Left Ventricular Remodeling After Myocardial Infarction

Abstract

L eft ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. 1,2 Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease ( Figure 1). This article will review postinfarction remodeling, pathophysiological mechanisms, and therapeutic intervention. Pathophysiology Postinfarction Left Ventricular RemodelingThe acute loss of myocardium results in an abrupt increase in loading conditions that induces a unique pattern of remodeling involving the infarcted border zone and remote noninfarcted myocardium. Myocyte necrosis and the resultant increase in load trigger a cascade of biochemical intracellular signaling processes that initiates and subsequently modulates reparative changes, which include dilatation, hypertrophy, and the formation of a discrete collagen scar. Ventricular remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar. This balance is determined by the size, location, and transmurality of the infarct, the extent of myocardial stunning, the patency of the infarct-related artery, and local tropic factors. 1,3 The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation. 4,5 The collagen framework couples adjacent myocytes by intercellular struts that align myofilaments to optimize force development, distribute force evenly to the ventricular walls, and prevent sarcomeric deformation. 5 Myocardial infarction results in the migration of macrophages, monocytes, and neutrophils into the infarct zone; this initiates intracellular signaling and neurohormonal activation, which localizes the inflammatory response. Changes in circulatory hemodynamics are determined primarily by the magnitude of myocyte loss, the stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and the release of natriuretic peptides.Postinfarction remodeling has been arbitrarily divided into an early phase (within 72 hours) and a late phase (beyond 72 hours). The early phase involves expansion of the infarct zone, 5 which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. The failure to normalize increa...

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Injectable Acellular Hydrogels for Cardiac Repair

“…Infarct expansion causes abnormal stress distributions in myocardial regions outside the infarction, especially in the adjacent border zone (BZ) region, putting this region at a mechanical disadvantage. With time, increased regional stress is the impetus for several maladaptive biologic processes, such as myocyte apoptosis and matrix metalloproteinase activation that inherently alter the contractile property of the normally perfused myocardium [11][12][13]. Once initiated, these maladaptive processes lead to a heart failure phenotype that is difficult to reverse by medical or surgical means.…”

Cardiomyocyte‐restricted over‐expression of C‐type natriuretic peptide prevents cardiac hypertrophy induced by myocardial infarction in mice

“…After MI, left ventricular (LV) remodelling occurs, in which the myocardium changes shape, size, and function in response to increased mechanical and neurohumoral stress. These adaptations include scar maturation and cardiac hypertrophy of remote myocardium to compensate for myocardial loss and increased wall stress [1,2]. Despite the apparent appropriateness of this remodelling, it constitutes an independent risk factor for the progression from LV dysfunction to overt congestive heart failure.…”