We have previously reported that regional wall motion abnormalities in a canine model of acute myocardial infarction may show substantial improvement in the first 6 weeks after infarction. To determine whether the mechanism of this improvement in function is the result of scar contraction within the infarct, we studied the relationship between changes in regional wall motion defined by cross-sectional echocardiography and the regional concentration of radioactive microspheres injected immediately before coronary occlusion and sampled 6 weeks after occlusion. Eight dogs underwent serial echocardiographic and microsphere blood flow measurements immediately before and 30 minutes, 48 hours, 1 week, 3 weeks, and 6 weeks after ligation of the left anterior descending or the left circumflex coronary artery. Wall motion and blood flow were measured in the short-axis section of the left ventricle at the level of the midpapillary muscle in each 10-degree radial segment around the circumference of the ventricle. Infarct histology was assessed at 6 weeks by means of the same radial coordinate system. Control data were collected in a similar manner from four dogs that underwent sham operations and had no histologic evidence of infarction. In all of the animals with infarcts, but not in the sham animals, the calculated preocclusion endocardial and epicardial blood flow values in the histologic infarct zone (252 ± 44 and 168 ± 17 ml/min/100 gm, respectively, mean ± SEM) were significantly higher than those in the normal opposite wall (endocardial: 106 ± 3 ml/min/100 gm, p < 0.01); epicardial: 108 ± 3 ml/min/100 gm, p < 0.01. The location and circumferential extent of myocardium showing this elevation of preocclusion blood flow correlated well (r = 0.93, p < 0.001) with the location and circumferential extent of the histologic infarct. The amount of wall motion abnormality, measured from the "correlation plot area," decreased significantly from its maximum value of 39 ± 3 degrees at 48 hours after coronary occlusion to 3 ± 1 degrees (p < 0.001) at 6 weeks after occlusion. The ratio of the preocclusion transmural blood flow in the infarct zone to that in the noninfarct zone, a measure of the condensation of the microspheres injected before coronary occlusion, and therefore of the degree of scar contraction at 6 weeks, correlated well (r = 0.83, p < 0.01) with the recovery of wall motion 6 weeks after infarction. These findings indicate that spontaneous recovery of regional wall motion in the chronic canine infarct is related to the degree of microsphere condensation and therefore to the process of scar contration.