COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.
Identifieur interne : 000039 ( Main/Corpus ); précédent : 000038; suivant : 000040COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.
Auteurs : Wolfgang Miesbach ; Michael MakrisSource :
- Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis [ 1938-2723 ]
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.
DOI: 10.1177/1076029620938149
PubMed: 32677459
PubMed Central: PMC7370334
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.</title><author><name sortKey="Miesbach, Wolfgang" sort="Miesbach, Wolfgang" uniqKey="Miesbach W" first="Wolfgang" last="Miesbach">Wolfgang Miesbach</name><affiliation><nlm:affiliation>Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Makris, Michael" sort="Makris, Michael" uniqKey="Makris M" first="Michael" last="Makris">Michael Makris</name><affiliation><nlm:affiliation>Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Sheffield Haemophilia and Thrombosis Centre, Royal Hallamshire Hospital, Sheffield, United Kingdom.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020 Jan-Dec</date><idno type="RBID">pubmed:32677459</idno><idno type="pmid">32677459</idno><idno type="doi">10.1177/1076029620938149</idno><idno type="pmc">PMC7370334</idno><idno type="wicri:Area/Main/Corpus">000039</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000039</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.</title><author><name sortKey="Miesbach, Wolfgang" sort="Miesbach, Wolfgang" uniqKey="Miesbach W" first="Wolfgang" last="Miesbach">Wolfgang Miesbach</name><affiliation><nlm:affiliation>Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Makris, Michael" sort="Makris, Michael" uniqKey="Makris M" first="Michael" last="Makris">Michael Makris</name><affiliation><nlm:affiliation>Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Sheffield Haemophilia and Thrombosis Centre, Royal Hallamshire Hospital, Sheffield, United Kingdom.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis</title><idno type="eISSN">1938-2723</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32677459</PMID><DateRevised><Year>2020</Year><Month>07</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1938-2723</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><PubDate><MedlineDate>2020 Jan-Dec</MedlineDate></PubDate></JournalIssue><Title>Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis</Title><ISOAbbreviation>Clin. Appl. Thromb. Hemost.</ISOAbbreviation></Journal><ArticleTitle>COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.</ArticleTitle><Pagination><MedlinePgn>1076029620938149</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1177/1076029620938149</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Miesbach</LastName><ForeName>Wolfgang</ForeName><Initials>W</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-4506-0061</Identifier><AffiliationInfo><Affiliation>Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Makris</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Sheffield Haemophilia and Thrombosis Centre, Royal 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PubStatus="medline"><Year>2020</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32677459</ArticleId><ArticleId IdType="doi">10.1177/1076029620938149</ArticleId><ArticleId IdType="pmc">PMC7370334</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>BMJ. 2003 Jun 21;326(7403):1358-62</Citation><ArticleIdList><ArticleId IdType="pubmed">12816821</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Immunol. 2013 Jan;13(1):34-45</Citation><ArticleIdList><ArticleId IdType="pubmed">23222502</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2011;6(8):e23710</Citation><ArticleIdList><ArticleId IdType="pubmed">21887302</ArticleId></ArticleIdList></Reference><Reference><Citation>J Thromb Haemost. 2020 May;18(5):1023-1026</Citation><ArticleIdList><ArticleId IdType="pubmed">32338827</ArticleId></ArticleIdList></Reference><Reference><Citation>J Pathol. 2004 Jun;203(2):631-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15141377</ArticleId></ArticleIdList></Reference><Reference><Citation>Thromb Res. 2020 Jul;191:145-147</Citation><ArticleIdList><ArticleId IdType="pubmed">32291094</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 2020 May 26;58(6):</Citation><ArticleIdList><ArticleId IdType="pubmed">32245835</ArticleId></ArticleIdList></Reference><Reference><Citation>Germs. 2019 Mar 01;9(1):35-42</Citation><ArticleIdList><ArticleId IdType="pubmed">31119115</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Respir Med. 2020 Apr;8(4):420-422</Citation><ArticleIdList><ArticleId IdType="pubmed">32085846</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Cardiol. 