Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease.

The mechanisms responsible for the development of reversible thallium-201 (TI-201) defects with dipyridamole stress in patients with coronary artery disease (CAD) is not well understood. Previous experimental animal studies have demonstrated coronary steal characterized by an absolute decrease in subendocardial flow distal to a stenosis in response to dipyridamole infusion. Accordingly, the purpose of this study was to determine if reversible TI-201 defects in response to dipyridamole infusion are reflective of myocardial ischemia or secondary to regional differences in flow reserve. Dipyridamole (0.56 mg/kg) TI-201 imaging was performed in 23 patients in whom serial electrocardiographic, hemodynamic, aortic and coronary sinus lactate, and coronary sinus adenosine measurements were obtained. All patients with CAD had TI-201 redistribution (3.8 +/- 2.0 defects/patient), and all patients without CAD had normal scans. Mean aortic pressure was similar in both groups and did not change in response to dipyridamole (non-CAD 103 +/- 11 vs CAD 99 +/- 15 mm Hg, p = NS). Pulmonary capillary wedge pressure was similar at baseline (non-CAD 11 +/- 4 vs CAD 13 +/- 5 mm Hg, p = NS) and did not change in response to the drug (non-CAD 14 +/- 3 vs CAD 15 +/- 7 mm Hg, p = NS). Lactate extraction fraction was similar at baseline (non-CAD 0.22 +/- 0.09 vs CAD 0.17 +/- 0.14, p = NS) and decreased similarly in both groups (non-CAD 0.08 +/- 0.06 vs CAD 0.05 +/- 0.12, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)