keywords: heart failure; inflammation; left ventricular remodeling; myocardial infarction; neurohormonal activation; wall stress.

Figure 1

Mechanisms of adverse ventricular remodeling after myocardial infarction. RAAS: renin-angiotensin-aldosterone system; SNS: sympathetic nervous system; ECM: extracellular collagen matrix.

Figure 2

Mechanical mechanisms of adverse LV remodeling.

Figure 3

Therapies for ventricular remodeling. ACE: angiotensin-converting enzyme; ARBs: Ang II receptor blockers; MRAs: mineralocorticoid receptor antagonists; ARNI: angiotensin receptor neprilysin inhibitor; SGLT2: sodium-glucose cotransporter 2; RNAs: ribonucleic acids; PCI: percutaneous coronary intervention; CABG: coronary artery bypass graft.