Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size.
We sought to identify advantages of contrast-enhanced magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling.
Although sequential measurements of ventricular volumes, internal dimensions, and total ventricular mass have provided important insights into postinfarction left ventricular remodeling, it has not been possible to define serial, directionally opposite changes in resorption of infarcted tissue and hypertrophy of viable myocardium and effects of these changes on commonly used indices of remodeling.
Using gadolinium-enhanced MRI, the time course and geometry of changes in infarcted and noninfarcted regions were assessed serially in dogs subjected to coronary occlusion for 45 min, 90 min, or permanently.
Infarct mass decreased progressively between three days and four to eight weeks following coronary occlusion; terminal values averaged 24 +/- 3% of those at three days. Radial infarct thickness also decreased progressively, whereas changes in circumferential and longitudinal extent of infarction were variable. The ability to define the circumferential endocardial and epicardial extents of infarction allowed radial thinning without epicardial expansion to be distinguished from true infarct expansion. The mass of noninfarcted myocardium increased by 15 +/- 2% following 90-min or permanent occlusion. However, the time course of growth of noninfarcted myocardium differed systematically from that of infarct resorption. Measurements of total ventricular mass frequently failed to reflect concurrent changes in infarcted and noninfarcted regions. Reperfusion accelerated infarct resorption. Histologic reductions in nucleus-to-cytoplasm ratios corresponded with increases in noninfarcted ventricular mass.
Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.
Fieno, DS; Hillenbrand, HB; Rehwald, WG; Harris, KR; Decker, RS; Parker, MA; Klocke, FJ; Kim, RJ; Judd, RM
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