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Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:1173-1179

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:1173-1179.)
© 1999 American Heart Association, Inc.


Vascular Biology

Endothelial Cell Dysfunction and Arterial Wall Hypertrophy Are Associated With Disturbed Carbohydrate Metabolism in Patients at Risk for Cardiovascular Disease

Christoph Thalhammer; Beate Balzuweit; Andreas Busjahn; Clemens Walter; Friedrich C. Luft; Hermann Haller

From the Franz Volhard Clinic at the Max Delbrück Center for Molecular Medicine, Universitätsklinikum Charité, Medical Faculty of Humboldt University, Campus Berlin-Buch, Berlin, Germany.

Correspondence to Hermann Haller, MD, Franz Volhard Clinic, Wiltberg Strasse 50, 13122 Berlin, Germany. E-mail haller{at}fvk-berlin.de

Abstract—To investigate the effects of fasting and postprandial glucose on endothelial cell function and intima-media thickness, we studied 60 men with cardiovascular risk factors. Postischemic, endothelium-dependent vasodilatation was measured after 3 minutes of ischemia at the radial artery with high-resolution echo tracking. Common carotid artery intima-media thickness was measured by B-mode ultrasound. Glucose tolerance was determined by a 75-g oral glucose load. Fasting glucose levels were inversely correlated with postischemic, endothelium-dependent vasodilatation (r=-0.24, P<0.05) and directly correlated with intima-media thickness (r=0.26, P<0.05). However, postischemic, endothelium-dependent vasodilatation and intima-media thickness were not correlated. All subjects with normal postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness, whereas some subjects with impaired postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness. Multiple regression analysis revealed a profound influence of age on intima-media thickness to the exclusion of all other variables. The same age-adjusted analysis for postischemic, endothelium-dependent vasodilatation accepted fasting glucose, followed by 2-hour postprandial glucose, as variables, but no others. Subjects with fasting glucose values >100 mg/dL showed reduced postischemic, endothelium-dependent vasodilatation (59 versus 120 µm, P<0.05) and a higher intima-media thickness (right: 0.76 versus 0.62 mm, P<0.05; left: 0.78 versus 0.63 mm, P<0.05) compared with those with fasting glucose values <100 mg/dL. Subjects with 2-hour postprandial glucose values >125 mg/dL had no reduced postischemic, endothelium-dependent vasodilatation compared with subjects with a 2-hour postprandial glucose >125 mg/dL; however, their intima-media thickness (right: 0.66 versus 0.62 mm; left: 0.68 versus 0.62 mm; P<0.05 for both) was greater. Thus, high fasting rather than postprandial glucose values are associated with both postischemic, endothelium-dependent vasodilatation and increased intima-media thickness. Postischemic endothelium-dependent vasodilatation may precede increased intima-media thickness.


Key Words: arteriosclerosis • impaired glucose tolerance • B-mode ultrasound • intima-media thickness • endothelial dysfunction




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