REGIONAL MYOCARDIAL BLOOD-FLOW IN STABLE ANGINA-PECTORIS ASSOCIATED WITH ISOLATED SIGNIFICANT NARROWING OF EITHER THE LEFT ANTERIOR DESCENDING OR LEFT CIRCUMFLEX CORONARY-ARTERY

Myocardial perfusion measurements were obtained with position emission tomography under basal conditions and after intravenous dipyridamole infusion (0.56 mg/kg over 4 minutes) to determine if myocardial perfusion is maximized in areas of resting wall motion abnormalities in patients with stable angina. Thirty-three patients with no history of myocardial infarction, and with coronary stenosis >50% involving the left anterior descending (n = 24) and left circumflex (n = 9) coronary arteries were evaluated. Quantitative perfusion images were recorded twice in each subject using nitrogen-13 ammonia at baseline and after intravenous administration of dipyridamole. Computer-assisted analysis of left ventriculograms showed abnormal wall motion in the stenosis-related regions in 16 patients (group 1), and normal regional function in 17 (group 2). The flow values in the anterior and posterolateral wall were considered to reflect left anterior and left circumflex coronary artery flow, respectively. Quantitative angiography showed that coronary stenosis severity was higher in group 1 than in group 2 (cross-sectional area reduction 94 +/- 7% vs 87 +/- 11%; p <0.05. Resting blood flow in the stenosis-related areas was significantly lower than in contralateral regions in group 1 (0.66 +/-0.19 vs 0.77 +/- 0.26 ml/min/g; p <0.05), but not in group 2 (0.73 +/- 0.18 vs 0.78 +/- 0.21 ml/min/g; p = NS). Dipyridamole significantly (p <0.01) increased myocardial blood flow in both stenotic and remote regions in both groups 1 (0.95 +/- 0.41 vs 1.57 +/- 0.70 ml/min/g) and (1.54 +/- 0.53 vs 2.01 +/- 0.84 ml/min/g). Thus, in patients with stable angina and no previous myocardial infarction, chronic wall motion abnormalities may be associated with reduced myocardial blood flow. A residual vascular tone can be maintained in hypoperfused dysfunction myocardial areas, suggesting that further factors, in addition to the restriction in oxygen delivery, can downregulate the metabolic demand of hibernating myocardium.