Published online before print July 5, 2005, doi: 10.1161/CIRCULATIONAHA.104.495127
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(Circulation. 2005;112:179-184.)
© 2005 American Heart Association, Inc.
Coronary Heart Disease |
Postprandial Myocardial Perfusion in Healthy Subjects and in Type 2 Diabetic Patients
From Metabolic Cardiology, Division of Metabolic Diseases, Department of Clinical and Experimental Medicine, University of Padova Medical School, Padua, Italy.
Correspondence to Roldano Scognamiglio, MD, Cardiologia Metabolica, Divisione di Malattie del Metabolismo, Policlinico Universitario, via Giustiniani 2, 35128 Padova, Italy. E-mail r.scognamiglio{at}unipd.it
Received July 26, 2004; revision received March 24, 2005; accepted March 30, 2005.
Background— In diabetic patients, postprandial hyperglycemia is a more powerful risk factor for cardiovascular disease than fasting hyperglycemia itself. A negative influence of acute hyperglycemia on systemic endothelial function (brachial artery) has been shown. However, myocardial perfusion during postprandial hyperglycemia has not been investigated.
Methods and Results— We evaluated the effects of a standardized mixed meal on myocardial perfusion in 20 healthy subjects and 20 consecutive patients with type 2 diabetes mellitus without macrovascular or microvascular complications. Myocardial perfusion was assessed in fasting and postprandial states by myocardial contrast echocardiography. Fasting myocardial flow velocity (ß, 0.65±0.27 versus 0.67±0.24; P=NS), myocardial blood volume (MBV; 8.3±1.2 versus 8.4±2; P=NS), and myocardial blood flow (5.4±1.5 versus 5.6±2; P=NS) did not differ between control subjects and diabetic patients. In the postprandial state, ß (0.67±0.24 versus 0.92±0.35; P<0.01), MBV (8.4±2 versus 10.9±2.7; P<0.01), and myocardial blood flow (5.6±2 versus 9.9±2.8; P<0.01) increased significantly in control subjects. In diabetic patients, ß increased (0.65±0.27 versus 0.8±0.24; P<0.01) but MBV (8.3±1.2 versus 4.3±1.3; P<0.01) and myocardial blood flow (5.4±1.5 versus 3.4±0.9; P<0.01) decreased significantly. Changes in MBV (expressed as [(MBVpostprandial–MBVfasting)/MBVfasting]x100) were significantly correlated with postprandial glycemia levels in diabetic patients.
Conclusions— Postprandial hyperglycemia determines myocardial perfusion defects in type 2 diabetic patients. They are secondary to deterioration in microvascular function causing a decrease in MBV. In diabetic patients without microvascular or macrovascular complications, postprandial myocardial perfusion defects may represent an early marker of the atherogenic process in the coronary circulation; hence, its reversal constitutes a potential goal of treatment.
Key Words: coronary disease • diabetes mellitus • microcirculation • perfusion
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