COVID-19 and thrombosis: From bench to bedside

Abstract

Coronavirus disease of 2019 (COVID-19) is the respiratory viral infection caused by the coronavirus SARS-CoV2 (Severe Acute Respiratory Syndrome Coronavirus 2). Despite being a respiratory illness, COVID-19 is found to increase the risk of venous and arterial thromboembolic events. Indeed, the link between COVID-19 and thrombosis is attracting attention from the broad scientific community. In this review we will analyze the current available knowledge of the association between COVID-19 and thrombosis. We will highlight mechanisms at both molecular and cellular levels that may explain this association. In addition, the article will review the antithrombotic properties of agents currently utilized or being studied in COVID-19 management. Finally, we will discuss current professional association guidance on prevention and treatment of thromboembolism associated with COVID-19.

Fig. 1

Dysregulated renin angiotensin aldosterone system in COVID-19. SARS-CoV2 has higher affinity to ACE2 receptor compared to other coronaviruses. ACE2 is a carboxypeptidase that converts angiotensin II (Ang II) to angiotensin 1-7. The binding between the spike protein (S-protein) of the virus and ACE2 is associated with downregulation of ACE2 activity. In its turn, this will lead to augmentation of Ang II signaling and pro-thrombotic pathways. On the other hand, the angiotensin 1-7 signaling which mediates anti-thrombotic pathways is diminished.

Fig. 2

Dysregulated innate immune response in COVID-19. Innate immunity plays critical role as an early defense mechanism against microbial infection including SARS-CoV2. However, uncontrolled innate immune response elicited by overactivated neutrophils will initiate coagulopathic pathways. These pathways may include excessive complement activation, cytokine storm and NETosis, each of which may cause thrombosis by various mechanisms.