Increased von Willebrand Factor Platelet-Binding Capacity Is Related to Poor Prognosis in COVID-19 Patients

Abstract

None

Thrombosis and Haemostasis 2023 Editors' Choice Papers

“…Amid the evolving landscape of COVID-19, exploring the potential of antiplatelet strategies stands as a promising avenue in addressing the thrombotic complications associated with this viral infection. Stefanini et al 29 reported higher sensitivity of platelets to ristocetin-induced agglutination in severe and short-term mortality COVID-19 patients compared with patients with mild symptoms, in line with previous observations on significant increase of von Willebrand factors (VWFs) circulating levels in COVID-19 patients and could be a useful tool to identify patients with high risk of clinical deterioration. Insights from the CORE-19 Registry revealed increased rates of arterial and VTE events, along with higher mortality in COVID-19 patients with prior cardiovascular risks, calling for exploration of the role of antithrombotic agents, particularly add-on antiplatelet therapy, through randomized controlled trials in the immediate postdischarge period.…”

Endotheliopathy in Acute COVID-19 and Long COVID

“…Moreover, patients receiving haemodialysis with severe COVID-19 had significantly higher vWf plasma levels [42]. All studies agree that thrombin formation via the intrinsic coagulation pathway and vWf reflect disease severity and poor prognosis in COVID-19 patients [164][165][166][167].…”

“…Significantly higher plasma vWf levels in severe COVID-19 patients receiving haemodialysis [42]. Increased vWf levels reflect disease severity and a poor prognosis in COVID-19 patients [164][165][166][167].…”

Breakthrough infections after COVID-19 vaccinations do not elicit platelet hyperactivation and are associated with high platelet–lymphocyte and low platelet–neutrophil aggregates

“…Since our flow cytometry panel did not include a DNA marker, we cannot exclude that the FSC high CD41 + events, which we identified as microthrombi based on previous work employing imaging flow cytometry [ 15 ], are not circulating megakaryocytes that have also been reported in severe COVID-19 [ [37] , [38] , [39] ]. High circulating microthrombi and low αIIbβ3 activation in ICU patients are not conflicting observations since ultralarge von Willebrand factor [ 40 , 41 ] and fibrin [ 42 ] can support the formation of microthrombi in a αIIbβ3-independent manner. We speculate that the presence of circulating microthrombi negatively correlated with lung function because microthrombi could obstruct the lung microcirculation and limit gas exchange, in line with the numerous reports of pulmonary microthrombosis in postmortem histopathologic studies [ 3 , 43 ].…”