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Plasma von Willebrand Factor and the Development of the Metabolic Syndrome in Patients with Hypertension

Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, United Kingdom

Address all correspondence and requests for reprints to: Dr. A. D. Blann, Ph.D., M.R.C.Path., Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, United Kingdom. E-mail: a.blann{at}bham.ac.uk.

Although the metabolic syndrome is associated with endothelial damage/dysfunction, the effect of risk factors and their relationship with the development of this condition are unclear. We hypothesized that plasma von Willebrand factor (vWf, marking endothelial damage/dysfunction) increases with the number of components of metabolic syndrome and that increased levels precede its development. To test this, fasting vWf, glucose and lipids were measured in 161 patients (mean age 63 ± 7 yr, 85% males) with hypertension. Using World Health Organization (WHO) criteria, 32 (19.9%), and using National Cholesterol Education Program (NCEP) criteria, 70 (43.5%) had metabolic syndrome. Plasma vWf was higher in these patients regardless of defining criteria and increased with the number of the components of metabolic syndrome (both P < 0.001). After 4 yr, patients who did not have metabolic syndrome at baseline were reassessed for the development of this condition. Of the 129 patients who did not meet the WHO criteria at baseline, 38 (29.5%) subsequently developed the condition, whereas 36 of the 91 (39.6%) who did not meet the NCEP criteria at baseline subsequently developed metabolic syndrome. Baseline vWf levels did not predict development of metabolic syndrome, regardless of criteria (P = 0.071 for WHO and P = 0.639 for NCEP). Our data suggest more severe endothelial damage/dysfunction with cumulative metabolic syndrome-related risk factors. The failure of plasma vWf to predict the development of metabolic syndrome suggests that endothelial damage/dysfunction is a consequence, not a cause, of these risk factors.

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