The suboptimal fibrinolytic response in COVID‐19 is dictated by high PAI‐1
Severe COVID‐19 disease is associated with thrombotic complications and extensive fibrin deposition. This study investigates whether the hemostatic complications in COVID‐19 disease arise due to dysregulation of the fibrinolytic system. This prospective study analyzed fibrinolytic profiles of 113 pa...
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| Veröffentlicht in: | Journal of thrombosis and haemostasis 2022-10, Vol.20 (10), p.2394-2406 |
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| creator | Whyte, Claire S. Simpson, Megan Morrow, Gael B. Wallace, Carol A. Mentzer, Alexander J. Knight, Julian C. Shapiro, Susan Curry, Nicola Bagot, Catherine N. Watson, Henry Cooper, Jamie G. Mutch, Nicola J. |
| description | Severe COVID‐19 disease is associated with thrombotic complications and extensive fibrin deposition. This study investigates whether the hemostatic complications in COVID‐19 disease arise due to dysregulation of the fibrinolytic system.
This prospective study analyzed fibrinolytic profiles of 113 patients hospitalized with COVID‐19 disease with 24 patients with non‐COVID‐19 respiratory infection and healthy controls. Antigens were quantified by Ella system or ELISA, clot lysis by turbidimetric assay, and plasminogen activator inhibitor‐1 (PAI‐1)/plasmin activity using chromogenic substrates. Clot structure was visualized by confocal microscopy.
PAI‐1 and its cofactor, vitronectin, are significantly elevated in patients with COVID‐19 disease compared with those with non‐COVID‐19 respiratory infection and healthy control groups. Thrombin activatable fibrinolysis inhibitor and tissue plasminogen activator were elevated in patients with COVID‐19 disease relative to healthy controls. PAI‐1 and tissue plasminogen activator (tPA) were associated with more severe COVID‐19 disease severity. Clots formed from COVID‐19 plasma demonstrate an altered fibrin network, with attenuated fiber length and increased branching. Functional studies reveal that plasmin generation and clot lysis were markedly attenuated in COVID‐19 disease, while PAI‐1 activity was elevated. Clot lysis time significantly correlated with PAI‐1 levels. Stratification of COVID‐19 samples according to PAI‐1 levels reveals significantly faster lysis when using the PAI‐1 resistant (tPA) variant, tenecteplase, over alteplase lysis.
This study shows that the suboptimal fibrinolytic response in COVID‐19 disease is directly attributable to elevated levels of PAI‐1, which attenuate plasmin generation. These data highlight the important prognostic potential of PAI‐1 and the possibility of using pre‐existing drugs, such as tenecteplase, to treat COVID‐19 disease and potentially other respiratory diseases. |
| doi_str_mv | 10.1111/jth.15806 |
| format | Article |
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This prospective study analyzed fibrinolytic profiles of 113 patients hospitalized with COVID‐19 disease with 24 patients with non‐COVID‐19 respiratory infection and healthy controls. Antigens were quantified by Ella system or ELISA, clot lysis by turbidimetric assay, and plasminogen activator inhibitor‐1 (PAI‐1)/plasmin activity using chromogenic substrates. Clot structure was visualized by confocal microscopy.
PAI‐1 and its cofactor, vitronectin, are significantly elevated in patients with COVID‐19 disease compared with those with non‐COVID‐19 respiratory infection and healthy control groups. Thrombin activatable fibrinolysis inhibitor and tissue plasminogen activator were elevated in patients with COVID‐19 disease relative to healthy controls. PAI‐1 and tissue plasminogen activator (tPA) were associated with more severe COVID‐19 disease severity. Clots formed from COVID‐19 plasma demonstrate an altered fibrin network, with attenuated fiber length and increased branching. Functional studies reveal that plasmin generation and clot lysis were markedly attenuated in COVID‐19 disease, while PAI‐1 activity was elevated. Clot lysis time significantly correlated with PAI‐1 levels. Stratification of COVID‐19 samples according to PAI‐1 levels reveals significantly faster lysis when using the PAI‐1 resistant (tPA) variant, tenecteplase, over alteplase lysis.
