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Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.
Crozatier et al. (1977) studied this question.