Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy
Essentials Total thrombus‐formation analysis system (T‐TAS) quantitatively measures platelet thrombus formation. We examined the utility of T‐TAS in patients with coronary artery disease. T‐TAS can discriminate different types of the antiplatelet therapy in the same measuring method. Genetic backgro...
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| Veröffentlicht in: | Journal of thrombosis and haemostasis 2016-04, Vol.14 (4), p.850-859 |
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| creator | Arima, Y. Kaikita, K. Ishii, M. Ito, M. Sueta, D. Oimatsu, Y. Sakamoto, K. Tsujita, K. Kojima, S. Nakagawa, K. Hokimoto, S. Ogawa, H. |
| description | Essentials
Total thrombus‐formation analysis system (T‐TAS) quantitatively measures platelet thrombus formation.
We examined the utility of T‐TAS in patients with coronary artery disease.
T‐TAS can discriminate different types of the antiplatelet therapy in the same measuring method.
Genetic background, cytochrome P‐450 2C19 genotypes, also influenced T‐TAS parameters.
Summary
Background
Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus‐formation analysis system (T‐TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL‐chip]; collagen plus tissue factor, atherome chip [AR‐chip]). We examined the utility of the T‐TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD).
Methods and Results
In this cross‐sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T‐TAS to measure the platelet thrombus‐formation area under the curve (AUC) at various shear rates (1500 s−1 [PL18‐AUC10] and 2000 s−1 [PL24‐AUC10] for the PL‐chip; 300 s−1 [AR10‐AUC30] for the AR‐chip). The on‐clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24‐AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9–387.1) in the control group, 256 ± 108 (95% CI 230.5–281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4–127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24‐AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4–200.6) than in the non‐PM group (87 ± 74, 95% CI 73.8–100.2).
Conclusions
Our findings suggest that the PL24‐AUC10 level measured by the T‐TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients. |
| doi_str_mv | 10.1111/jth.13256 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1780006624</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4017966201</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3886-9f0e8c56709a257fc8822f2c2f5a29525e751922916716a97bfaf24ad93505b03</originalsourceid><addsrcrecordid>eNp1kU1OHDEQha0oKBDIIheILGWVxYB_8N8SIRISIWUD65anu8x41N3uuDyg3uUIuQX34iQxzEx28aas8lev_PQI-cjZKa_nbF1Wp1wKpd-QI66kXRgr9dv93Ul5SN4jrhnjTgn2jhwKbYwUzh6RpwtEQBxgLDQFOvW-QA_l-fefDnJ8gI6WVU7DMt3DGNtYZvoYy6o2gZZUfL973mCdCCkPvsQ0Uj_6fsaIFGcsMNA40jblNPo8U58L1NJFBI9ApzpRlyPN0EJ8iON9nS5x_5GXTdlP8wk5CL5H-LCrx-Tu69Xt5fXi5ue375cXN4tWWqsXLjCwrdKGOS-UCa21QgTRiqC8qOYVGMWdEI5rw7V3Zhl8EOe-c1IxtWTymHze6k45_doAlmadNrnawYYbyxjTWpxX6suWanNCzBCaKcehums4a14iaWokzWsklf20U9wsB-j-kfsMKnC2BR5jD_P_lZoft9dbyb9O0pxr</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1780006624</pqid></control><display><type>article</type><title>Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Arima, Y. ; Kaikita, K. ; Ishii, M. ; Ito, M. ; Sueta, D. ; Oimatsu, Y. ; Sakamoto, K. ; Tsujita, K. ; Kojima, S. ; Nakagawa, K. ; Hokimoto, S. ; Ogawa, H.</creator><creatorcontrib>Arima, Y. ; Kaikita, K. ; Ishii, M. ; Ito, M. ; Sueta, D. ; Oimatsu, Y. ; Sakamoto, K. ; Tsujita, K. ; Kojima, S. ; Nakagawa, K. ; Hokimoto, S. ; Ogawa, H.</creatorcontrib><description>Essentials
Total thrombus‐formation analysis system (T‐TAS) quantitatively measures platelet thrombus formation.
We examined the utility of T‐TAS in patients with coronary artery disease.
