Myocardial blood flow, metabolism, and inotropic reserve in dogs with dysfunctional noninfarcted collateral-dependent myocardium.

UNLABELLED There is intense controversy as to the mechanisms underlying chronic but reversible left ventricular (LV) ischemic dysfunction. The aim of this study was to investigate the physiology underlying this condition in a canine model of noninfarcted collateral-dependent myocardium. METHODS Six mongrel dogs were instrumented with ameroid constrictors on the left circumflex and right coronary arteries and a partial occluder on the left anterior descending coronary artery. The animals were followed up for 6 mo. Every 6 wk, measurements of regional wall thickening (M-mode echo), myocardial blood flow ((13)N-ammonia PET), oxygen consumption ((11)C-acetate PET), and glucose uptake ((18)F-FDG PET) were obtained. After 6 mo, myocardial blood flow reserve (during adenosine infusion) and regional contractile reserve (during infusion of a low dose of dobutamine) were also investigated. RESULTS Following ameroid implantation, regional thickening decreased in the posterior wall (to 34% +/- 13% of baseline; P < 0.001) but not in the septum. Resting myocardial blood flow (56 +/- 10 vs. 58 +/- 15 mL.[min.100 g](-1)), myocardial oxygen consumption (21 +/- 3 vs. 22 +/- 3 J.[beat.100 g](-1)), and insulin-stimulated glucose uptake (39 +/- 8 vs. 42 +/- 11 micromol.[min.100 g](-1)) were similar among dysfunctional and normal segments. Myocardial blood flow reserve was blunted in dysfunctional versus normal segments (3.7 +/- 0.5 vs. 5.2 +/- 1.5; P = 0.06). With dobutamine, wall thickening (to 69% +/- 8% and 77% +/- 11%, respectively) and oxygen consumption (to 36 +/- 5 and 39 +/- 5 J.[beat.100 g](-1), respectively) improved to the same extent in both segments. As a consequence, mechanical efficiency decreased in septal but remained unchanged in posterior segments during infusion of dobutamine. Biopsy specimens from both walls were free from any morphological alterations. CONCLUSION Our data indicate that ameroid occlusion in dogs induces sustained reduction in regional contraction, which occurs despite normal levels of transmural blood flow and recruitable inotropic reserve. Since myocardial perfusion reserve was blunted, such perfusion-contraction mismatch could reflect repetitive stunning.