Hypoxic Hypoperfusion Fails to Induce Myocardial Hibernation in Anesthetized Swine

Background: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA) results in chronically dysfunctional myocardium with the partial ability to recover after revascularization. We attempted to establish an ALCAPA syndrome in anes thetized pigs for 24 hours and to compare it with stunned and infarcted myocardium. Methods and Results: In group 1 (n = 12), a bypass graft was interposed between the pul monary artery and the left anterior descending coronary artery (LAD). Reduction of flow in the LAD with gradual increases in flow from the pulmonary artery resulted in an incre mental reduction of segment shortening (8.9 ± 5.3% at 24 hours vs 26.6 ± 10% at baseline, P < .005). In group 2 (n = 5), 2 cycles of 10-minute LAD occlusion resulted in decreased segment shortening with slow recovery (at 24 hours 18.7 ± 1.3% vs 24.2 ± 4% at bascline, P < .05). In group 3 (n = 6), 1-hour LAD occlusion reduced segment shortening at 24 hours to 4.7 ± 5.2% (P < .005 vs baseline). Histological analysis of the LAD territory revealed severe degeneration, myolysis, and alteration of the chromatin structure in group 1 compa rable to ischemic cell death in group 3, whereas control areas and the LAD area in group 2 showed only minor structural alterations. Infarct size/risk area, as measured by tetrazolium staining, was 49.8 ± 11.2% in group 1,9.3 ± 8.1 % in group 2 (P < .005), and 60.3 ± 9% in group 3. Conclusion: Hypoxic myocardial hypoperfusion from the pulmonary artery results in myo cardial necrosis in anesthetized pigs. These findings are in contrast to the concept of myocar dial hibernation in the ALCAPA syndrome because in this model, hypoxic hypoperfusion failed to induce adaptation to preserve myocardial structure.