Hyperresponsiveness of platelets in ischemic stroke

Summary Platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activa...

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Veröffentlicht in:Thrombosis and haemostasis 2007-06, Vol.97 (6), p.974-978
Hauptverfasser: Fateh-Moghadam, Suzanne, Htun, Patrik, Tomandl, Bernd, Sander, Dirk, Stellos, Konstantinos, Geisler, Tobias, Langer, Harald, Walton, Kodwo, Handschu, Rene, Garlichs, Christoph, Daniel, Werner G., Gawaz, Meinrad
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container_end_page 978
container_issue 6
container_start_page 974
container_title Thrombosis and haemostasis
container_volume 97
creator Fateh-Moghadam, Suzanne
Htun, Patrik
Tomandl, Bernd
Sander, Dirk
Stellos, Konstantinos
Geisler, Tobias
Langer, Harald
Walton, Kodwo
Handschu, Rene
Garlichs, Christoph
Daniel, Werner G.
Gawaz, Meinrad
description Summary Platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n=74) or stroke (n=64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP]=0.002, p[arachidonic acid]=0.047, p[epinephrine]=0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0–5.2] versus 2.9, [2.3–4.0], p=0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.
doi_str_mv 10.1160/th06-12-0725
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The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n=74) or stroke (n=64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP]=0.002, p[arachidonic acid]=0.047, p[epinephrine]=0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0–5.2] versus 2.9, [2.3–4.0], p=0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.</description><identifier>ISSN: 0340-6245</identifier><identifier>EISSN: 2567-689X</identifier><identifier>DOI: 10.1160/th06-12-0725</identifier><identifier>PMID: 17549300</identifier><identifier>CODEN: THHADQ</identifier><language>eng</language><publisher>Stuttgart: Schattauer Verlag für Medizin und Naturwissenschaften</publisher><subject>Adenosine Diphosphate - metabolism ; Adult ; Aged ; Arachidonic Acid - metabolism ; Biological and medical sciences ; Biomarkers - blood ; Blood coagulation. 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The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n=74) or stroke (n=64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP]=0.002, p[arachidonic acid]=0.047, p[epinephrine]=0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0–5.2] versus 2.9, [2.3–4.0], p=0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.</description><subject>Adenosine Diphosphate - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Arachidonic Acid - metabolism</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood coagulation. Blood cells</subject><subject>Blood Platelets - metabolism</subject><subject>Brain Ischemia - blood</subject><subject>Brain Ischemia - complications</subject><subject>Brain Ischemia - mortality</subject><subject>Collagen - metabolism</subject><subject>Epinephrine - metabolism</subject><subject>Female</subject><subject>flow cytometry</subject><subject>Follow-Up Studies</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Ischemic Attack, Transient - blood</subject><subject>Ischemic Attack, Transient - diagnosis</subject><subject>Ischemic Attack, Transient - etiology</subject><subject>Ischemic Attack, Transient - mortality</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Molecular and cellular biology</subject><subject>Platelet Activation</subject><subject>Platelet Aggregation</subject><subject>Platelet diseases and coagulopathies</subject><subject>Platelet Function Tests</subject><subject>Platelets and Blood Cells</subject><subject>Predictive Value of Tests</subject><subject>Recurrence</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>ROC Curve</subject><subject>Severity of Illness Index</subject><subject>Stroke</subject><subject>Stroke - blood</subject><subject>Stroke - diagnosis</subject><subject>Stroke - etiology</subject><subject>Stroke - mortality</subject><subject>Time Factors</subject><subject>Transient ischemic attack</subject><issn>0340-6245</issn><issn>2567-689X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNq1kT1vFDEQhlcIRI5AR42ugSYs2F5_bRlFwCFFogkSneX1zWod1vbi8Qbl3-PTnUgFFVTWyI_eZ_RO07yk5B2lkrwvE5EtZS1RTDxqNkxI1Urdf3vcbEjHSSsZF2fNM8RbQqjkvXjanFEleN8Rsmm63f0COQMuKaK_gwiI2zRul9kWmKHg1setRzdB8G6LJafv8Lx5MtoZ4cXpPW--fvxwc7Vrr798-nx1ed06JWRpOR0VWE76ASi3go_7UUo7WjFo1ttej5QNWmvRKQKkF6x3daLacQlSa7DdefPmmLvk9GMFLCbUTWCebYS0olFEKEYJqeDbI-hyQswwmiX7YPO9ocQcSjI3OyINZeZQUsVfnXLXIcD-AT61UoHXJ8Cis_OYbXQeHzitScc4rdzFkSuThwDmNq051kb-pPVHurZpS7Er5N-RZcopDAmrxca9mSyEhMUeZpdigVjqR3ZTvZDxiCsY1UkTbFzRZb8UoxlTBqf000wlzNUV_qELF3Dezn_1uf_v634B3WL5IA</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Fateh-Moghadam, Suzanne</creator><creator>Htun, Patrik</creator><creator>Tomandl, Bernd</creator><creator>Sander, Dirk</creator><creator>Stellos, Konstantinos</creator><creator>Geisler, Tobias</creator><creator>Langer, Harald</creator><creator>Walton, Kodwo</creator><creator>Handschu, Rene</creator><creator>Garlichs, Christoph</creator><creator>Daniel, Werner G.