Mechanical circulatory support is associated with loss of platelet receptors glycoprotein Ibα and glycoprotein VI.

Background Ventricular assist devices (VADs) and extracorporeal membrane oxygenation (ECMO) are associated with bleeding, not fully explained by anti-coagulant or anti-platelet use. Exposure of platelets to elevated shear in vitro leads to increased shedding. Objectives Here we investigated whether loss of platelet receptors occurs in vivo, and the relationship with acquired Von Willebrand Syndrome (AVWS) Methods Platelet counts, coagulation tests and Von Willebrand factor (VWF) analyses were performed on samples from 21 continuous flow VAD (CF-VAD), 20 ECMO, 12 heart failure and 7 aortic stenosis patients. Levels of platelet receptors were measured by flow cytometry or enzyme-linked immunosorbent assay (ELISA). Results The loss of high molecular weight (HMW) VWF multimers was observed in 18/19 CF-VADs and 14/20 ECMO patients, consistent with AVWS. Platelet receptor shedding was demonstrated by elevated soluble GPVI levels in plasma and significantly reduced surface GPIbα and GPVI in CF-VADs and ECMO patients compared to healthy donors. Platelet receptor levels were also significantly reduced in heart failure patients. Conclusions This data links AVWS and increased platelet receptor shedding in patients with CF-VADs or ECMO for the first time. Loss of platelet surface receptors GPIbα and GPVI in heart failure, CF-VADs and ECMO patients may contribute to ablated platelet adhesion/activation and limit thrombus formation under high/pathological shear conditions. This article is protected by copyright. All rights reserved.