Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors.

Abstract

Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.

Relationship between infarct size and severity measured by gated SPECT and long-term left ventricular remodelling after acute myocardial infarction

“…We observed that infarct size and severity could be significant predictors of LV remodelling. Several clinical studies demonstrated that various parameters are predictive of remodelling, including anterior infarct location, patency of the infarctrelated artery, perfusion and functional parameters [4][5][6][7][8][9][10][11][12][13]. In agreement with these previous findings, the present study showed a number of baseline parameters predictive of remodelling, infarct severity demonstrating the best predictive value.…”

“…It represents an important cause of heart failure and is a predictor of mortality [2,3]. Several factors have been demonstrated to influence the evolution of LV volumes after AMI, among which there are size, location and transmurality of the infarction, residual viability in the infarct territory and patency of the infarct-related artery [4]. The relative role of these factors, however, is still unclear.…”

Prognostication of late left ventricular systolic dysfunction in patients with acute coronary syndrome during the acute period

“…In part of patients with remaining large-scale myocardial damage, failed or delayed normalization of blood circulation in the CA resulted in the myocardial function remaining low or decreasing further due to LV remodeling processes. Gaudron and Gianuzi et al indicated that progressing late LV remodeling that results in LV systolic dysfunction develops in one-fifth of patients who had MI (21,22). According to Zhang et al, late remodeling of the myocardium occurs if MI involves more than 15% of the myocardium in case of anterior MI and more than 20% of the myocardium in case of inferior MI (23).…”

Patterns of Left Ventricular Dilatation With an Opened Artery After Acute Myocardial Infarction

“…The study findings are consistent with our current understanding of infarct physiology, myocardial functional recovery, and remodeling. Infarct size, 4 anterior infarct location, 9 perfusion status of the infarct-related artery, 6 heart failure on admission, 10 and a restricted pattern of LV filling 11 have all been identified as major predictors of LV dilatation after infarction. These observations demonstrate that after acute myocardial infarction, even with patent infarct-related arteries and a relatively small initial end-systolic volume, many patients remain at risk for ventricular remodeling despite an early favorable examination.…”

“…1 It has long been recognized that early infarct expansion is the result of lengthening of the noncontractile region undergoing a stress response with secondary volume overload hypertrophy, a process which maybe progressive over time. [2][3][4] The extent of the initial myocardial damage is linked both to the magnitude and, to a lesser degree, the timing of left ventricular (LV) dilatation and ultimately survival. 5 Moreover, ventricular remodeling (enlargement) is influenced not only by infarct size but also the type of infarct healing and coexistent LV wall stresses.…”