2020 Feb;17(2):116-129</Citation><ArticleIdList><ArticleId IdType="pubmed">31427727</ArticleId></ArticleIdList></Reference><Reference><Citation>Postgrad Med J. 2005 Jun;81(956):e3</Citation><ArticleIdList><ArticleId IdType="pubmed">15937197</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurol. 2004 Oct;251(10):1227-31</Citation><ArticleIdList><ArticleId IdType="pubmed">15503102</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2020 May 2;395(10234):1417-1418</Citation><ArticleIdList><ArticleId IdType="pubmed">32325026</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2020 Apr 30;382(18):1708-1720</Citation><ArticleIdList><ArticleId IdType="pubmed">32109013</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2020 Mar 28;395(10229):1054-1062</Citation><ArticleIdList><ArticleId IdType="pubmed">32171076</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1986-94</Citation><ArticleIdList><ArticleId IdType="pubmed">12682352</ArticleId></ArticleIdList></Reference><Reference><Citation>J Thromb Haemost. 2020 Jun;18(6):1421-1424</Citation><ArticleIdList><ArticleId IdType="pubmed">32271988</ArticleId></ArticleIdList></Reference><Reference><Citation>Hypertension. 2001 May;37(5):1336-40</Citation><ArticleIdList><ArticleId IdType="pubmed">11358950</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2000 Nov 15;165(10):5671-9</Citation><ArticleIdList><ArticleId IdType="pubmed">11067924</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2020 May 13;:</Citation><ArticleIdList><ArticleId IdType="pubmed">32402155</ArticleId></ArticleIdList></Reference><Reference><Citation>J Thromb Haemost. 2020 Apr;18(4):844-847</Citation><ArticleIdList><ArticleId IdType="pubmed">32073213</ArticleId></ArticleIdList></Reference><Reference><Citation>JAMA Intern Med. 2020 Mar 13;:</Citation><ArticleIdList><ArticleId IdType="pubmed">32167524</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation><ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId></ArticleIdList></Reference><Reference><Citation>mBio. 2018 Oct 9;9(5):</Citation><ArticleIdList><ArticleId IdType="pubmed">30301856</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2002 Jun 20;417(6891):822-8</Citation><ArticleIdList><ArticleId IdType="pubmed">12075344</ArticleId></ArticleIdList></Reference><Reference><Citation>Intensive Care Med. 2020 Apr;46(4):586-590</Citation><ArticleIdList><ArticleId IdType="pubmed">32125455</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cardiovasc Pharmacol. 1995;25 Suppl 2:S13-9</Citation><ArticleIdList><ArticleId IdType="pubmed">8699851</ArticleId></ArticleIdList></Reference><Reference><Citation>JAMA. 2020 Feb 24;:</Citation><ArticleIdList><ArticleId IdType="pubmed">32091533</ArticleId></ArticleIdList></Reference><Reference><Citation>J Surg Res. 2019 Jun;238:175-185</Citation><ArticleIdList><ArticleId IdType="pubmed">30771687</ArticleId></ArticleIdList></Reference><Reference><Citation>JAMA. 2020 Feb 7;:</Citation><ArticleIdList><ArticleId IdType="pubmed">32031570</ArticleId></ArticleIdList></Reference><Reference><Citation>Virulence. 2014 Jan 1;5(1):4-11</Citation><ArticleIdList><ArticleId IdType="pubmed">24335434</ArticleId></ArticleIdList></Reference><Reference><Citation>J Thromb Haemost. 2020 Jul;18(7):1752-1755</Citation><ArticleIdList><ArticleId IdType="pubmed">32267998</ArticleId></ArticleIdList></Reference><Reference><Citation>Intensive Care Med. 2004 Apr;30(4):580-8</Citation><ArticleIdList><ArticleId IdType="pubmed">14997295</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Microbiol. 2016 Aug;14(8):523-34</Citation><ArticleIdList><ArticleId IdType="pubmed">27344959</ArticleId></ArticleIdList></Reference><Reference><Citation>Antiviral Res. 2013 Oct;100(1):286-95</Citation><ArticleIdList><ArticleId IdType="pubmed">24012996</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Infect Dis. 2018 Apr 17;66(9):1467-1469</Citation><ArticleIdList><ArticleId IdType="pubmed">29177461</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2020 Feb 15;395(10223):497-506</Citation><ArticleIdList><ArticleId IdType="pubmed">31986264</ArticleId></ArticleIdList></Reference><Reference><Citation>J Am Coll Cardiol. 2020 Jun 16;75(23):2950-2973</Citation><ArticleIdList><ArticleId IdType="pubmed">32311448</ArticleId></ArticleIdList></Reference><Reference><Citation>Sci China Life Sci. 2020 Mar;63(3):364-374</Citation><ArticleIdList><ArticleId IdType="pubmed">32048163</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect. 2016 Nov;73(5):468-475</Citation><ArticleIdList><ArticleId IdType="pubmed">27519621</ArticleId></ArticleIdList></Reference><Reference><Citation>Physiol Rev. 2018 Jul 1;98(3):1627-1738</Citation><ArticleIdList><ArticleId IdType="pubmed">29873596</ArticleId></ArticleIdList></Reference><Reference><Citation>J Thromb Haemost. 2020 May;18(5):1094-1099</Citation><ArticleIdList><ArticleId IdType="pubmed">32220112</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2020 Apr 23;382(17):e38</Citation><ArticleIdList><ArticleId IdType="pubmed">32268022</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2020 Feb 15;395(10223):507-513</Citation><ArticleIdList><ArticleId IdType="pubmed">32007143</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Respir Med. 2020 May;8(5):475-481</Citation><ArticleIdList><ArticleId IdType="pubmed">32105632</ArticleId></ArticleIdList></Reference><Reference><Citation>Expert Rev Cardiovasc Ther. 2010 Dec;8(12):1723-9</Citation><ArticleIdList><ArticleId 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