Prolonged recovery is common after acute SARS‐CoV‐2 infection; however, the pathophysiological mechanisms underpinning Long COVID syndrome remain unknown. VWF/ADAMTS‐13 imbalance, dysregulated angiogenesis, and immunothrombosis are hallmarks of acute COVID‐19. We… Click to show full abstract
Prolonged recovery is common after acute SARS‐CoV‐2 infection; however, the pathophysiological mechanisms underpinning Long COVID syndrome remain unknown. VWF/ADAMTS‐13 imbalance, dysregulated angiogenesis, and immunothrombosis are hallmarks of acute COVID‐19. We hypothesized that VWF/ADAMTS‐13 imbalance persists in convalescence together with endothelial cell (EC) activation and angiogenic disturbance. Additionally, we postulate that ongoing immune cell dysfunction may be linked to sustained EC and coagulation activation.
               
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