The Emerging Threat of (Micro)Thrombosis in COVID-19 and Its Therapeutic Implications

Jun 27, 2020Circulation research

The Growing Risk of Tiny Blood Clots in COVID-19 and Possible Treatments

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Abstract

Thrombotic complications in COVID-19 are associated with severe disease and increased mortality.

COVID-19 is linked to various thrombotic issues, including microvascular thrombosis, venous thromboembolic disease, and stroke.
Thrombotic complications serve as indicators of severe COVID-19 and correlate with multiorgan failure.
SARS-CoV-2 may invade endothelial cells through ACE-2, leading to inflammation and a prothrombotic state.
Immunothrombosis, characterized by the recruitment of immune cells and coagulation activation, contributes to complications like deep vein thrombosis and pulmonary embolism.
Plasma D-dimer levels and thrombocytopenia are emerging as prognostic markers for COVID-19 severity.
Antithrombotic therapies, such as heparin and FXII inhibitors, are being explored for preventing thrombotic complications in COVID-19 patients.

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The recent emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing global pandemic has presented a health emergency of unprecedented magnitude. Recent clinical data has highlighted that coronavirus disease 2019 (COVID-19) is associated with a significant risk of thrombotic complications ranging from microvascular thrombosis, venous thromboembolic disease, and stroke. Importantly, thrombotic complications are markers of severe COVID-19 and are associated with multiorgan failure and increased mortality. The evidence to date supports the concept that the thrombotic manifestations of severe COVID-19 are due to the ability of SARS-CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on the endothelial cell surface. However, in patients with COVID-19 the subsequent endothelial inflammation, complement activation, thrombin generation, platelet, and leukocyte recruitment, and the initiation of innate and adaptive immune responses culminate in immunothrombosis, ultimately causing (micro)thrombotic complications, such as deep vein thrombosis, pulmonary embolism, and stroke. Accordingly, the activation of coagulation (eg, as measured with plasma D-dimer) and thrombocytopenia have emerged as prognostic markers in COVID-19. Given thrombotic complications are central determinants of the high mortality rate in COVID-19, strategies to prevent thrombosis are of critical importance. Several antithrombotic drugs have been proposed as potential therapies to prevent COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat, and dipyridamole, many of which also possess pleiotropic anti-inflammatory or antiviral effects. The growing awareness and mechanistic understanding of the prothrombotic state of COVID-19 patients are driving efforts to more stringent diagnostic screening for thrombotic complications and to the early institution of antithrombotic drugs, for both the prevention and therapy of thrombotic complications. The shifting paradigm of diagnostic and treatment strategies holds significant promise to reduce the burden of thrombotic complications and ultimately improve the prognosis for patients with COVID-19.

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