Anticoagulant treatment in COVID-19: a narrative review

Abstract

The actual Coronavirus Disease (COVID 19) pandemic is due to Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the coronavirus family. Besides the respiratory involvement, COVID 19 patients frequently develop a pro-coagulative state caused by virus-induced endothelial dysfunction, cytokine storm and complement cascade hyperactivation. It is common to observe diffuse microvascular thrombi in multiple organs, mostly in pulmonary microvessels. Thrombotic risk seems to be directly related to disease severity and worsens patients' prognosis. Therefore, the correct understanding of the mechanisms underlying COVID-19 induced prothrombotic state can lead to a thorough assessment of the possible management strategies. Hence, we review the pathogenesis and therapy of COVID 19-related thrombosis disease, focusing on the available evidence on the possible treatment strategies and proposing an algorithm for the anticoagulation strategy based on disease severity.

Keywords: Anticoagulation; COVID-19; SARS-CoV-2; Thrombosis.

Fig. 1

Hypercoagulable state pathogenesis in Covid 19 (C3 complement component 3, C5 complement component 5, C3a complement-activated product 3, C5a complement-activated product 5, IL-6 interleukin 6, eNOS endothelial nitric oxide synthase, ADMA asymmetric dimethylarginine)

Fig. 2

Proposed algorithm for anticoagulation strategy in COVID-19 patients (LMWH low molecular weight heparin, q12h every 12 h, q24h every 24 h, ISTH-DIC score International Society on Thrombosis and Hemostasis (ISTH) scoring system)