Clinical and In Vitro Evidence that LVAD-Induced Von Willebrand Factor Degradation May Alter Angiogenesis
Contributor: Darien Allen
GI bleeds in continuous-flow left ventricular assist device (CF-LVAD) patients are an increasing problem. Bartoli et al posit a two-hit hypothesis to explain the increased risk of mucosal bleeds in this population:
Hit 1: CF-LVAD-induced shear stress activates von Willebrand factor (VWF) multimers leading to enzymatic and mechanical degradation into variably sized fragments and acquired VWF deficiency. CF-LVAD induced VWF deficiency reduces VWF-collagen and VWF-platelet binding resulting in increased risk of mucosal bleeding.
Hit 2: Higher circulating concentrations of VWF fragments lead to altered angiogenesis and likely contribute to the development of angiodysplasia.
Early right ventricular assist device utilization in patients undergoing continuous-flow left ventricular assist device implantation: Insight from INTERMACS
Contributor: Steven Stroud
Frustrated by limited, single small center risk scores for RV failure? Kiernan and colleagues analyzed the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) to identify factors associated with RV failure following continuous flow left ventricular assist device (CF-LVAD) support.
Old drug… new trick? Treatment with sildenafil may prevent device thrombosis and ischemic stroke in LVAD patients.
Contributor: Chris Sobowale
Bleeding and thrombosis account for almost half of adverse events in patients with CF-LVADs.
Saeed et al analyzed 144 HeartMate II (HMII) CF-LVAD patients in a single center, retrospective study. Patients in the sildenafil groups were on sildenafil for pulmonary hypertension or right ventricular dysfunction for at least 30 days after discharge from CF-LVAD implant. Patients were divided into four groups:
- Low level hemolysis not on sildenafil (n=31)
- Low level hemolysis on sildenafil (n= 16)
- No low level hemolysis not on sildenafil n= (76)
- No low level hemolysis on sildenafil (n=21)