Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Abstract
To study endocardial wall motion and thickness as indexes of infarction, 2-dimensional echocardiography was used to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Dogs (13) were studied 48 h after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 ms at 1 cm intervals from apex to base in an open-chest, anesthetized preparation were analyzed with a computer-aided contouring system for quantification of segmental %EM and %Th at 16 equally spaced points/slice. Slices corresponding to each 2-dimensional echocardiographic cross section were examined pathologically for evidence of infarction. Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM yielded clear separation with little overlap (-12.5% infarcted vs. 37.4% normal for thickness; -11.3 vs. 25.7% for motion, P .mchlt. 0.001 for both). Endocardial motion was less precise than thickening in distinguishing infarct from either distant normal zones or zones directly adjacent to infarct. Although wall thickening was useful in separating out true subendocardial infarct, change in systolic thickening was not accurate in detecting the transmural extent of infarction. In 827 individual 2-dimensional echocardiographic segments with varying degrees of transmural involvement, segments with 1-20% extent of transmural infarction showed reduced thickening compared with noninfarcted segments (39.9 vs. 15.2%, P < 0.001). Myocardial segments with 21-100% transmural infarction showed systolic thinning (-8.9 to -13.3%). There was no significant augmentation in the severity of systolic thinning as an extent of transmural infarction increased from 21-100%. Wall motion abnormalities apparently are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. There apparently is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. There is evidently no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21-100%. This threshold phenomenon may preclude accurate estimation of infarct size by 2-dimensional echocardiography. Evidence of any systolic thickening suggests less than 20% transmural extent of infarction.