Postinfarction left ventricular remodeling

Left ventricular hypertrophy and the development of chronic heart failure are potent predictors of survival after myocardial infarction. Gaudron et al showed that 26% of patients developed limited left ventricular dilation within 4 weeks after their first infarction. Since this helped to restore the resting cardiac index and stroke index and preserve exercise performance, it remained compensatory. A somewhat smaller group (20%) developed progressive structural left ventricular dilation, which was compensatory at first, then progressed to noncompensatory dilation, finally resulting in severe global left ventricular dysfunction. In these patients, dysfunction of the initially normally contracting myocardium was probably responsible for depressing the global ejection fraction.

The acute loss of myocardium causes an abrupt increase in loading conditions that induces a unique pattern of remodeling, involving the infarcted border zone and remote noninfarcted myocardium. 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, which may cause early ventricular rupture or aneurysm. Infarct expansion results from the degradation of the intermyocyte collagen struts by serine proteases and the activation of matrix metalloproteinases released from neutrophils. It occurs within hours of myocyte injury, results in wall thinning and ventricular dilatation, and elevates diastolic and systolic wall stresses. Increased wall stress is a powerful stimulus for hypertrophy and a major determinant of ventricular performance. Late remodeling involves the left ventricle globally and is associated with time-dependent dilation, distortion of ventricular shape, and mural hypertrophy. Progressive thinning and lengthening in the remote, noninfarcted, wall may continue for at least 6 months and possibly for years. Compensatory hypertrophy appears to be a delayed and limited adaptation during the first year. Myocyte hypertrophy and changes in the ventricular architecture are meant to distribute the increased wall stresses more evenly as the extracellular matrix forms a collagen scar to stabilize the distending forces and prevent further deformation. The failure to normalize increased wall stresses causes progressive dilation, recruitment of border zone myocardium into the scar, and deterioration in contractile function.

The progressive dilation that continues after the infarct zone has healed histologically is associated with the development of progressive left ventricular dysfunction and congestive heart failure. Furthermore, the increase in left ventricular size after myocardial infarction correlates with mortality and the risk of a major cardiovascular adverse event.

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