Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu
Objective Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myelo...
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| Veröffentlicht in: | Herz 2016-02, Vol.41 (1), p.57-62 |
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| creator | Procter, Nathan E.K. Ball, Jocasta Ngo, Doan T.M. Chirkov, Yuliy Y. Isenberg, Jeffrey S. Hylek, Elaine M. Stewart, Simon Horowitz, John D. |
| description | Objective
Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myeloperoxidase (MPO) and C-reactive protein (CRP)] and impaired nitric oxide (NO) signaling.
Methods
Clinical and biochemical determinants of adenosine diphosphate (ADP)-induced platelet aggregation were sought in patients (
n
= 106) hospitalized with AF via univariate and multivariate analysis.
Results
Hyper-responsiveness of platelets to ADP was directly (
r
= 0.254,
p
|
| doi_str_mv | 10.1007/s00059-015-4335-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1850775033</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3953554571</sourcerecordid><originalsourceid>FETCH-LOGICAL-c427t-e737f0cc03f9b4b2db74b721a2db067a525aa45e8e80c1ed5d9f80582193e7123</originalsourceid><addsrcrecordid>eNqFkU9LAzEQxYMoWqsfwIssePGyOkk2yeamFP-BoAc9h-x2to1sd2uSIvvtTWkVEcRTJuT33mTmEXJC4YICqMsAAELnQEVecC7yYYeMqEw3KTXbJSPgBeRac3VADkN4gwRqBvvkgEnKRSHLEbl6bm3EFmM2H5bo7WzmcWYr17o4ZK7LljY67GLIPlycZzZ6Z9uscZV3bRK6vjsie41tAx5vzzF5vb15mdznj093D5Prx7wumIo5Kq4aqGvgja6Kik0rVVSKUZsqkMoKJqwtBJZYQk1xKqa6KUGUjGqOijI-Jucb36Xv31cYolm4UGP6RYf9KhhaClBKAOf_o0orxrSgMqFnv9C3fuW7NEiipGCSKVj3phuq9n0IHhuz9G5h_WAomHUSZpOESQs26yTMkDSnW-dVtcDpt-Jr9QlgGyCkp26G_kfrP10_AXFPkvk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1765262702</pqid></control><display><type>article</type><title>Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Procter, Nathan E.K. ; Ball, Jocasta ; Ngo, Doan T.M. ; Chirkov, Yuliy Y. ; Isenberg, Jeffrey S. ; Hylek, Elaine M. ; Stewart, Simon ; Horowitz, John D.</creator><creatorcontrib>Procter, Nathan E.K. ; Ball, Jocasta ; Ngo, Doan T.M. ; Chirkov, Yuliy Y. ; Isenberg, Jeffrey S. ; Hylek, Elaine M. ; Stewart, Simon ; Horowitz, John D.</creatorcontrib><description><![CDATA[Objective
Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myeloperoxidase (MPO) and C-reactive protein (CRP)] and impaired nitric oxide (NO) signaling.
Methods
Clinical and biochemical determinants of adenosine diphosphate (ADP)-induced platelet aggregation were sought in patients (
n
= 106) hospitalized with AF via univariate and multivariate analysis.
Results
Hyper-responsiveness of platelets to ADP was directly (
r
= 0.254,
p
< 0.01) correlated with plasma concentrations of thrombospondin-1 (TSP-1), a matricellular protein that impairs NO responses and contributes to development of oxidative stress. In turn, plasma TSP-1 concentrations were directly correlated with MPO concentrations (
r
= 0.221,
p
< 0.05), while MPO concentrations correlated with those of asymmetric dimethylarginine (ADMA,
r
= 0.220,
p
< 0.05), and its structural isomer symmetric dimethylarginine (SDMA,
r
= 0.192,
p
= 0.05). Multivariate analysis identified TSP-1 (β = 0.276,
p
< 0.05) concentrations, as well as female sex (β = 0.199,
p
< 0.05), as direct correlates of platelet aggregability, and SDMA concentrations (β = − 0.292,
p
< 0.05) as an inverse correlate.
