Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

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Abstract
The region of preserved myocardium between a subendocardial myocardial infarct (SEMI) and the endocardium was quantitated in dogs and determinations were made as to whether this preserved zone was within the region at risk and whether infarct extension could occur in this region. The existence of a similar subendocardial region in patients with SEMI was also evaluated. A 40-min temporary occlusion of the left anterior descending coronary artery (LAD) in 8 dogs resulted in a 35 .+-. 5% transmural infarct with 8 .+-. 1% subendocardial preservation as assessed by point-counting of the histologic specimens. In vivo perfusion of coronary vessels with Microfil showed that this preserved subendocardial zone was within the region at risk. The preserved subendocardial zone had significantly fewer cell layers in the dogs ventilated with room air than in dogs ventilated with 100% O2 (8 .+-. 4 vs. 19 .+-. 4, P < 0.001), which suggests that diffusion from the ventricular cavity was the mechanism of cell preservation. The inspired O2 concentration did not influence the size of the SEMI. Reocclusion of the LAD for 24 h in an additional 8 dogs, 1 wk after a SEMI had been created by a 40-min temporary occlusion, resulted in both subendocardial and subepicardial extension involving 5 .+-. 1% and 29 .+-. 9%, respectively, of the transmural myocardium at the infarct center. Subendocardial infarct extension of a similar dimension to that in dogs ventilated on 100% O2 was observed in postmortem material from 8 patients with infarct extension. The preserved layers of subendocardium presumably receive sufficient nutrients from the ventricular cavity to maintain the viability of this region during temporary, but not permanent, reduction of blood supply from the coronary arteries.