A comparison of quantitative echocardiographic methods for delineating infarct-induced abnormal wall motion.

Abstract

Current echocardiographic methods for quantitating abnormal regional left ventricular wall motion rely primarily on changes in endocardial excusion from end-diastole to end-systole. Recent studies demonstrating important spatial and temporal heterogeneity in wall motion within ischemic regions, however, raise questions about the validity of this approach. To determine the optimal method for defining abnormal left ventricular wall motion, we used a canine preparation of acute experimental infarction to examine four quantitative methods of wall motion analysis. The circumferential extent of abnormal wall motion assessed by each method was compared with the circumferential extent of infarction (defined by triphenyltetrazolium chloride staining) and the circumferential extent of reduced transmural blood flow (determined by radiolabeled microsphere techniques) 6 hr after acute coronary occlusion. The following methods of quantitating abnormal wall motion were examined: (1) determination of end-diastolic to end-systolic endocardial excursion (less than 0.20 end-diastolic radius), (2) determination of the extent of maximal dyskinesis (systolic bulging), and (3) and (4) two derived correlation methods that consider the entire course of systolic radial motion by correlating the observed echocardiographic field-by-field (every 16.7 msec) motion of each of 36 evenly spaced endocardial targets with the course of normal motion established from pooled normal data. Results obtained with the correlation methods showed a better correlation with the triphenyltetrazolium chloride-defined circumferential extent of infarction (r = .87 and r = .78) than did determinations of reduced end-diastolic to end-systolic endocardial excursion (r = .35) or the extent of maximal dyskinesis (r = .37). Similarly, the best correlation with the extent of reduced flow was obtained with one of the correlation methods (r = .80). We conclude that correlation methods that "integrate" endocardial motion over the entire systolic contraction sequence provide better definition of ischemic left ventricular dysfunction than do methods that consider motion at only single points in time.