COVID-19 and Microvascular Thrombosis
In addition to macrovascular complications, there is a strong association of COVID-19 with microvascular thrombosis. Pulmonary microvascular thrombosis has been previously described in autopsies as a complication of severe ARDS and has subsequently been reported to complicate ARDS during outbreaks of other coronaviruses, including SARS-CoV and MERS-CoV.36–41 However, this feature appears more pronounced in severe SARS-CoV-2 infection, with histology from patients with COVID-19-associated respiratory failure demonstrating a 9-fold increase in the prevalence of alveolar-capillary microthrombi when compared with patients with influenza.42 In this regard, autopsy findings have shown that, in addition to the expected features of diffuse alveolar damage found in ARDS, platelet-fibrin thrombi are a common microscopic finding in the small pulmonary vasculature, occurring in 80% to 100% of lungs examined at autopsy.43–45 In combination with other reported thrombotic events, the emerging microvascular thrombotic complications indicate a strong interaction between the SARS-CoV-2 and coagulation. Below, we review the underlying known mechanisms for thrombosis and the growing body of work that implicates SARS-CoV-2 as a key player driving many molecular processes underpinning pathological thrombosis.