Acquired blood platelet disorder in patients with end-stage heart failure after implantation of a continuous centrifugal- flow left ventricular assist device: A prospective cohort study

Background: Continuous-flow left ventricular assist devices (CF-LVADs) are an established therapy for advanced heart failure. Thrombosis and hemorrhage are common complications after CF-LVAD implantation, which may be explained by deviceinduced platelet activation. Few data on the effect of CF-LVAD implantation on platelets are available to date. Objectives: The aim of this study was to characterize the change in the platelet activation status after CF-LVAD. Methods: Platelet phenotype and reactivity were determined with flow cytometry in 32 adults with end-stage heart failure before and 4 to 6 weeks after CF-LVAD implantation. Sixteen adults with a biological aortic valve prosthesis (AVP) using the same antiplatelet regimen were included to discriminate between the effects of CF-LVAD and the antiplatelet regimen. Plasma markers for platelet activation were determined with enzyme-linked immunosorbent assay. Results: Median (IQR) plasma levels of soluble P-selectin increased from 115.6 (79.1142.7) ng/mL to 144.5 (100.4-197.5) ng/mL after CF-LVAD implantation (P <.001). Median (IQR) ss-thromboglobulin levels were 60.5 (37.8-81.5) ng/mL before implantation and remained high after LVAD implantation [60.0 (42.0-69.5) ng/mL]. The platelet P-selectin expression after stimulation with ADP (30 and 60 mu M) or PAR1-activating peptide (12.5 and 25 mu M) was reduced by 17% to 21%, and fibrinogen binding was reduced by 37% to 86%. Platelet responses to agonists were similar in patients with a CF-LVAD and patients with an AVP, except for fibrinogen binding in response to 12.5 mu M PAR1-AP, which was lower in patients with a CF-LVAD (P <.001). Conclusions: Combined, these data provide evidence for systemic platelet activation and an acquired platelet disorder after CF-LVAD implantation. This might contribute to the risk of both hemorrhage and thrombosis associated with CF-LVADs.