Coagulopathy, thromboembolic complications, and the use of heparin in COVID-19 pneumonia

Abstract

The SARS-CoV-2 (COVID-19) is causing a pandemic and potentially fatal disease of global public health concern. Viral infections are known to be associated with coagulation impairment; thus, thrombosis, hemorrhage, or both may occur. Understanding the pathophysiologic mechanisms underlying the development of coagulation disorders during viral infection is essential for the development of therapeutic strategies. Coagulopathy in COVID-19 infection is emerging as a precipitant factor for severe respiratory complications and death. An increase in coagulation markers, such as fibrinogen and D-dimer, has been found in severe COVID-19 cases. Heparin, clinically used as an anticoagulant, also has anti-inflammatory properties, including binding of inflammatory cytokines, inhibition of neutrophil chemotaxis, and protection of endothelial cells, and a potential antiviral effect. We hypothesized that low-molecular-weight heparin may attenuate cytokine storm in COVID-19 patients; therefore, low-molecular-weight heparin could be a valid adjunctive therapeutic drug for the treatment of COVID-19 pneumopathy. In this paper, we review potential mechanisms involved in coagulation impairment after viral infection and the possible role of heparin in the treatment of COVID-19 patients.

Keywords: COVID-19; Coagulopathy; D-dimer; Low-molecular-weight heparin; Pneumonia; Thrombosis.

Fig 1

Mechanisms of coagulation impairment in COVID-19 infection. ∗Elevated levels of plasminogen/plasmin are found in several medical conditions, including hypertension, diabetes, cardiovascular disease, cerebrovascular disease, and chronic renal disease. IL6, Interleukin 6; IL8, interleukin 8; TNF-α, tumor necrosis factor α.

Fig 2

Potential effects of low-molecular-weight heparin (LMWH) in COVID-19 disease.