Key result
An in vitro laboratory vortexer and an LVAD mock circulatory loop reproduced the pathologic degradation of vWF (decreased large multimers and increased fragments) seen during LVAD support.
Why the study?
Do in vitro vortexer and mock circulatory loop models reproduce LVAD-associated von Willebrand factor degradation?
Do in vitro vortexer and mock circulatory loop models reproduce LVAD-associated von Willebrand factor degradation?
A simple vortexer and a mock circulatory loop can accurately reproduce the pathologic degradation of von Willebrand factor seen in LVAD patients, providing useful preclinical models for studying LVAD-associated bleeding.
Answers are grounded in this paper and cite their sources.
No immediate clinical change; extends preclinical tools for LVAD bleeding research.
Evidence suggests a major role for von Willebrand factor (vWF) in left ventricular assist device (LVAD)-associated bleeding. However, the mechanisms of vWF degradation during LVAD support are not well understood. We developed: (i) a simple and inexpensive vortexer model; and (ii) a translational LVAD mock circulatory loop to perform preclinical investigations of LVAD-associated vWF degradation. Whole blood was obtained from LVAD patients (n = 8) and normal humans (n = 15). Experimental groups included: (i) blood from continuous-flow LVAD patients (baseline vs. post-LVAD, n = 8); (ii) blood from normal humans (baseline vs. 4 h in vitro laboratory vortexer, ∼ 2400 rpm, shear stress ∼175 dyne/cm(2) , n = 8); and (iii) blood from normal humans (baseline vs. 12 h HeartMate II mock circulatory loop, 10 000 rpm, n = 7). vWF multimers and degradation fragments were characterized with electrophoresis and immunoblotting. Blood from LVAD patients, blood exposed to in vitro supraphysiologic shear stress, and blood circulated through an LVAD mock circulatory loop demonstrated a similar profile of decreased large vWF multimers and increased vWF degradation fragments. A laboratory vortexer and an LVAD mock circulatory loop reproduced the pathologic degradation of vWF that occurs during LVAD support. Both models are appropriate for preclinical studies of LVAD-associated vWF degradation.
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Restle et al. (2015) studied LVAD-associated von Willebrand factor degradation (n=23). In vitro laboratory vortexer and LVAD mock circulatory loop vs. Baseline was evaluated on vWF multimers and degradation fragments. An in vitro laboratory vortexer and an LVAD mock circulatory loop reproduced the pathologic degradation of vWF (decreased large multimers and increased fragments) seen during LVAD support.
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