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COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.
Clin Appl Thromb Hemost. 2020 Jan-Dec; 26:1076029620938149.CA

Abstract

The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.

Authors+Show Affiliations

Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany.Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom. Sheffield Haemophilia and Thrombosis Centre, Royal Hallamshire Hospital, Sheffield, United Kingdom.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32677459

Citation

Miesbach, Wolfgang, and Michael Makris. "COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation." Clinical and Applied Thrombosis/hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis, vol. 26, 2020, p. 1076029620938149.
Miesbach W, Makris M. COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation. Clin Appl Thromb Hemost. 2020;26:1076029620938149.
Miesbach, W., & Makris, M. (2020). COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation. Clinical and Applied Thrombosis/hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis, 26, 1076029620938149. https://doi.org/10.1177/1076029620938149
Miesbach W, Makris M. COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation. Clin Appl Thromb Hemost. 2020 Jan-Dec;26:1076029620938149. PubMed PMID: 32677459.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation. AU - Miesbach,Wolfgang, AU - Makris,Michael, PY - 2020/7/18/entrez PY - 2020/7/18/pubmed PY - 2020/8/1/medline KW - COVID-19 KW - anticoagulation KW - thrombosis SP - 1076029620938149 EP - 1076029620938149 JF - Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis JO - Clin. Appl. Thromb. Hemost. VL - 26 N2 - The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19. SN - 1938-2723 UR - https://www.unboundmedicine.com/medline/citation/32677459/COVID_19:_Coagulopathy_Risk_of_Thrombosis_and_the_Rationale_for_Anticoagulation_ L2 - https://journals.sagepub.com/doi/10.1177/1076029620938149?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -