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 (beta, 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, beta (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, beta 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 [(MBV(postprandial)-MBV(fasting))/MBV(fasting)]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.
BACKGROUND: In diabeticpatients, 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 (beta, 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 diabeticpatients. In the postprandial state, beta (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 diabeticpatients, beta 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 [(MBV(postprandial)-MBV(fasting))/MBV(fasting)]x100) were significantly correlated with postprandial glycemia levels in diabeticpatients. CONCLUSIONS: Postprandial hyperglycemia determines myocardial perfusion defects in type 2 diabeticpatients. They are secondary to deterioration in microvascular function causing a decrease in MBV. In diabeticpatients 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.