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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 (201Tl) 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 eht 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 muCi) 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 104 +/- 6 min (p = .0001) after production of the stenosis and slowed even further to 169 +/- 21 min (p = .003) after dipyridamole.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial thallium-201 (201Tl) uptake and clearance after intravenous administration of dipyridamole (150 micrograms/kg) were determined in 12 open-chest anesthetized dogs with a partial coronary artery stenosis. 201Tl (1.5 mCi) was injected intravenously and myocardial biopsy specimens were obtained 10 min, 60 min, and 2 hr after injection. Serial changes in 201Tl activity in the normal zone and in the zone of partial stenosis were correlated with microsphere-determined regional blood flow and distal coronary pressure. Another nine dogs with equivalent stenosis not given dipyridamole before 201Tl served as controls. In the 12 dogs given dipyridamole, 201Tl activity at 10 min in the zone of stenosis was reduced to 42 +/- 5% of initial normal zone activity (p less than .001) and remained at 44 +/- 3% of initial normal zone activity at 2 hr. There was a good correlation (.81) between the percent reduction in myocardial 201Tl activity and the percent reduction of peak hyperemic flow as determined by measuring the percentage difference in peak coronary flow after a transient 10 sec occlusion under control and stenotic conditions. In contrast, 201Tl clearance was rapid in the normal zone, with 201Tl activity decreasing to 55 +/- 3% of initial normal zone activity by 2 hr. A redistribution pattern was produced because of the disparate clearance rates from hyperperfused and relatively hypoperfused myocardial regions. The relative 201Tl defect decreased from 58% to 11% from 10 min to 2 hr. In the normal zone dipyridamole increased epicardial flow from 1.03 +/- 0.09 (SEM) to 3.52 +/- 0.36 ml/min/g (p less than .0001) and endocardial flow from 1.19 +/- 0.09 to 2.96 +/- 0.20 ml/min/g (p = .0001). In the zone of partial stenosis the increase in epicardial flow after dipyridamole was less marked (1.01 +/- 0.10 to 1.55 +/- 0.15 ml/min/g; p = .009) and endocardial flow decreased (0.84 +/- 0.11 to 0.64 +/- 0.15 ml/min/g; p = .04). Coronary perfusion pressure distal to the stenotic zone fell from 65 +/- 3 to 50 +/- 3 mm Hg after dipyridamole. In the nine control dogs with equivalent stenosis, 201Tl uptake and washout were not significantly different in the stenotic zone compared with the normal zone. These data indicate that dipyridamole-induced vasodilation in the presence of a partial stenosis results in diminished uptake and delayed clearance compared with increased uptake and more rapid clearance in normally perfused myocardium producing an initial 201Tl defect with delayed redistribution.(ABSTRACT TRUNCATED AT 400 WORDS)

The initial myocardial uptake of thallium-201 depends on myocardial blood flow distribution. The phenomenon of delayed thallium redistribution after transiently or chronically altered myocardial perfusion has been described. The net myocardial accumulation of thallium-201 after injection depends upon the net balance between continuing myocardial extraction from low levels of recirculating thallium in the blood compartment and the net rate of efflux of thallium from the myocardium into the extracardiac blood pool. These experiments were designed to measure separately the myocardial extraction and intrinsic myocardial efflux of thallium-201 at normal and at reduced rates of myocardial blood flow. The average myocardial extraction fraction at normal blood flow in 10 anesthetized dogs was 82 +/- 6% (+/- SD) at normal coronary arterial perfusion pressures and increased insignificantly, to 85 +/- 7%, at coronary perfusion pressures of 10--35 mm Hg. At normal coronary arterial perfusion pressures in 12 additional dogs, the intrinsic thallium washout in the absence of systemic recirculation had a half-time (T 1/2) of 54 +/- 7 minutes. The intrinsic cellular washout rate began to increase as distal perfusion pressures fell below 60 mm Hg and increased markedly to a T 1/2 of 300 minutes at perfusion pressures of 25--30 mm Hg. A second, more rapid component of intrinsic thallium washout (T 1/2 2.5 minutes) representing approximately 7% of the total initially extracted myocardial thallium was observed. The faster washout component is presumed to be due to washout of interstitial thallium unextracted by myocardial cells, whereas the slower component is presumed due to intracellular washout. The net clearance time of thallium measured after i.v. injection is much longer than the intrinsic myocardial cellular washout rate because of continuous replacement of myocardial thallium from systemic recirculation. Myocardial redistribution of thallium-201 in states of chronically reduced perfusion cannot be the result of increased myocardial extraction efficiency, but rather, is the result of the slower intrinsic cellular washout rate at reduced perfusion levels.