title: Early loss of postextrasystolic potentiation in acutely ischemic myocardium: evaluation by contrast two-dimensional echocardiography.
abstract: Studies in animals with acutely ischemic hearts have suggested that postextrasystolic potentiation (PESP) may predict the viability of dysfunctional myocardium. Most of these data have been obtained with sonomicrometers and therefore the presence and extent of PESP throughout the entire region at risk has not been defined. In this study we used contrast two-dimensional echocardiography (2DE) to define region at risk in vivo, and then with quantitative 2DE we examined the proportion of the region at risk that demonstrated PESP, the degree of the potentiation, and the time course of this response. The region at risk was divided into a central (inner 50%) and two peripheral (25% each) ischemic zones. Adjacent contrast-enhanced myocardium was divided into near and far border zones that were equal in size to the adjacent peripheral ischemic zone. Systolic thickening was analyzed within each zone along multiple radii at 5, 30, and 120 min after coronary occlusion. PESP was absent in the central ischemic zone at all three times. In the peripheral ischemic zone at 5 min, a small amount of PESP was detected (-4.1% vs + 3.1% for nonpotentiated and potentiated thickening, respectively; p less than .01). At 30 min after occlusion, no potentiation was seen in the region at risk and PESP was confined to the contrast-enhanced near and far border zones. These findings persisted at 120 min. These data indicate that the response to PESP is localized to perfused myocardium by 30 min after acute occlusion. PESP is therefore of limited value in predicting the presence of ischemic, potentially viable myocardium early in the course of acute infarction.
authors.forename: T
authors.initials: T
authors.lastname: Force
authors.forename: A J
authors.initials: AJ
authors.lastname: Kemper
authors.forename: C
authors.initials: C
authors.lastname: Cohen
authors.forename: A F
authors.initials: AF
authors.lastname: Parisi
mesh_terms: D000818:Animals; D005117:Cardiac Complexes, Premature / Q000175:diagnosis*; D002304:Cardiac Pacing, Artificial; D003250:Constriction; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology; D004285:Dogs; D004452:Echocardiography / Q000379:methods*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D013997:Time Factors