Functional significance of hypertrophy of the noninfarcted myocardium after myocardial infarction in humans.

Abstract

Hypertrophy of the noninfarcted left ventricle as a chronic response to myocardial infarction has been demonstrated in animals and at autopsy in humans. However, the functional significance of postmyocardial infarction hypertrophy is a subject of dispute. The purpose of this study was to determine the time course of development of postmyocardial infarction hypertrophy of the noninfarcted myocardium in humans and to assess its functional significance. Subcostal view, two-dimensional echocardiograms were recorded at rest and during peak exercise, 6 and 40 weeks postmyocardial infarction in 45 patients (16 anterior, 20

S100B Expression Modulates Left Ventricular Remodeling After Myocardial Infarction in Mice

“…These findings are in agreement with those of a previous study in a rat model showing that induction of additional myocardial hypertrophy with an inhibitor of longchain fatty oxidation reduced LV dilation and preserved function 13 days after MI. 25,26 Global changes in cardiac mass and wall thickness after infarction represent the sum of both myocyte hypertrophy and loss or apoptosis. Overlapping pathways can trigger both hypertrophy and apoptosis, and over a chronic course, they can lead to dilated cardiomyopathy and heart failure.…”

Subendocardial fibrosis in remote myocardium results from reduction of coronary driving pressure during acute infarction in rats

“…In part, this may be due to the relatively early hemodynamic measurements undertaken in the present study. Although studies performed in humans 14 and in dogs 15 suggest that an initial transitory improvement may occur in post-MI hemodynamics, in rats these parameters usually deteriorated during the first 24 hours 12 and beyond [16][17][18][19] . Further ischemia at the SE region may occur during the progression of remodeling as a consequence of reduced coronary blood flow reserve [20][21][22] .…”

Structural basis of end-stage failure in ischemic cardiomyopathy in humans.

“…In addition, both forms of ischemic damage reduce the amount of functioning myocardium, increasing the load on the surviving region of the ventricle, which undergoes compensatory reactive hypertrophy. [6][7][8][9] This growth process may expand the length of the unaffected myocytes more than myocyte diameter, contributing to chamber dilation and relative thinning of the wall.10,11 Ventricular dilation has repeatedly been demonstrated to constitute an unfavorable outcome of the ischemic cardiomyopathic heart acutely and chronically. [12][13][14][15][16] Moreover, this anatomic factor has been shown to limit survival in both humans and animal models.9 Therefore, the present investigation was undertaken to analyze the quantitative structural properties of hearts removed from patients undergoing cardiac transplantation as a result of chronic ischemic heart disease and refractory congestive heart failure.…”