Regional Myocardial Blood Flow Redistribution as a Cause of Postprandial Angina Pectoris

Abstract

Postprandial angina pectoris has been recognized for more than two centuries and can be identified in up to 10% of patients with chronic ischemic heart disease. Redistribution of myocardial blood flow, from a region supplied by a severely stenotic coronary artery to those supplied by less diseased or normal vessels, is a potential mechanism of postprandial angina. To test this hypothesis, we have determined the effects of a standard liquid meal on whole heart and regional myocardial blood flow, measured by means of dynamic positron emission tomography (PET) with 15O-labeled water in 14 patients with a reproducible history of postprandial angina and 7 matched control subjects. The standard liquid meal precipitated angina pectoris in all patients. Baseline whole heart blood flow was similar and increased normally after the meal in patients (0.97+/-0.14 to 1.14+/-0.25 mL.min(-1).g(-1), P<.04) as in control subjects (0.92+/-0.12 to 1.02+/-0.13 mL.min(-1).g(-1), P<.02). In contrast, the coefficient of variation of blood flow increased significantly after the standard liquid meal in patients (34+/-9%, P<.05 versus baseline) but not in control subjects (17+/-7%, P=NS versus baseline). In patients, analysis of regional myocardial blood flow demonstrated decreased myocardial blood flow in territories supplied by stenotic arteries (1.01+/-0.35 to 0.76+/-0.27 mL.min(-1).g(-1), P<.03), but there was an increase in blood flow in territories supplied by normal arteries (0.89+/-0.16 to 1.34+/-0.25 mL.min(-1).g(-1), P<.001) after the meal. The standard liquid meal induced angina pectoris in patients with coronary artery disease. Although whole heart blood flow increased appropriately for the greater cardiac work, there was a redistribution of regional blood flow from territories supplied by severely stenosed coronary arteries to those supplied by less diseased or normal arteries. This redistribution may be the cause of myocardial ischemia in postprandial angina.