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  • von Willebrand factor, endothelial dysfunction, and cardiovascular disease
  • Vischer UM
  • J Thromb Haemost 2006[Jun]; 4 (6): 1186-93
  • von Willebrand factor (VWF), a glycoprotein involved in arterial thrombus formation, is released into the circulation by secretion from endothelial cells. Plasma VWF levels are determined by genetic factors including ABO blood groups and VWF mutations, and by non-genetic factors including aging, impaired nitric oxide production, inflammation, free radical production and diabetes. Plasma VWF levels have been proposed as a risk factor for cardiovascular events. Although they are only weakly associated with the risk of coronary heart disease (CHD) in the general population, they are a more promising CHD risk factor in high-risk populations with previous cardiovascular events, diabetes or old age. However, is it still unclear whether VWF levels directly determine the rate and severity of arterial thrombus formation or whether they merely reflect alteration in other endothelial functions. The future status of VWF levels as a cardiovascular risk factor depends on additional studies on the genetic determinants of both VWF levels and cardiovascular outcomes. Further studies on VWF levels as a predictor of the risk of stroke (rather than CHD) in elderly or other high-risk population are also promising. Such studies could lead to the clinical use of plasma VWF levels to refine the estimation of the cardiovascular risk and of the expected benefit of antithrombotic agents.
  • |Animals[MESH]
  • |Atherosclerosis/metabolism/physiopathology[MESH]
  • |Biomarkers/blood/metabolism[MESH]
  • |Cardiovascular Diseases/*metabolism[MESH]
  • |Endothelium, Vascular/*metabolism[MESH]
  • |Humans[MESH]
  • |Platelet Glycoprotein GPIb-IX Complex/metabolism[MESH]
  • |Risk Factors[MESH]
  • |Thrombosis/metabolism/physiopathology[MESH]
  • |von Willebrand Factor/*metabolism[MESH]





  • *{{pmid16706957}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=16706957 von Willebrand factor, endothelial dysfunction, and cardiovascular disease ]</b> J Thromb Haemost 2006; 4(6) ; 1186-93 Vischer UM

        *16706957*

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    J Thromb Haemost

    1186 6.4 2006