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Coronavirus-2019 (COVID-19) infection is responsible for the pandemic outbreak across the world. The pathophysiology of COVID-19 has been characterized by endothelial dysfunction, and a thromboinflammatory state. Severe infection and poor clinical outcomes have been associated with diffuse endothelial dysfunction and a hyperinflammatory state leading to a cytokine storm which further enhances thrombotic complications. 1, 2 The pathophysiology uniquely affects the lungs in its early stages as evidenced by autopsy reports of diffuse alveolar damage along with pulmonary intravascular microthrombi in the absence of known venous thromboembolism (VTE). 3 Multiple retrospective and prospective clinical trials have evaluated thromboinflammatory biomarkers linking them to poor prognosis among patients with COVID-19 infection. 4–6 The thrombotic biomarkers evaluated include D-dimer levels, fibrinogen …