This study shows that the suboptimal fibrinolytic response in COVID‐19 disease is directly attributable to elevated levels of PAI‐1, which attenuate plasmin generation. These data highlight the important prognostic potential of PAI‐1 and the possibility of using pre‐existing drugs, such as tenecteplase, to treat COVID‐19 disease and potentially other respiratory diseases.</description><identifier>ISSN: 1538-7836</identifier><identifier>ISSN: 1538-7933</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/jth.15806</identifier><identifier>PMID: 35780481</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Antigens ; Carboxypeptidase B2 ; Chromogenic Compounds ; Confocal microscopy ; COVID-19 ; COVID-19 Drug Treatment ; Disease ; Enzyme-linked immunosorbent assay ; Fibrin ; Fibrinolysin - pharmacology ; Fibrinolysis ; Hemostatics - pharmacology ; Humans ; Lysis ; Original ; PAI‐1 ; Plasmin ; Plasminogen Activator Inhibitor 1 ; Plasminogen activator inhibitors ; Prospective Studies ; Respiration ; Respiratory diseases ; t-Plasminogen activator ; Tenecteplase ; Thrombin ; Thrombosis - drug therapy ; Tissue Plasminogen Activator - pharmacology ; Tissue polypeptide antigen ; TPA ; Vitronectin</subject><ispartof>Journal of thrombosis and haemostasis, 2022-10, Vol.20 (10), p.2394-2406</ispartof><rights>2022 The Authors.Journal of Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis.</rights><rights>2022 The Authors. published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis.</rights><rights>2022 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis.</rights><rights>2022. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4876-8f26a8e6cd4e2e205f26aab6378f82f305fcdc1d016a95a695986b71522ec2783</citedby><cites>FETCH-LOGICAL-c4876-8f26a8e6cd4e2e205f26aab6378f82f305fcdc1d016a95a695986b71522ec2783</cites><orcidid>0000-0002-4030-619X ; 0000-0003-3812-7026 ; 0000-0002-1402-2134 ; 0000-0003-0402-0802 ; 0000-0002-3849-0688 ; 0000-0002-4502-2209 ; 0000-0002-0377-5536 ; 0000-0002-6439-9706 ; 0000-0002-7452-0813 ; 0000-0001-9299-6754 ; 0000-0001-8127-6102 ; 0000-0002-3824-8808</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35780481$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Whyte, Claire S.</creatorcontrib><creatorcontrib>Simpson, Megan</creatorcontrib><creatorcontrib>Morrow, Gael B.</creatorcontrib><creatorcontrib>Wallace, Carol A.</creatorcontrib><creatorcontrib>Mentzer, Alexander J.</creatorcontrib><creatorcontrib>Knight, Julian C.</creatorcontrib><creatorcontrib>Shapiro, Susan</creatorcontrib><creatorcontrib>Curry, Nicola</creatorcontrib><creatorcontrib>Bagot, Catherine N.</creatorcontrib><creatorcontrib>Watson, Henry</creatorcontrib><creatorcontrib>Cooper, Jamie G.</creatorcontrib><creatorcontrib>Mutch, Nicola J.</creatorcontrib><title>The suboptimal fibrinolytic response in COVID‐19 is dictated by high PAI‐1</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Severe COVID‐19 disease is associated with thrombotic complications and extensive fibrin deposition. This study investigates whether the hemostatic complications in COVID‐19 disease arise due to dysregulation of the fibrinolytic system.
This prospective study analyzed fibrinolytic profiles of 113 patients hospitalized with COVID‐19 disease with 24 patients with non‐COVID‐19 respiratory infection and healthy controls. Antigens were quantified by Ella system or ELISA, clot lysis by turbidimetric assay, and plasminogen activator inhibitor‐1 (PAI‐1)/plasmin activity using chromogenic substrates. Clot structure was visualized by confocal microscopy.
