Limitations of postextrasystolic potentiation in identifying ischemic myocardium.

To evaluate the usefulness of postextrasystolic potentiation in differentiating ischemic yet viable myocardium from infarcted myocardium, 20 dogs were chronically instrumented with left ventricular pressure gauges, left circumflex coronary artery flow probes, occluders, pacing wires, and ultrasonic segment-length transducers. Ten dogs had acute (1 h) coronary occlusions followed by reperfusion (4 days) and were then killed. Ten more dogs had more prolonged (1 mo) occlusions and were then killed. Timed premature ventricular contractions were induced, and the postextrasystolic beat was evaluated. In ischemic segments that were hypokinetic, postextrasystolic potentiation of shortening occurred in both groups. In ischemic segments that were akinetic or dyskinetic, potentiation of shortening did not occur in either group. Both groups showed recovery of shortening, and histologically normal myocardium was identified in the region between the segments in all animals. Thus, akinetic and dyskinetic segments did not show postextrasystolic potentiation of shortening, even though the tissue was viable and showed functional recovery. Failure to improve shortening after a premature ventricular beta in an ischemic segment does not necessarily indicate nonviable myocardium.