Mechanism of persistent S-T segment elevation after anterior myocardial infarction

Abstract

Persistent S-T segment elevation after anterior myocardial infarction, reliably predicts the presence of advanced left ventricular asynergy. The genesis of this persistent S-T elevation is unknown, although recent observations suggest that ischemia within or surrounding the infarct zone might be involved. To explore this possibility, a body surface mapping system was utilized to assess the torso distribution of these repolarization potentials, as well as the responsiveness of the S-T segment elevation to three randomized interventions designed to alter the myocardial oxygen supply/demand ratio (40 percent oxygen, sublingual nitroglycerin and isometric exercise). S-T segment amplitude measured 75 msec after the J point (as well as two measurements from time-normalized ST-T segments) was not significantly altered by any intervention in 11 patients, thus indicating that ischemia was an unlikely cause of the persistent S-T elevation. Moreover, plots of the integrated area of the first three eighths of both the QRS complex (Q wave zone) and the ST-T segment (S-T segment) revealed that the initial repolarization maximum (corresponding to the persistent S-T segment elevation) was spatially concordant with the initial depolarization minimum (reflecting precordial Q waves). Because large Q waves usually indicate transmural scar, this surface distribution supports the conclusion that ischemia is not responsible for persistent S-T segment elevation and suggests that the sources for these repolarization potentials are not located in the infarcted area.