T‐TAS can discriminate different types of the antiplatelet therapy in the same measuring method.
Genetic background, cytochrome P‐450 2C19 genotypes, also influenced T‐TAS parameters.
Summary
Background
Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus‐formation analysis system (T‐TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL‐chip]; collagen plus tissue factor, atherome chip [AR‐chip]). We examined the utility of the T‐TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD).
Methods and Results
In this cross‐sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T‐TAS to measure the platelet thrombus‐formation area under the curve (AUC) at various shear rates (1500 s−1 [PL18‐AUC10] and 2000 s−1 [PL24‐AUC10] for the PL‐chip; 300 s−1 [AR10‐AUC30] for the AR‐chip). The on‐clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24‐AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9–387.1) in the control group, 256 ± 108 (95% CI 230.5–281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4–127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24‐AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4–200.6) than in the non‐PM group (87 ± 74, 95% CI 73.8–100.2).
Conclusions
Our findings suggest that the PL24‐AUC10 level measured by the T‐TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.</description><identifier>ISSN: 1538-7933</identifier><identifier>ISSN: 1538-7836</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/jth.13256</identifier><identifier>PMID: 26773298</identifier><language>eng</language><publisher>England: Elsevier Limited</publisher><subject>Aged ; antiplatelet therapy ; Area Under Curve ; Aspirin - administration & dosage ; Blood Platelets - drug effects ; clopidogrel ; Coronary Artery Disease - blood ; Coronary Artery Disease - drug therapy ; Cross-Sectional Studies ; CYP2C19 ; Cytochrome P-450 CYP2C19 - genetics ; Electrocardiography ; Female ; Genotype ; Humans ; Male ; Middle Aged ; new device ; percutaneous coronary intervention ; Phenotype ; Platelet Aggregation ; Platelet Aggregation Inhibitors - blood ; Platelet Aggregation Inhibitors - therapeutic use ; Platelet Function Tests ; Polymorphism, Genetic ; Thrombosis - blood ; Thrombosis - drug therapy ; Thrombosis - genetics ; Ticlopidine - administration & dosage ; Ticlopidine - analogs & derivatives</subject><ispartof>Journal of thrombosis and haemostasis, 2016-04, Vol.14 (4), p.850-859</ispartof><rights>2016 International Society on Thrombosis and Haemostasis</rights><rights>2016 International Society on Thrombosis and Haemostasis.</rights><rights>Copyright © 2016 International Society on Thrombosis and Haemostasis</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3886-9f0e8c56709a257fc8822f2c2f5a29525e751922916716a97bfaf24ad93505b03</citedby><cites>FETCH-LOGICAL-c3886-9f0e8c56709a257fc8822f2c2f5a29525e751922916716a97bfaf24ad93505b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26773298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arima, Y.</creatorcontrib><creatorcontrib>Kaikita, K.</creatorcontrib><creatorcontrib>Ishii, M.</creatorcontrib><creatorcontrib>Ito, M.</creatorcontrib><creatorcontrib>Sueta, D.</creatorcontrib><creatorcontrib>Oimatsu, Y.</creatorcontrib><creatorcontrib>Sakamoto, K.</creatorcontrib><creatorcontrib>Tsujita, K.</creatorcontrib><creatorcontrib>Kojima, S.</creatorcontrib><creatorcontrib>Nakagawa, K.</creatorcontrib><creatorcontrib>Hokimoto, S.</creatorcontrib><creatorcontrib>Ogawa, H.</creatorcontrib><title>Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Essentials
Total thrombus‐formation analysis system (T‐TAS) quantitatively measures platelet thrombus formation.
We examined the utility of T‐TAS in patients with coronary artery disease.
T‐TAS can discriminate different types of the antiplatelet therapy in the same measuring method.
Genetic background, cytochrome P‐450 2C19 genotypes, also influenced T‐TAS parameters.
Summary
Background
Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus‐formation analysis system (T‐TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL‐chip]; collagen plus tissue factor, atherome chip [AR‐chip]). We examined the utility of the T‐TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD).
