Vascular Damage and Coagulopathy during COVID-19 Infections

Dear Colleagues,

The pathogenic coronavirus has been wreaking havoc worldwide since January. Reports of thrombotic complications in patients with Covid-19 are increasingly prominent, and growing evidence strongly suggests that some of the clinical features of Covid-19 infection are driven by a localized thrombotic phenomenon. More specifically, there is increasing recognition that the Covid-19-associated hemostasis abnormality may be resulting in localized thrombosis in the lungs. Histologic analysis of pulmonary vessels in patients with Covid-19 revealed severe endothelial injury associated with intracellular SARS-CoV-2 virus and disrupted endothelial cell membranes together with widespread thrombosis and occlusion of alveolar capillaries. The Covid-19 acquired coagulopathy involves venous, arterial, and microcirculatory systems, and offers unique features in comparison with the thrombogenicity observed in previous viral or bacterial illness.
The pathophysiological mechanisms are complex and most likely involve endothelial cell activation and endothelitis, vWF release, cytokine storms and hyperinflammation, procoagulant microparticle release, lupus anticoagulant generation, platelet activation, neutrophils extracellular traps (NETs), alteration of the fibrinolytic pathways, hypoxia, hyperviscosity, and altered shear stress. On top of these proposed pro-thrombotic routes, at sites of endothelial injury, imbalance between ACE2 and ACE1 activity could contribute to unopposed angiotensin II accumulation which further exacerbates tissue injury and promotes both inflammation and thrombosis.
Several questions remain unanswered: Are we facing in situ pulmonary thrombosis or pulmonary embolism? What is the contribution of vWF, NETs, and microparticles to thrombus growth? What are the optimal antithrombotic strategies for both the prevention and treatment of venous thromboembolic events?
The development of vasculitis including the recent outbreak of Kawasaki disease still remains to be fully characterized. The impact of “host damage-control” strategies including anti-complement and anti-inflammatory approaches are appealing leads, and finally, the restoration of the ACE2/ACE1 (role of ACEi, ARB, statins) imbalance within the vascular wall is a key approach that deserves further insights.
From a more practical point of view, the definition of the optimal anticoagulant strategy (type, dose, and duration) and the role for anti-platelet therapy or combined strategies are today’s hot topics.
The present Special Issue aims to provide significant development in the management of vascular damages and coagulopathy burden during SARS-CoV-2 infection.

Prof. Dr. Olivier Morel
Dr. Benjamin Marchandot
Guest Editors

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