Abstract
During the last decade the use of ventricular assist devices (VADs) for patients with severe heart failure has increased tremendously. However, flow disturbances, mainly high shear induced by the device is associated with bleeding complications. Shear stress-induced changes in VWF conformation are associated with a loss of high molecular weight multimers (HMW) of VWF and an increased risk of bleeding. This phenomenon and its cause will be elaborated and reviewed in the following.
Highlights
In 1958, Edward Heyde observed a link between the presence of aortic stenosis (AS) and gastrointestinal (GI)-bleeding of idiopathic origin in 10 patients [1, 2]
Recent studies in mice models reported that plasmin can function as a back-up for ADAMTS-13 to proteolyze von Willebrand factor (VWF) and mitigate thrombocytopenic purpura (TTP) symptoms, but only in conditions of supraphysiological increased plasmin activity to overcome the inhibition by α2antiplasmin and plasminogen activator inhibitor 1 (PAI-1) [17]
Sakatsume et al reported that patients with continuous flow left ventricular assist device (LVAD) support and with GI-bleeding exhibited a more severe loss of VWF high molecular weight multimers (HMW)-multimers compared to patients without GI-bleeding [61]
Summary
During the last decade the use of ventricular assist devices (VADs) for patients with severe heart failure has increased tremendously. Flow disturbances, mainly high shear induced by the device is associated with bleeding complications. Shear stress-induced changes in VWF conformation are associated with a loss of high molecular weight multimers (HMW) of VWF and an increased risk of bleeding. This phenomenon and its cause will be elaborated and reviewed in the following. Reviewed by: Shiu-Ki Rocky Hui, Baylor College of Medicine, United States Coen Maas, University Medical Center Utrecht, Netherlands. Specialty section: This article was submitted to Hematology, a section of the journal
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