tetano
Editor, Senior Moderator
Vasc Med
. 2020 Jun 19;1358863X20932640.
doi: 10.1177/1358863X20932640. Online ahead of print.
COVID-19-associated Coagulopathy: An Exploration of Mechanisms
Meaghan E Colling[SUP] 1 [/SUP], Yogendra Kanthi[SUP] 2 [/SUP]
Affiliations
Abstract
An ongoing global pandemic of viral pneumonia (coronavirus disease [COVID-19]), due to the virus SARS-CoV-2, has infected millions of people and remains a threat to many more. Most critically ill patients have respiratory failure and there is an international effort to understand mechanisms and predictors of disease severity. Coagulopathy, characterized by elevations in D-dimer and fibrin(ogen) degradation products (FDPs), is associated with critical illness and mortality in patients with COVID-19. Furthermore, increasing reports of microvascular and macrovascular thrombi suggest that hemostatic imbalances may contribute to the pathophysiology of SARS-CoV-2 infection. We review the laboratory and clinical findings of patients with COVID-19-associated coagulopathy, and prior studies of hemostasis in other viral infections and acute respiratory distress syndrome. We hypothesize that an imbalance between coagulation and inflammation may result in a hypercoagulable state. Although thrombosis initiated by the innate immune system is hypothesized to limit SARS-CoV-2 dissemination, aberrant activation of this system can cause endothelial injury resulting in loss of thromboprotective mechanisms, excess thrombin generation, and dysregulation of fibrinolysis and thrombosis. The role various components including neutrophils, neutrophil extracellular traps, activated platelets, microparticles, clotting factors, inflammatory cytokines, and complement play in this process remains an area of active investigation and ongoing clinical trials target these different pathways in COVID-19.
Keywords: COVID-19; NETs; anticoagulation; antiplatelet; coagulation; coronavirus; inflammation; neutrophils; thrombosis; vascular endothelium; venous thromboembolism (VTE).
. 2020 Jun 19;1358863X20932640.
doi: 10.1177/1358863X20932640. Online ahead of print.
COVID-19-associated Coagulopathy: An Exploration of Mechanisms
Meaghan E Colling[SUP] 1 [/SUP], Yogendra Kanthi[SUP] 2 [/SUP]
Affiliations
- PMID: 32558620
- DOI: 10.1177/1358863X20932640
Abstract
An ongoing global pandemic of viral pneumonia (coronavirus disease [COVID-19]), due to the virus SARS-CoV-2, has infected millions of people and remains a threat to many more. Most critically ill patients have respiratory failure and there is an international effort to understand mechanisms and predictors of disease severity. Coagulopathy, characterized by elevations in D-dimer and fibrin(ogen) degradation products (FDPs), is associated with critical illness and mortality in patients with COVID-19. Furthermore, increasing reports of microvascular and macrovascular thrombi suggest that hemostatic imbalances may contribute to the pathophysiology of SARS-CoV-2 infection. We review the laboratory and clinical findings of patients with COVID-19-associated coagulopathy, and prior studies of hemostasis in other viral infections and acute respiratory distress syndrome. We hypothesize that an imbalance between coagulation and inflammation may result in a hypercoagulable state. Although thrombosis initiated by the innate immune system is hypothesized to limit SARS-CoV-2 dissemination, aberrant activation of this system can cause endothelial injury resulting in loss of thromboprotective mechanisms, excess thrombin generation, and dysregulation of fibrinolysis and thrombosis. The role various components including neutrophils, neutrophil extracellular traps, activated platelets, microparticles, clotting factors, inflammatory cytokines, and complement play in this process remains an area of active investigation and ongoing clinical trials target these different pathways in COVID-19.
Keywords: COVID-19; NETs; anticoagulation; antiplatelet; coagulation; coronavirus; inflammation; neutrophils; thrombosis; vascular endothelium; venous thromboembolism (VTE).