{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T03:47:24Z","timestamp":1793159244530,"version":"4.5.0"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"24","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2020,12,15]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">To assess differences in platelet inhibition during ticagrelor monotherapy (TIC) or dual therapy with ticagrelor and aspirin (TIC+ASP) in patients after percutaneous coronary intervention using a comprehensive panel of functional tests.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In a single\u2010center parallel group, open label, randomized controlled trial, 110 participants were randomized to receive either TIC (n=55) or TIC+ASP (n=55) for 4\u00a0weeks. The primary outcome was the platelet aggregation response with 10\u00a0\u03bcmol\/L thrombin receptor activation peptide\u20106 (TRAP\u20106). The secondary outcomes were platelet aggregation responses and binding of surface activation markers with a panel of other activators. The mean percentage aggregation for 10\u00a0\u03bcmol\/L TRAP\u20106 was similar for the TIC and TIC+ASP groups (mean difference+4.29; 95% CI, \u22120.87 to +9.46). Aggregation was higher in the TIC group compared with the TIC+ASP group with 1\u00a0\u03bcg\/mL (+6.47; +2.04 to +10.90) and 0.5\u00a0\u03bcg\/mL (+14.00; +7.63 to +20.39) collagen related peptide. Aggregation responses with 5\u00a0\u03bcmol\/L TRAP\u20106, 5\u00a0\u03bcmol\/L or 2.5\u00a0\u03bcmol\/L thromboxane A\n              <jats:sub>2<\/jats:sub>\n              receptor agonist and surface activation marker binding with 5\u00a0\u03bcmol\/L TRAP\u20106 or 0.5\u00a0\u03bcg\/mL collagen related peptide were the same between the treatment groups.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Patients with PCI show similar levels of inhibition of most platelet activation pathways with TIC compared with dual therapy with TIC + ASP. However, the greater aggregation response with collagen related peptide during TIC indicates incomplete inhibition of glycoprotein VI (collagen) receptor\u2010mediated platelet activation. This difference in pharmacodynamic response to anti\u2010platelet medication may contribute to the lower bleeding rates observed with TIC compared with dual antiplatelet therapy in recent clinical trials.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Registration Information<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              URL:\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.isrctn.com\">https:\/\/www.isrctn.com<\/jats:ext-link>\n              ; Unique Identifier ISRCTN84335288.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.120.016495","type":"journal-article","created":{"date-parts":[[2020,12,11]],"date-time":"2020-12-11T10:50:14Z","timestamp":1607683814000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["Pharmacodynamic Comparison of Ticagrelor Monotherapy Versus Ticagrelor and Aspirin in Patients After Percutaneous Coronary Intervention: The TEMPLATE (Ticagrelor Monotherapy and Platelet Reactivity) Randomized Controlled Trial"],"prefix":"10.1161","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4638-601X","authenticated-orcid":false,"given":"Thomas W.","family":"Johnson","sequence":"first","affiliation":[{"name":"Bristol Heart InstituteUniversity Hospitals Bristol &amp; 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Weston NHS Foundation Trust Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Riyaad","family":"Aungraheeta","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Reilly\u2010Stitt","sequence":"additional","affiliation":[{"name":"Bristol Heart InstituteUniversity Hospitals Bristol &amp; Weston NHS Foundation Trust Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth","family":"Bowles","sequence":"additional","affiliation":[{"name":"Bristol Heart InstituteUniversity Hospitals Bristol &amp; Weston NHS Foundation Trust Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barnaby C.","family":"Reeves","sequence":"additional","affiliation":[{"name":"Clinical Trials and Evaluation Unit Bristol Trials CentreBristol Medical SchoolUniversity of Bristol Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris A.","family":"Rogers","sequence":"additional","affiliation":[{"name":"Clinical Trials and Evaluation Unit Bristol Trials CentreBristol Medical SchoolUniversity of Bristol Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart J","family":"Mundell","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Baumbach","sequence":"additional","affiliation":[{"name":"William Harvey Research InstituteQueen Mary University of London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew D.","family":"Mumford","sequence":"additional","affiliation":[{"name":"Bristol Heart InstituteUniversity Hospitals Bristol &amp; 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