angiodysplasia/protease

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[A hemostatic disorder caused by high shear stress: acquired von Willebrand syndrome].

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The von Willebrand factors (VWFs) play critical role in hemostasis and thrombosis formation. VWFs are produced in and secreted as large multimers from endothelial cells, and shear stress-dependently cleaved into 2-80 multimers by their specific protease, ADATS13. Because high molecular weight VWFs

No evidence for increased intraoperative bleeding in aortic-valve stenosis: a comparative analysis of haemotherapy in 136 patients undergoing aortic-valve replacement.

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OBJECTIVE An association of aortic-valve stenosis and abnormal bleeding, particularly from gastrointestinal angiodysplasia, has been reported. In this setting, high-shear stress generated by the transvalvular gradient leads to a conformational change of plasmic von Willebrand factor, making this

Acquired von Willebrand Syndrome Associated with Cardiovascular Diseases.

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The blood glycoprotein von Willebrand factor (VWF) plays an important role in hemostasis and thrombosis.VWF is produced and secreted as large multimers by endothelial cells and megakaryocytes. It is then cleaved in a sheer-stress dependent manner by a specific protease, ADAMTS13, into multimers

Clinical and In Vitro Evidence That Left Ventricular Assist Device-Induced von Willebrand Factor Degradation Alters Angiogenesis.

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Background Gastrointestinal bleeding from angiodysplasia is a major problem in continuous-flow left ventricular assist device (LVAD) patients. LVAD shear stress causes pathologic degradation of VWF (von Willebrand factor). A mechanistic relationship between VWF degradation and angiodysplasia has not

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