Echocardiographic Detection of Regional Myocardial Infarction

Posterior wall velocities have been advanced as a useful technic for the assessment of left ventricular function. To evaluate the echocardiographic effects of regional myocardial infarction on posterior wall motion (PWM), measurements were obtained in 22 open-chest dogs. Coronary artery ligation produced infarction of the apex in 11 dogs (group I) and the posterior wall in 11 dogs (group II). Echoes were thus received from noninfarcted myocardium in group I and from infarcted myocardium in group II. Postinfarct recordings in group I showed no significant changes in posterior wall velocities or excursion. In contrast, group II showed striking changes in the contour of PWM with a large initial posterior displacement (aneurysmal bulging) during isometric contraction, followed by a slow anterior movement during ventricular ejection and then a rapid anterior recoil motion during isometric relaxation. Mean posterior wall velocity fell from 31 ± se 3 mm/sec preinfarct to 13 ± 4 postinfarct ( P < 0.01); from 33 ± 4 to 21 ± 5 mm/sec during atrial pacing pre- and postinfarction ( P < 0.05); from 30 ± 3 to 18 ± 3 mm/sec during volume loading with dextran 20 ml/kg ( P < 0.01); and from 32 ± 4 to 5 ± 2 mm/sec during aortic constriction ( P < 0.01). Corresponding reductions in posterior wall systolic excursion were observed. Simultaneous hemodynamic measurements revealed moderate depression of ventricular performance in group II, but there was no significant correlation between the changes in hemodynamic parameters and echocardiographic velocities following infarction. We conclude that the marked changes in PWM following posterior infarction were due to echocardiographic detection of dyskinesis in the infarcted area rather than to generalized changes in ventricular function. Posterior wall velocities are not a reliable index of left ventricular performance when localized dyskinesis, as indicated by abnormal PWM, is present.