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

To study endocardial wall motion and thickness as indexes of infarction, we used two-dimensional echocardiography to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Thirteen dogs were studied 48 hours after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 msec 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 per slice. Slices corresponding to each two-dimensional echocardiographic cross section were examined pathologically for evidence of infarction. Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM both yielded clear separation with little overlap (- 12.5% infarcted vs 37.4% normal for thickness; - 11.3 vs 25.7% for motion, p <<0.001 for both). Endocardial motion was less precise than thickening, however, 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 two 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), whereas 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 the extent of transmural infarction increased from 21% to 100%. We conclude that: (1) Wall motion abnormalities are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. (2) There is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. (3) There is no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21% to 100%. This 'threshold' phenomenon may therefore preclude accurate estimation of infarct size by two-dimensional echocardiography. (4) Evidence of any systolic thickening indicates less than 20% transmural extent of infarction.