Intrinsic washout rates of thallium-201 in normal and ischemic myocardium after dipyridamole-induced vasodilation

Abstract

Infusion of dipyridamole has been suggested as an alternative to exercise stress for myocardial perfusion imaging for detection of ischemia, but the mechanism and significance of thallium-201 (2901Tl) redistribution after administration of dipyridamole are uncertain. If disparate intrinsic cellular efflux rates of 201Tl from normal and relatively underperfused myocardium in response to dipyridamole-induced vasodilation were observed, this could explain delayed 201Tl redistribution. We investigated the effect of an intravenous infusion of 0.15 mg/kg dipyridamole on the intrinsic myocardial washout rate of 201Tl as measured with a gamma-detector probe after intracoronary injection (50 μCi) of the radionuclide in open-chested anesthetized dogs. In six normal dogs the t 1/2 for intrinsic 201Tl washout from the myocardium was 89 ± 11 min (SE) at control conditions and became more rapid at 59 ± 10 min (p = .0001) after dipyridamole. This corresponded to a significant increase in microsphere-determined epicardial (0.95 ± 0.11 to 2.23 ± 0.46 ml/min/g; p = .01) and endocardial (0.86 ± 0.10 to 1.53 ± 0.27; p = .029) flows. In 12 dogs with a critical coronary stenosis, the 201Tl intrinsic washout rate slowed from 70 ± 5 to 108 ± 6 min (p = .0001) after production of the stenosis and slowed even further to 169 ± 21 min (p = .003) after dipyridamole. Compared to conditions with the stenosis alone, dipyridamole-induced vasodilation caused a fall in mean aortic pressure (91 ± 5 to 74 ± 6 mm Hg; p