PAI‐1 and its cofactor, vitronectin, are significantly elevated in patients with COVID‐19 disease compared with those with non‐COVID‐19 respiratory infection and healthy control groups. Thrombin activatable fibrinolysis inhibitor and tissue plasminogen activator were elevated in patients with COVID‐19 disease relative to healthy controls. PAI‐1 and tissue plasminogen activator (tPA) were associated with more severe COVID‐19 disease severity. Clots formed from COVID‐19 plasma demonstrate an altered fibrin network, with attenuated fiber length and increased branching. Functional studies reveal that plasmin generation and clot lysis were markedly attenuated in COVID‐19 disease, while PAI‐1 activity was elevated. Clot lysis time significantly correlated with PAI‐1 levels. Stratification of COVID‐19 samples according to PAI‐1 levels reveals significantly faster lysis when using the PAI‐1 resistant (tPA) variant, tenecteplase, over alteplase lysis.
This study shows that the suboptimal fibrinolytic response in COVID‐19 disease is directly attributable to elevated levels of PAI‐1, which attenuate plasmin generation. These data highlight the important prognostic potential of PAI‐1 and the possibility of using pre‐existing drugs, such as tenecteplase, to treat COVID‐19 disease and potentially other respiratory diseases.</description><subject>Antigens</subject><subject>Carboxypeptidase B2</subject><subject>Chromogenic Compounds</subject><subject>Confocal microscopy</subject><subject>COVID-19</subject><subject>COVID-19 Drug Treatment</subject><subject>Disease</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibrin</subject><subject>Fibrinolysin - pharmacology</subject><subject>Fibrinolysis</subject><subject>Hemostatics - pharmacology</subject><subject>Humans</subject><subject>Lysis</subject><subject>Original</subject><subject>PAI‐1</subject><subject>Plasmin</subject><subject>Plasminogen Activator Inhibitor 1</subject><subject>Plasminogen activator inhibitors</subject><subject>Prospective Studies</subject><subject>Respiration</subject><subject>Respiratory diseases</subject><subject>t-Plasminogen activator</subject><subject>Tenecteplase</subject><subject>Thrombin</subject><subject>Thrombosis - drug therapy</subject><subject>Tissue Plasminogen Activator - pharmacology</subject><subject>Tissue polypeptide antigen</subject><subject>TPA</subject><subject>Vitronectin</subject><issn>1538-7836</issn><issn>1538-7933</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kc1OGzEUhS1UBJSy4AUqS920i4DtmbE9m0oohRKEoIu0W8vjuZNxNBkHewaUXR-hz8iT1CEJCgi88c_97tG5PggdU3JC4zqddvUJzSThO-iAZokcCJnwD1vnffQxhCkhNM8Y2UP7SSYkSSU9QDfjGnDoCzfv7Ew3uLKFt61rFp012EOYuzYAti0e3v4Z_Xj8-4_m2AZcWtPpDkpcLHBtJzX-dTZaFj-h3Uo3AY7W-yH6fXE-Hl4Orm9_joZn1wOTSsEHsmJcS-CmTIEBI9nyrgueCFlJViXxwZSGloRynWea51kueSFoxhgYFic6RN9XuvO-mEFpoO28btTcxyH8Qjlt1ctKa2s1cfcqT9I8TVkU-LoW8O6uh9CpmQ0Gmka34PqgGJcpyYUgPKJfXqFT1_s2jqdYtMSJSMRS8NuKMt6F4KF6NkOJWqakYkrqKaXIft52_0xuYonA6Qp4sA0s3ldSV-PLjWSy6oD46_cWvArGQmugtB5Mp0pn3zDyHxvZrgU</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Whyte, Claire S.</creator><creator>Simpson, Megan</creator><creator>Morrow, Gael B.</creator><creator>Wallace, Carol A.</creator><creator>Mentzer, Alexander J.</creator><creator>Knight, Julian C.</creator><creator>Shapiro, Susan</creator><creator>Curry, Nicola</creator><creator>Bagot, Catherine N.</creator><creator>Watson, Henry</creator><creator>Cooper, Jamie G.</creator><creator>Mutch, Nicola J.