Arvan S, Varat M A
Am J Cardiol. 1984 Jun 1;53(11):1542-6. doi: 10.1016/0002-9149(84)90576-9.
Twenty-three patients with an anterior wall myocardial infarction (MI) and persistent ST-segment elevations (Group I) were examined for wall motion abnormalities using 2-dimensional (2-D) echocardiography. Twenty-two (96%) had dyskinetic wall motion of the infarcted area and 10 (43%) had a left ventricular aneurysm. Among 15 patients who had a chronic anterior wall MI without ST-segment elevation (Group II), 13 (86%) had akinesia of the infarcted segment. To document that dyskinetic wall motion caused the persistent electrocardiographic ST-segment elevations, 15 patients with an acute anterior wall MI (Group III) were followed by serial 2-D echocardiography for 2 to 24 months (mean 8). Of the 10 patients who had dyskinetic wall motion abnormalities on their initial 2-D echocardiogram, persistent ST-segment elevation developed in 9. All 5 patients with akinetic or severely hypokinetic wall motion abnormalities on their first 2-D echocardiogram did not show ST-segment elevation on late follow-up surface electrocardiograms. Infarct size as determined by peak creatine kinase levels for the former subgroup was greater than that for the latter subgroup (2243 +/- 429 vs 899 +/- 320 IU, respectively, p less than 0.01). In conclusion, persistent ST-segment elevation after an acute anterior wall MI is indicative of dyskinetic wall motion rather than aneurysm formation. Dyskinesia precedes the appearance of ST-segment elevation and is probably responsible for these changes on the surface electrocardiogram. Infarct size is larger in persons in whom dyskinetic wall motion abnormalities are likely to develop.