Acquired von Willebrand factor deficiency is reduced in HeartMate 3 patients†.

Abstract

The acquired von Willebrand syndrome (AvWS), which is associated with left ventricular assist device support, is caused by the loss of the von Willebrand factor (vWF) high molecular weight multimers (HMWMs). We investigated whether the implantation of the left ventricular assist device HeartMate 3 (HM 3) is superior to the HeartWare ventricular assist device (HVAD) in preserving the multimeric structure of vWF. In total, 70 patients with implanted HM 3 (n = 35) or HVAD (n = 35) were retrospectively investigated. HMWMs, intermediate molecular weight multimers and low molecular weight multimers were quantified by using a densitometric methodology. vWF antigen, vWF activity and vWF collagen-binding activity, as well as demographic and clinical data, were analysed. AvWS, which is characterized by a decrease in vWF HMWMs, was found in 97.1% of patients in the HM 3 group and 100% of patients in the HVAD group. Compared to normal pooled plasma, HM 3 induced a reduction in HMWMs (40.7 ± 8.2% vs 26.7 ± 7.5%, P < 0.01) and an increase in low molecular weight multimers (31.3 ± 11.8% vs 42.7 ± 9.8%, P < 0.01), whereas HVAD patients exhibited an increase in the percentage of intermediate molecular weight multimers (28.0 ± 5.0% vs 38.4 ± 7.7%, P < 0.01) in addition to a decrease in the percentage of HMWM (23.0 ± 11.0%, P < 0.01). A comparison of both left ventricular assist device types showed a difference in vWF multimeric structure (HMWMs: P < 0.01, intermediate molecular weight multimer: P = 0.05, low molecular weight multimer: P = 0.03). Furthermore, vWF activity was elevated in patients with an implanted HM 3 device (153.7 ± 54.4%) compared to those with an HVAD device (126.3 ± 39.7%, P = 0.02). Patients with an implanted HM 3 had more intact HMWMs and a higher vWF activity during device support. This may reduce the manifestation of AvWS in HM 3 patients and could thus lead to a lower bleeding complication rate.