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><general>John Wiley and Sons Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4030-619X</orcidid><orcidid>https://orcid.org/0000-0003-3812-7026</orcidid><orcidid>https://orcid.org/0000-0002-1402-2134</orcidid><orcidid>https://orcid.org/0000-0003-0402-0802</orcidid><orcidid>https://orcid.org/0000-0002-3849-0688</orcidid><orcidid>https://orcid.org/0000-0002-4502-2209</orcidid><orcidid>https://orcid.org/0000-0002-0377-5536</orcidid><orcidid>https://orcid.org/0000-0002-6439-9706</orcidid><orcidid>https://orcid.org/0000-0002-7452-0813</orcidid><orcidid>https://orcid.org/0000-0001-9299-6754</orcidid><orcidid>https://orcid.org/0000-0001-8127-6102</orcidid><orcidid>https://orcid.org/0000-0002-3824-8808</orcidid></search><sort><creationdate>202210</creationdate><title>The suboptimal fibrinolytic response in COVID‐19 is dictated by high PAI‐1</title><author>Whyte, Claire S. ; Simpson, Megan ; Morrow, Gael B. ; Wallace, Carol A. ; Mentzer, Alexander J. ; Knight, Julian C. ; Shapiro, Susan ; Curry, Nicola ; Bagot, Catherine N. ; Watson, Henry ; Cooper, Jamie G. ; Mutch, Nicola J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4876-8f26a8e6cd4e2e205f26aab6378f82f305fcdc1d016a95a695986b71522ec2783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antigens</topic><topic>Carboxypeptidase B2</topic><topic>Chromogenic Compounds</topic><topic>Confocal microscopy</topic><topic>COVID-19</topic><topic>COVID-19 Drug Treatment</topic><topic>Disease</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibrin</topic><topic>Fibrinolysin - pharmacology</topic><topic>Fibrinolysis</topic><topic>Hemostatics - pharmacology</topic><topic>Humans</topic><topic>Lysis</topic><topic>Original</topic><topic>PAI‐1</topic><topic>Plasmin</topic><topic>Plasminogen Activator Inhibitor 1</topic><topic>Plasminogen activator inhibitors</topic><topic>Prospective Studies</topic><topic>Respiration</topic><topic>Respiratory diseases</topic><topic>t-Plasminogen activator</topic><topic>Tenecteplase</topic><topic>Thrombin</topic><topic>Thrombosis - drug therapy</topic><topic>Tissue Plasminogen Activator - pharmacology</topic><topic>Tissue polypeptide antigen</topic><topic>TPA</topic><topic>Vitronectin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Whyte, Claire S.</creatorcontrib><creatorcontrib>Simpson, Megan</creatorcontrib><creatorcontrib>Morrow, Gael B.</creatorcontrib><creatorcontrib>Wallace, Carol A.</creatorcontrib><creatorcontrib>Mentzer, Alexander J.</creatorcontrib><creatorcontrib>Knight, Julian C.</creatorcontrib><creatorcontrib>Shapiro, Susan</creatorcontrib><creatorcontrib>Curry, Nicola</creatorcontrib><creatorcontrib>Bagot, Catherine N.</creatorcontrib><creatorcontrib>Watson, Henry</creatorcontrib><creatorcontrib>Cooper, Jamie G.</creatorcontrib><creatorcontrib>Mutch, Nicola J.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Whyte, Claire S.</au><au>Simpson, Megan</au><au>Morrow, Gael B.</au><au>Wallace, Carol A.</au><au>Mentzer, Alexander J.</au><au>Knight, Julian C.</au><au>Shapiro, Susan</au><au>Curry, Nicola</au><au>Bagot, Catherine N.</au><au>Watson, Henry</au><au>Cooper, Jamie G.</au><au>Mutch, Nicola J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The suboptimal fibrinolytic response in COVID‐19 is dictated by high PAI‐1</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2022-10</date><risdate>2022</risdate><volume>20</volume><issue>10</issue><spage>2394</spage><epage>2406</epage><pages>2394-2406</pages><issn>1538-7836</issn><issn>1538-7933</issn><eissn>1538-7836</eissn><abstract>Severe COVID‐19 disease is associated with thrombotic complications and extensive fibrin deposition. This study investigates whether the hemostatic complications in COVID‐19 disease arise due to dysregulation of the fibrinolytic system.
