Dipyridamole-induced increased glucose uptake in patients with single-vessel coronary artery disease assessed with PET

Background. The aim of this study was to determine the relationship between vasodilatation-induced ischemia and poststress glucose uptake. Coronary va sodilators may induce myocardial ischemia due to coronary steal through col lateral circulation or transmural blood flow redistribution with diminished subendocardial perfusion. Myocardial ischemia can be demonstrated by incre ased glucose uptake as previously shown in patients with exercise-induced i schemia. Methods and Results. We studied 11 patients with single-vessel disease and no history of myocardial infarction. Five patients had no collateral circul ation, and 6 had angiographic evidence of collateral vessels. We measured m yocardial blood flow (MBF) and glucose uptake at baseline and after the adm inistration of dipyridamole (0.56 mg/kg) with positron emission tomography, using O-15 water and fluorine 18 deoxyglucose (FDG) as perfusion and gluco se tracers. MBF at baseline was 0.82 +/- 0.13 mL/g/min in normal areas and 0.80 +/- 0.15 mL/g/min in areas supplied by stenotic arteries. MBF during d ipyridamole was 2.05 +/- 0.66 and 1.19 +/- 0.66 mL/g/min in normal areas an d areas with stenotic arteries, respectively (P less than or equal to .001) . FDG uptake at baseline was 1.36 +/- 0.55 in normal areas and 1.57 +/- 0.6 2 in areas supplied by stenotic arteries. FDG uptake after dipyridamole inf usion was 1.79 +/- 1.1 and 4.04 +/- 0.84 in normal areas and areas with ste notic arteries, respectively (P less than or equal to .001). MBF and FDG up take were not different between patients with collateral circulation and th ose without collateral circulation, Conclusions. Increased myocardial glucose uptake was consistently observed after dipyridamole administration in those areas with diminished coronary v asodilatory capacity. The similar MBF and FDG findings in patients with and without collateral circulation may indicate that transmural blood flow red istribution appears to be a possible mechanism of dipyridamole-induced myoc ardial ischemia.