Conclusion
We conclude that platelet hyperaggregability, where present in the context of AF, may be engendered by impaired availability of NO, as well as via MPO-related inflammatory activation.]]></description><identifier>ISSN: 0340-9937</identifier><identifier>EISSN: 1615-6692</identifier><identifier>DOI: 10.1007/s00059-015-4335-y</identifier><identifier>PMID: 26135468</identifier><identifier>CODEN: HERZDW</identifier><language>eng</language><publisher>Munich: Springer Medizin</publisher><subject>Aged ; Aged, 80 and over ; Atrial Fibrillation - immunology ; Atrial Fibrillation - pathology ; Cardiology ; Female ; Humans ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Myocarditis - immunology ; Myocarditis - pathology ; Nitric Oxide - blood ; Nitric Oxide - immunology ; Original Article ; Peroxidase - blood ; Peroxidase - immunology ; Platelet Aggregation - immunology ; Reactive Oxygen Species - blood ; Reactive Oxygen Species - immunology</subject><ispartof>Herz, 2016-02, Vol.41 (1), p.57-62</ispartof><rights>Urban & Vogel 2015</rights><rights>Springer Medizin Verlag 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c427t-e737f0cc03f9b4b2db74b721a2db067a525aa45e8e80c1ed5d9f80582193e7123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00059-015-4335-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00059-015-4335-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26135468$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Procter, Nathan E.K.</creatorcontrib><creatorcontrib>Ball, Jocasta</creatorcontrib><creatorcontrib>Ngo, Doan T.M.</creatorcontrib><creatorcontrib>Chirkov, Yuliy Y.</creatorcontrib><creatorcontrib>Isenberg, Jeffrey S.</creatorcontrib><creatorcontrib>Hylek, Elaine M.</creatorcontrib><creatorcontrib>Stewart, Simon</creatorcontrib><creatorcontrib>Horowitz, John D.</creatorcontrib><title>Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu</title><title>Herz</title><addtitle>Herz</addtitle><addtitle>Herz</addtitle><description><![CDATA[Objective
Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myeloperoxidase (MPO) and C-reactive protein (CRP)] and impaired nitric oxide (NO) signaling.
Methods
Clinical and biochemical determinants of adenosine diphosphate (ADP)-induced platelet aggregation were sought in patients (
n
= 106) hospitalized with AF via univariate and multivariate analysis.
Results
Hyper-responsiveness of platelets to ADP was directly (
r
= 0.254,
p
< 0.01) correlated with plasma concentrations of thrombospondin-1 (TSP-1), a matricellular protein that impairs NO responses and contributes to development of oxidative stress. In turn, plasma TSP-1 concentrations were directly correlated with MPO concentrations (
r
= 0.221,
p
< 0.05), while MPO concentrations correlated with those of asymmetric dimethylarginine (ADMA,
r
= 0.220,
p
< 0.05), and its structural isomer symmetric dimethylarginine (SDMA,
r
= 0.192,
p
= 0.05). Multivariate analysis identified TSP-1 (β = 0.276,
p
< 0.05) concentrations, as well as female sex (β = 0.199,
p
< 0.05), as direct correlates of platelet aggregability, and SDMA concentrations (β = − 0.292,
p
< 0.05) as an inverse correlate.
Conclusion
We conclude that platelet hyperaggregability, where present in the context of AF, may be engendered by impaired availability of NO, as well as via MPO-related inflammatory activation.]]></description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Atrial Fibrillation - immunology</subject><subject>Atrial Fibrillation - pathology</subject><subject>Cardiology</subject><subject>Female</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocarditis - immunology</subject><subject>Myocarditis - pathology</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide - immunology</subject><subject>Original Article</subject><subject>Peroxidase - blood</subject><subject>Peroxidase - immunology</subject><subject>Platelet Aggregation - immunology</subject><subject>Reactive Oxygen Species - blood</subject><subject>Reactive Oxygen Species - immunology</subject><issn>0340-9937</issn><issn>1615-6692</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU9LAzEQxYMoWqsfwIssePGyOkk2yeamFP-BoAc9h-x2to1sd2uSIvvtTWkVEcRTJuT33mTmEXJC4YICqMsAAELnQEVecC7yYYeMqEw3KTXbJSPgBeRac3VADkN4gwRqBvvkgEnKRSHLEbl6bm3EFmM2H5bo7WzmcWYr17o4ZK7LljY67GLIPlycZzZ6Z9uscZV3bRK6vjsie41tAx5vzzF5vb15mdznj093D5Prx7wumIo5Kq4aqGvgja6Kik0rVVSKUZsqkMoKJqwtBJZYQk1xKqa6KUGUjGqOijI-Jucb36Xv31cYolm4UGP6RYf9KhhaClBKAOf_o0orxrSgMqFnv9C3fuW7NEiipGCSKVj3phuq9n0IHhuz9G5h_WAomHUSZpOESQs26yTMkDSnW-dVtcDpt-Jr9QlgGyCkp26G_kfrP10_AXFPkvk</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Procter, Nathan E.K.