Abstract
Bleeding is an important source of morbidity in patients with a left ventricular assist device (LVAD). Evidence suggests a major role for von Willebrand factor (vWF). However, limited data exist to explain the mechanism(s) of vWF degradation. We investigated whether high shear stress and/or ADAMTS-13, the vWF cleaving protease, alter vWF metabolism. To investigate specific the mechanisms of vWF degradation independent of plasma cells and proteins, isolated vWF and ADAMTS-13 were used.
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