Two-dimensional echocardiography was employed to define the natural history of regional wall motion abnormalities in a canine model of acute experimental myocardial infarction. Serial short-axis two-dimensional echocardiograms were recorded in 11 closed chest dogs before coronary occlusion and 10, 30, 60, 180 and 360 minutes after permanent coronary ligation. Radiolabeled microsphere-derived blood flows were obtained in each study period and the histochemical (triphenyltetrazolium chloride) extent of infarction was determined at 6 hours. Previously published methods were used to quantitate field by field (every 16.7 ms) excursion of 36 evenly spaced endocardial targets. The circumferential extent of abnormal wall motion was followed sequentially using previously published definitions of abnormality: 1) systolic fractional radial change of less than 20%; 2) dyskinesia (systolic bulging) at the point in time (echocardiographic field) in which there is maximal dyskinesia; and 3) correlation with composite normal ray motion falling outside the 95% confidence limits defined in the control period. On the basis of the triphenyltetrazolium chloride staining pattern, the ventricle was divided into five zones: central infarct zone, zone with greater than 25% transmural infarction, total infarct zone, border zones and normal zone. Mean systolic fractional radial change was calculated for each zone and used as an index of the magnitude of abnormal wall motion. Regardless of the definition of abnormality employed, the circumferential extent of abnormal wall motion manifested at 10 minutes after occlusion did not significantly change, even up to 6 hours later. Similarly, 10 minutes after coronary occlusion the three infarct zones and border zones demonstrated significantly reduced systolic fractional radial change. This remained stable over the remainder of the 6 hour study period. It is concluded that once established at 10 minutes after coronary occlusion, the circumferential extent and magnitude of abnormal wall motion do not significantly change in the immediate postinfarct (6 hour) period.