Methods and Results
In this cross‐sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T‐TAS to measure the platelet thrombus‐formation area under the curve (AUC) at various shear rates (1500 s−1 [PL18‐AUC10] and 2000 s−1 [PL24‐AUC10] for the PL‐chip; 300 s−1 [AR10‐AUC30] for the AR‐chip). The on‐clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24‐AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9–387.1) in the control group, 256 ± 108 (95% CI 230.5–281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4–127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24‐AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4–200.6) than in the non‐PM group (87 ± 74, 95% CI 73.8–100.2).
Conclusions
Our findings suggest that the PL24‐AUC10 level measured by the T‐TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.</description><subject>Aged</subject><subject>antiplatelet therapy</subject><subject>Area Under Curve</subject><subject>Aspirin - administration & dosage</subject><subject>Blood Platelets - drug effects</subject><subject>clopidogrel</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Cross-Sectional Studies</subject><subject>CYP2C19</subject><subject>Cytochrome P-450 CYP2C19 - genetics</subject><subject>Electrocardiography</subject><subject>Female</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>new device</subject><subject>percutaneous coronary intervention</subject><subject>Phenotype</subject><subject>Platelet Aggregation</subject><subject>Platelet Aggregation Inhibitors - blood</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Platelet Function Tests</subject><subject>Polymorphism, Genetic</subject><subject>Thrombosis - blood</subject><subject>Thrombosis - drug therapy</subject><subject>Thrombosis - genetics</subject><subject>Ticlopidine - administration & dosage</subject><subject>Ticlopidine - analogs & derivatives</subject><issn>1538-7933</issn><issn>1538-7836</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1OHDEQha0oKBDIIheILGWVxYB_8N8SIRISIWUD65anu8x41N3uuDyg3uUIuQX34iQxzEx28aas8lev_PQI-cjZKa_nbF1Wp1wKpd-QI66kXRgr9dv93Ul5SN4jrhnjTgn2jhwKbYwUzh6RpwtEQBxgLDQFOvW-QA_l-fefDnJ8gI6WVU7DMt3DGNtYZvoYy6o2gZZUfL973mCdCCkPvsQ0Uj_6fsaIFGcsMNA40jblNPo8U58L1NJFBI9ApzpRlyPN0EJ8iON9nS5x_5GXTdlP8wk5CL5H-LCrx-Tu69Xt5fXi5ue375cXN4tWWqsXLjCwrdKGOS-UCa21QgTRiqC8qOYVGMWdEI5rw7V3Zhl8EOe-c1IxtWTymHze6k45_doAlmadNrnawYYbyxjTWpxX6suWanNCzBCaKcehums4a14iaWokzWsklf20U9wsB-j-kfsMKnC2BR5jD_P_lZoft9dbyb9O0pxr</recordid><startdate>201604</startdate><enddate>201604</enddate><creator>Arima, Y.</creator><creator>Kaikita, K.</creator><creator>Ishii, M.</creator><creator>Ito, M.</creator><creator>Sueta, D.</creator><creator>Oimatsu, Y.</creator><creator>Sakamoto, K.</creator><creator>Tsujita, K.</creator><creator>Kojima, S.</creator><creator>Nakagawa, K.</creator><creator>Hokimoto, S.</creator><creator>Ogawa, H.</creator><general>Elsevier Limited</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>7T5</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>201604</creationdate><title>Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy</title><author>Arima, Y. ; Kaikita, K. ; Ishii, M. ; Ito, M. ; Sueta, D. ; Oimatsu, Y. ; Sakamoto, K. ; Tsujita, K. ; Kojima, S. ; Nakagawa, K. ; Hokimoto, S. ; Ogawa, H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3886-9f0e8c56709a257fc8822f2c2f5a29525e751922916716a97bfaf24ad93505b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>antiplatelet therapy</topic><topic>Area Under Curve</topic><topic>Aspirin - administration & dosage</topic><topic>Blood Platelets - drug effects</topic><topic>clopidogrel</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Cross-Sectional Studies</topic><topic>CYP2C19</topic><topic>Cytochrome P-450 CYP2C19 - genetics</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>new device</topic><topic>percutaneous coronary intervention</topic><topic>Phenotype</topic><topic>Platelet Aggregation</topic><topic>Platelet Aggregation Inhibitors - blood</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Platelet Function Tests</topic><topic>Polymorphism, Genetic</topic><topic>Thrombosis - blood</topic><topic>Thrombosis - drug therapy</topic><topic>Thrombosis - genetics</topic><topic>Ticlopidine - administration & dosage</topic><topic>Ticlopidine - analogs & derivatives</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arima, Y.