</creator><creator>Ball, Jocasta</creator><creator>Ngo, Doan T.M.</creator><creator>Chirkov, Yuliy Y.</creator><creator>Isenberg, Jeffrey S.</creator><creator>Hylek, Elaine M.</creator><creator>Stewart, Simon</creator><creator>Horowitz, John D.</creator><general>Springer Medizin</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TS</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20160201</creationdate><title>Platelet hyperaggregability in patients with atrial fibrillation</title><author>Procter, Nathan E.K. ; Ball, Jocasta ; Ngo, Doan T.M. ; Chirkov, Yuliy Y. ; Isenberg, Jeffrey S. ; Hylek, Elaine M. ; Stewart, Simon ; Horowitz, John D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-e737f0cc03f9b4b2db74b721a2db067a525aa45e8e80c1ed5d9f80582193e7123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Atrial Fibrillation - immunology</topic><topic>Atrial Fibrillation - pathology</topic><topic>Cardiology</topic><topic>Female</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocarditis - immunology</topic><topic>Myocarditis - pathology</topic><topic>Nitric Oxide - blood</topic><topic>Nitric Oxide - immunology</topic><topic>Original Article</topic><topic>Peroxidase - blood</topic><topic>Peroxidase - immunology</topic><topic>Platelet Aggregation - immunology</topic><topic>Reactive Oxygen Species - blood</topic><topic>Reactive Oxygen Species - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Procter, Nathan E.K.</creatorcontrib><creatorcontrib>Ball, Jocasta</creatorcontrib><creatorcontrib>Ngo, Doan T.M.</creatorcontrib><creatorcontrib>Chirkov, Yuliy Y.</creatorcontrib><creatorcontrib>Isenberg, Jeffrey S.</creatorcontrib><creatorcontrib>Hylek, Elaine M.</creatorcontrib><creatorcontrib>Stewart, Simon</creatorcontrib><creatorcontrib>Horowitz, John D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Herz</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Procter, Nathan E.K.</au><au>Ball, Jocasta</au><au>Ngo, Doan T.M.</au><au>Chirkov, Yuliy Y.</au><au>Isenberg, Jeffrey S.</au><au>Hylek, Elaine M.</au><au>Stewart, Simon</au><au>Horowitz, John D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu</atitle><jtitle>Herz</jtitle><stitle>Herz</stitle><addtitle>Herz</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>41</volume><issue>1</issue><spage>57</spage><epage>62</epage><pages>57-62</pages><issn>0340-9937</issn><eissn>1615-6692</eissn><coden>HERZDW</coden><abstract><![CDATA[Objective
Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myeloperoxidase (MPO) and C-reactive protein (CRP)] and impaired nitric oxide (NO) signaling.
Methods
Clinical and biochemical determinants of adenosine diphosphate (ADP)-induced platelet aggregation were sought in patients (
n
= 106) hospitalized with AF via univariate and multivariate analysis.
Results
Hyper-responsiveness of platelets to ADP was directly (
r
= 0.254,
p
< 0.01) correlated with plasma concentrations of thrombospondin-1 (TSP-1), a matricellular protein that impairs NO responses and contributes to development of oxidative stress. In turn, plasma TSP-1 concentrations were directly correlated with MPO concentrations (
r
= 0.221,
p
< 0.05), while MPO concentrations correlated with those of asymmetric dimethylarginine (ADMA,
r
= 0.220,
p
< 0.05), and its structural isomer symmetric dimethylarginine (SDMA,
r
= 0.192,
p
= 0.05). Multivariate analysis identified TSP-1 (β = 0.276,
p
< 0.05) concentrations, as well as female sex (β = 0.199,
p
< 0.05), as direct correlates of platelet aggregability, and SDMA concentrations (β = − 0.292,
p
< 0.05) as an inverse correlate.
Conclusion
We conclude that platelet hyperaggregability, where present in the context of AF, may be engendered by impaired availability of NO, as well as via MPO-related inflammatory activation.]]></abstract><cop>Munich</cop><pub>Springer Medizin</pub><pmid>26135468</pmid><doi>10.1007/s00059-015-4335-y</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Herz, 2016-02, Vol.41 (1), p.57-62 |
| issn | 0340-9937 1615-6692 |
| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Aged Aged, 80 and over Atrial Fibrillation - immunology Atrial Fibrillation - pathology Cardiology Female Humans Internal Medicine Male Medicine Medicine & Public Health Myocarditis - immunology Myocarditis - pathology Nitric Oxide - blood Nitric Oxide - immunology Original Article Peroxidase - blood Peroxidase - immunology Platelet Aggregation - immunology Reactive Oxygen Species - blood Reactive Oxygen Species - immunology |
| title | Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu |
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