Abstract
Early in the COVID-19 pandemic, it became clear that coagulopathy leading to macrovascular and microvascular thrombotic events was a considerable potential complication for patients with COVID-19.1 Increased inflammation and coagulopathy were independently associated with critical illness and all-cause mortality and had a synergistic role in the pathogenesis of COVID-19.2 Early observations of a benefit from heparin3 in a selected cohort of severely ill patients with COVID-19 in China, followed by reports of increased thromboembolic events in patients with COVID-19 (both in and outside of intensive care units [ICUs]) despite the use of standard-dose venous thromboembolism prophylaxis,4,5 led many physicians to use increased anticoagulant doses, even without robust data available.
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