</creatorcontrib><creatorcontrib>Kaikita, K.</creatorcontrib><creatorcontrib>Ishii, M.</creatorcontrib><creatorcontrib>Ito, M.</creatorcontrib><creatorcontrib>Sueta, D.</creatorcontrib><creatorcontrib>Oimatsu, Y.</creatorcontrib><creatorcontrib>Sakamoto, K.</creatorcontrib><creatorcontrib>Tsujita, K.</creatorcontrib><creatorcontrib>Kojima, S.</creatorcontrib><creatorcontrib>Nakagawa, K.</creatorcontrib><creatorcontrib>Hokimoto, S.</creatorcontrib><creatorcontrib>Ogawa, H.</creatorcontrib><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><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arima, Y.</au><au>Kaikita, K.</au><au>Ishii, M.</au><au>Ito, M.</au><au>Sueta, D.</au><au>Oimatsu, Y.</au><au>Sakamoto, K.</au><au>Tsujita, K.</au><au>Kojima, S.</au><au>Nakagawa, K.</au><au>Hokimoto, S.</au><au>Ogawa, H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2016-04</date><risdate>2016</risdate><volume>14</volume><issue>4</issue><spage>850</spage><epage>859</epage><pages>850-859</pages><issn>1538-7933</issn><issn>1538-7836</issn><eissn>1538-7836</eissn><abstract>Essentials
Total thrombus‐formation analysis system (T‐TAS) quantitatively measures platelet thrombus formation.
We examined the utility of T‐TAS in patients with coronary artery disease.
T‐TAS can discriminate different types of the antiplatelet therapy in the same measuring method.
Genetic background, cytochrome P‐450 2C19 genotypes, also influenced T‐TAS parameters.
Summary
Background
Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus‐formation analysis system (T‐TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL‐chip]; collagen plus tissue factor, atherome chip [AR‐chip]). We examined the utility of the T‐TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD).
Methods and Results
In this cross‐sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T‐TAS to measure the platelet thrombus‐formation area under the curve (AUC) at various shear rates (1500 s−1 [PL18‐AUC10] and 2000 s−1 [PL24‐AUC10] for the PL‐chip; 300 s−1 [AR10‐AUC30] for the AR‐chip). The on‐clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24‐AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9–387.1) in the control group, 256 ± 108 (95% CI 230.5–281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4–127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24‐AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4–200.6) than in the non‐PM group (87 ± 74, 95% CI 73.8–100.2).
Conclusions
Our findings suggest that the PL24‐AUC10 level measured by the T‐TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.</abstract><cop>England</cop><pub>Elsevier Limited</pub><pmid>26773298</pmid><doi>10.1111/jth.13256</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of thrombosis and haemostasis, 2016-04, Vol.14 (4), p.850-859 |
| issn | 1538-7933 1538-7836 1538-7836 |
| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aged antiplatelet therapy Area Under Curve Aspirin - administration & dosage Blood Platelets - drug effects clopidogrel Coronary Artery Disease - blood Coronary Artery Disease - drug therapy Cross-Sectional Studies CYP2C19 Cytochrome P-450 CYP2C19 - genetics Electrocardiography Female Genotype Humans Male Middle Aged new device percutaneous coronary intervention Phenotype Platelet Aggregation Platelet Aggregation Inhibitors - blood Platelet Aggregation Inhibitors - therapeutic use Platelet Function Tests Polymorphism, Genetic Thrombosis - blood Thrombosis - drug therapy Thrombosis - genetics Ticlopidine - administration & dosage Ticlopidine - analogs & derivatives |
| title | Assessment of platelet‐derived thrombogenicity with the total thrombus‐formation analysis system in coronary artery disease patients receiving antiplatelet therapy |
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