This prospective study analyzed fibrinolytic profiles of 113 patients hospitalized with COVID‐19 disease with 24 patients with non‐COVID‐19 respiratory infection and healthy controls. Antigens were quantified by Ella system or ELISA, clot lysis by turbidimetric assay, and plasminogen activator inhibitor‐1 (PAI‐1)/plasmin activity using chromogenic substrates. Clot structure was visualized by confocal microscopy.
PAI‐1 and its cofactor, vitronectin, are significantly elevated in patients with COVID‐19 disease compared with those with non‐COVID‐19 respiratory infection and healthy control groups. Thrombin activatable fibrinolysis inhibitor and tissue plasminogen activator were elevated in patients with COVID‐19 disease relative to healthy controls. PAI‐1 and tissue plasminogen activator (tPA) were associated with more severe COVID‐19 disease severity. Clots formed from COVID‐19 plasma demonstrate an altered fibrin network, with attenuated fiber length and increased branching. Functional studies reveal that plasmin generation and clot lysis were markedly attenuated in COVID‐19 disease, while PAI‐1 activity was elevated. Clot lysis time significantly correlated with PAI‐1 levels. Stratification of COVID‐19 samples according to PAI‐1 levels reveals significantly faster lysis when using the PAI‐1 resistant (tPA) variant, tenecteplase, over alteplase lysis.
This study shows that the suboptimal fibrinolytic response in COVID‐19 disease is directly attributable to elevated levels of PAI‐1, which attenuate plasmin generation. These data highlight the important prognostic potential of PAI‐1 and the possibility of using pre‐existing drugs, such as tenecteplase, to treat COVID‐19 disease and potentially other respiratory diseases.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>35780481</pmid><doi>10.1111/jth.15806</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4030-619X</orcidid><orcidid>https://orcid.org/0000-0003-3812-7026</orcidid><orcidid>https://orcid.org/0000-0002-1402-2134</orcidid><orcidid>https://orcid.org/0000-0003-0402-0802</orcidid><orcidid>https://orcid.org/0000-0002-3849-0688</orcidid><orcidid>https://orcid.org/0000-0002-4502-2209</orcidid><orcidid>https://orcid.org/0000-0002-0377-5536</orcidid><orcidid>https://orcid.org/0000-0002-6439-9706</orcidid><orcidid>https://orcid.org/0000-0002-7452-0813</orcidid><orcidid>https://orcid.org/0000-0001-9299-6754</orcidid><orcidid>https://orcid.org/0000-0001-8127-6102</orcidid><orcidid>https://orcid.org/0000-0002-3824-8808</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of thrombosis and haemostasis, 2022-10, Vol.20 (10), p.2394-2406 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Antigens Carboxypeptidase B2 Chromogenic Compounds Confocal microscopy COVID-19 COVID-19 Drug Treatment Disease Enzyme-linked immunosorbent assay Fibrin Fibrinolysin - pharmacology Fibrinolysis Hemostatics - pharmacology Humans Lysis Original PAI‐1 Plasmin Plasminogen Activator Inhibitor 1 Plasminogen activator inhibitors Prospective Studies Respiration Respiratory diseases t-Plasminogen activator Tenecteplase Thrombin Thrombosis - drug therapy Tissue Plasminogen Activator - pharmacology Tissue polypeptide antigen TPA Vitronectin |
| title | The suboptimal fibrinolytic response in COVID‐19 is dictated by high PAI‐1 |
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