Effects of HeartWare ventricular assist device on the von Willebrand factor: results of an academic Belgian center

Abstract

BackgroundLeft Ventricular Assist Device (LVAD) is a promising therapy for patients with advanced heart failure (HF), but bleeding complications remain an important issue. Previous series show that acquired von Willebrand syndrome was present in up to 100 % of first generation LVAD recipients. We report the effects of new generation LVADs on vW factor (vWF) metabolism and activity in our center.MethodsFifteen LVAD recipients (HeartWare®, Framingham, MA, USA) were compared to 12 HF patients, matched for age and body mass index. vWF antigen and activity, as well as D-dimers, were measured on hemostasis analyzers. A vWF LVAD-induced alteration was evocated when the [vWF activity]/[vWF antigen] ratio was <0.6. ADAMTS13 and high molecular weight multimers of vWF were also assessed.ResultsLVAD recipients had similar levels of endothelial vWF production than the HF subjects (137 ± 14.5 vs. 147 ± 11.7 %; respectively, p = 0.611) but a decreased vWF activity (90 ± 11 vs. 132.6 ± 13 %; respectively, p = 0.017). [vWF activity]/[vWF antigen] ratio was 0.65 ± 0.02 in the LVAD recipients and 0.92 ± 0.06 in the subjects with HF (p = 0.001). ADAMTS13 activity was 80.3 ± 4.7 % in LVAD recipients and 96.2 ± 3.5 % in the HF patients (p = 0.016). LVAD patients disclosed markedly elevated D-dimers (3217.7 ± 735 vs. 680.6 ± 223.2 ng/mL FEU in the HF patients, p = 0.006). The LVAD patients experienced one major hemorrhagic event and one systemic thrombotic event during the median follow-up of 345 days.ConclusionsLVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic and thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation.Trial registrationISRCTN39517567Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0334-z) contains supplementary material, which is available to authorized users.

In Vitro Benchmarking Study of Ventricular Assist Devices in Current Clinical Use

“…Varying levels of shear stress in the CentriMag, HMII and HVAD could explain different collagen binding activity between devices. This observation is consistent with previous findings revealing that HMII and HVAD patients have similarly reduced vWF multimers and vWF activity, which might explain gastrointestinal bleeding episodes in HMII treated patients (17,41). Notably, the HMII device generates higher levels of shear stress than the newer HeartMate 3 (HM3; Abbott, Thoratec, Pleasanton, CA, US) device.…”

“…These findings are consistent with the enhanced vWF degradation profile and decreased CBA observed in HMII and HVAD patients (41,47). Thus our more extensive in vitro results could relate to the prominence of thrombosis and bleeding identified in HMII and HVAD patients.…”

“…(a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) and unfold vWF multimers. Activated ADAMTS13 binds to and cleaves high molecular weight (HMW) vWF, however, excess cleavage results in enhanced vWF multimer degradation and reduced vWF activity (41,42).…”

Antithrombotic therapy in ventricular assist device (VAD) management: From ancient beliefs to updated evidence. A narrative review

“…However, these slight differences are unlikely to be clinically significant, as reported in studies performed in patients undergoing coronary artery bypass [ 46 ]. Moreover, in patients with centrifugal devices, the vWF antigen and vWF activity did not differ among individuals with blood group “O” compared to the other blood groups [ 47 ].…”

Acquired von Willebrand syndrome in patients on long-term left ventricular assist device support: Results of a Belgian center

“…However, information concerning the changes in VWF parameters on long-term support (> 4 months to years after LVAD implant) and after heart transplantation is scarce [2]. In addition, only a few studies describe ADAMTS13 parameters after LVAD implantation and found either normal or decreased ADAMTS13 activities [6][7][8]. Hence, the aim of this study was a long-term follow up of VWF (VWF multimer size, antigen and activity) and ADAMTS13 (ADAMTS13 antigen and activity) parameters in LVAD patients and in those patients undergoing heart transplantation.…”