</creator><creator>Gawaz, Meinrad</creator><general>Schattauer Verlag für Medizin und Naturwissenschaften</general><general>Schattauer GmbH</general><general>Schattauer</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Hyperresponsiveness of platelets in ischemic stroke</title><author>Fateh-Moghadam, Suzanne ; Htun, Patrik ; Tomandl, Bernd ; Sander, Dirk ; Stellos, Konstantinos ; Geisler, Tobias ; Langer, Harald ; Walton, Kodwo ; Handschu, Rene ; Garlichs, Christoph ; Daniel, Werner G. ; Gawaz, Meinrad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c756t-41f7ea409be14a54fdf66afa5b829a98f12b8885370e09529c88818c46e688ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adenosine Diphosphate - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Arachidonic Acid - metabolism</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Blood coagulation. Blood cells</topic><topic>Blood Platelets - metabolism</topic><topic>Brain Ischemia - blood</topic><topic>Brain Ischemia - complications</topic><topic>Brain Ischemia - mortality</topic><topic>Collagen - metabolism</topic><topic>Epinephrine - metabolism</topic><topic>Female</topic><topic>flow cytometry</topic><topic>Follow-Up Studies</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Ischemic Attack, Transient - blood</topic><topic>Ischemic Attack, Transient - diagnosis</topic><topic>Ischemic Attack, Transient - etiology</topic><topic>Ischemic Attack, Transient - mortality</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Molecular and cellular biology</topic><topic>Platelet Activation</topic><topic>Platelet Aggregation</topic><topic>Platelet diseases and coagulopathies</topic><topic>Platelet Function Tests</topic><topic>Platelets and Blood Cells</topic><topic>Predictive Value of Tests</topic><topic>Recurrence</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>ROC Curve</topic><topic>Severity of Illness Index</topic><topic>Stroke</topic><topic>Stroke - blood</topic><topic>Stroke - diagnosis</topic><topic>Stroke - etiology</topic><topic>Stroke - mortality</topic><topic>Time Factors</topic><topic>Transient ischemic attack</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fateh-Moghadam, Suzanne</creatorcontrib><creatorcontrib>Htun, Patrik</creatorcontrib><creatorcontrib>Tomandl, Bernd</creatorcontrib><creatorcontrib>Sander, Dirk</creatorcontrib><creatorcontrib>Stellos, Konstantinos</creatorcontrib><creatorcontrib>Geisler, Tobias</creatorcontrib><creatorcontrib>Langer, Harald</creatorcontrib><creatorcontrib>Walton, Kodwo</creatorcontrib><creatorcontrib>Handschu, Rene</creatorcontrib><creatorcontrib>Garlichs, Christoph</creatorcontrib><creatorcontrib>Daniel, Werner G.</creatorcontrib><creatorcontrib>Gawaz, Meinrad</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fateh-Moghadam, Suzanne</au><au>Htun, Patrik</au><au>Tomandl, Bernd</au><au>Sander, Dirk</au><au>Stellos, Konstantinos</au><au>Geisler, Tobias</au><au>Langer, Harald</au><au>Walton, Kodwo</au><au>Handschu, Rene</au><au>Garlichs, Christoph</au><au>Daniel, Werner G.</au><au>Gawaz, Meinrad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperresponsiveness of platelets in ischemic stroke</atitle><jtitle>Thrombosis and haemostasis</jtitle><addtitle>Thromb Haemost</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>97</volume><issue>6</issue><spage>974</spage><epage>978</epage><pages>974-978</pages><issn>0340-6245</issn><eissn>2567-689X</eissn><coden>THHADQ</coden><abstract>Summary Platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n=74) or stroke (n=64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP]=0.002, p[arachidonic acid]=0.047, p[epinephrine]=0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0–5.2] versus 2.9, [2.3–4.0], p=0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.</abstract><cop>Stuttgart</cop><pub>Schattauer Verlag für Medizin und Naturwissenschaften</pub><pmid>17549300</pmid><doi>10.1160/th06-12-0725</doi><tpages>5</tpages></addata></record>
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source MEDLINE; Thieme Connect Journals
subjects Adenosine Diphosphate - metabolism
Adult
Aged
Arachidonic Acid - metabolism
Biological and medical sciences
Biomarkers - blood
Blood coagulation. Blood cells
Blood Platelets - metabolism
Brain Ischemia - blood
Brain Ischemia - complications
Brain Ischemia - mortality
Collagen - metabolism
Epinephrine - metabolism
Female
flow cytometry
Follow-Up Studies
Fundamental and applied biological sciences. Psychology
Hematologic and hematopoietic diseases
Humans
Ischemic Attack, Transient - blood
Ischemic Attack, Transient - diagnosis
Ischemic Attack, Transient - etiology
Ischemic Attack, Transient - mortality
Logistic Models
Male
Medical sciences
Middle Aged
Molecular and cellular biology
Platelet Activation
Platelet Aggregation
Platelet diseases and coagulopathies
Platelet Function Tests
Platelets and Blood Cells
Predictive Value of Tests
Recurrence
Risk Assessment
Risk Factors
ROC Curve
Severity of Illness Index
Stroke
Stroke - blood
Stroke - diagnosis
Stroke - etiology
Stroke - mortality
Time Factors
Transient ischemic attack
title Hyperresponsiveness of platelets in ischemic stroke
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