Clinical and In Vitro Evidence That Left Ventricular Assist Device-Induced von Willebrand Factor Degradation Alters Angiogenesis.
Publication/Presentation Date
9-1-2018
Abstract
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 been explored. We tested 2 novel hypotheses: (1) clinical hypothesis: VWF fragments are elevated in LVAD patients that develop angiodysplasia and (2) in vitro hypothesis: VWF fragments generated during LVAD support alter angiogenesis, which may contribute to angiodysplasia. Methods and Results Clinical study: Paired blood samples were collected from continuous-flow LVAD patients (n=35). VWF was quantified with immunoblotting. In vitro experiments: (1) To investigate whether LVAD support alters angiogenesis, human endothelial cells were cultured with LVAD patient plasma (n=11). To investigate mechanism, endothelial cells were cultured with VWF fragments produced by exposing human VWF and ADAMTS-13 (VWF protease) to LVAD-like shear stress (175 dyne/cm
Volume
11
Issue
9
First Page
004638
Last Page
004638
ISSN
1941-3297
Published In/Presented At
Bartoli, C. R., Zhang, D. M., Hennessy-Strahs, S., Kang, J., Restle, D. J., Bermudez, C., Atluri, P., & Acker, M. A. (2018). Clinical and In Vitro Evidence That Left Ventricular Assist Device-Induced von Willebrand Factor Degradation Alters Angiogenesis. Circulation. Heart failure, 11(9), e004638. https://doi.org/10.1161/CIRCHEARTFAILURE.117.004638
Disciplines
Medicine and Health Sciences
PubMedID
30354363
Department(s)
Department of Surgery
Document Type
Article