Mechanism of impaired myocardial function during progressive coronary stenosis in conscious pigs: Hibernation versus stunning?

The major goal of this study was to determine whether impaired myocardial contractile function during the development of progressive coronary artery stenosis induced by ameroid constriction in conscious pigs reflected myocardial 'hibernation' or 'stunning.' Minipigs were instrumented with a coronary ameroid constrictor and hydraulic occluder, regional wall thickness crystals, a left ventricular (LV) pressure gauge, and aortic and left atrial catheters. In the seven pigs in which it was measured, systolic wall thickening (WT) distal to the ameroid fell by a maximum of 56±6% at 20±3 days after ameroid implantation and then began to recover. At 1 day after ameroid implantation, brief complete coronary artery occlusion (CAO) resulted in wall thinning distal to the ameroid (-113±4%) and transmural decreases in myocardial blood flow in endocardial (from 0.82±0.08 to 0.02±0.01 mL/min per gram) and epicardial (from 0.73±0.13 to 0.03±0.02 mL/min per grain) layers. At 20±3 days, baseline myocardial blood flow was not altered either in endocardial (0.92±0.10 mL/min per gram) or epicardial (0.85±0.12 mL/min per gram) layers,whereas brief complete coronary artery occlusion still reduced WT (-83±12%) and myocardial blood flow in endocardial (to 0.21±0.03 mL/min per gram) and epicardial (to 0.43±0.12 mL/min per gram) layers, indicating that the coronary artery was not totally occluded. Pathology in four pigs demonstrated no gross necrotic myocardium shortly after this time point. Transient reductions in WT distal to the ameroid were observed during progressive coronary artery stenosis in response to spontaneous increases in activity. Beat-by-beat analysis of these episodes revealed that acute reductions in WT followed increases in LV dP/dt and heart rate and exhibited delayed recovery. These data suggest that the reduced function during ameroid-induced coronary stenosis reflected cumulative myocardia/stunning rather than a primary deficit in coronary blood flow or 'hibernating myocardium.'