{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T14:07:18Z","timestamp":1772114838806,"version":"3.50.1"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"23","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,12,3]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              After a loading dose of ticagrelor, the rate of high on\u2010treatment platelet reactivity remains elevated, which increases periprocedural myocardial infarction and injury. This indicates that faster platelet inhibition with crushed ticagrelor (\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              ) or eptifibatide is needed to reduce high on\u2010treatment platelet reactivity. The efficacy of\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              versus eptifibatide bolus plus clopidogrel is unknown.\n            <\/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              A total of 100 P2Y\n              <jats:sub>12<\/jats:sub>\n              na\u00efve, troponin\u2010negative patients with acute coronary syndrome were randomized to\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              (180\u00a0mg) versus eptifibatide bolus (180\u00a0\u03bcg\/kg\u00d72 intravenous boluses) plus clopidogrel (600\u00a0mg) at the time of percutaneous coronary intervention. High on\u2010treatment platelet reactivity was markedly higher with\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              versus eptifibatide bolus plus clopidogrel (42% versus 0%;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001) at 30\u00a0minutes and persisted up to 2\u00a0hours (12% versus 0%;\n              <jats:italic>P<\/jats:italic>\n              =0.01, respectively). Platelet aggregation by adenosine diphosphate dropped faster from baseline with eptifibatide bolus plus clopidogrel versus\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              (0.5 versus 2\u00a0hours, respectively) and was higher with\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              versus eptifibatide bolus plus clopidogrel at 0.5, 2, and 4\u00a0hours after loading dose (53\u00b112% versus 1.3\u00b12%; 35\u00b111% versus 0.34\u00b11.0%; and 23\u00b19% versus 3.5\u00b12%, respectively;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001). Eptifibatide bolus plus clopidogrel, but not\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              , significantly inhibited platelet aggregation induced by thrombin\u2010receptor activating peptide. Periprocedural myocardial infarction and injury was higher with\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              versus eptifibatide bolus plus clopidogrel (48% versus 28%, respectively;\n              <jats:italic>P<\/jats:italic>\n              =0.035). Post\u2013percutaneous coronary intervention hemoglobin levels were not different between 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\">\n              Eptifibatide bolus plus clopidogrel led to faster and more potent platelet inhibition than\n              <jats:styled-content style=\"fixed-case\">CTIC<\/jats:styled-content>\n              and reduced periprocedural myocardial infarction and injury in troponin\u2010negative acute coronary syndrome patients undergoing percutaneous coronary intervention, with no significant hemoglobin drop after percutaneous coronary intervention.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Clinical Trial Registration<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">URL<\/jats:styled-content>\n              :\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/www.clinicaltrials.gov\">http:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n              . Unique identifier:\n              <jats:styled-content style=\"fixed-case\">NCT<\/jats:styled-content>\n              02925923.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.012844","type":"journal-article","created":{"date-parts":[[2019,11,26]],"date-time":"2019-11-26T10:00:24Z","timestamp":1574762424000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":12,"title":["Effects of Crushed Ticagrelor Versus Eptifibatide Bolus Plus Clopidogrel in Troponin\u2010Negative Acute Coronary Syndrome Patients Undergoing Percutaneous Coronary Intervention: A Randomized Clinical Trial"],"prefix":"10.1161","volume":"8","author":[{"given":"Moazez J.","family":"Marian","sequence":"first","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hussein","family":"Abu Daya","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arka","family":"Chatterjee","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Firas","family":"Al Solaiman","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark F.","family":"Sasse","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William S.","family":"Fonbah","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raymond W.","family":"Workman","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brittany E.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah E.","family":"Carlson","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brigitta C.","family":"Brott","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sumanth D.","family":"Prabhu","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Massoud A.","family":"Leesar","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehv717"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehv320"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2015.11.044"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1160\/TH16-08-0670"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/s40262-015-0320-0"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.117.005562"},{"key":"e_1_3_1_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcin.2012.01.006"},{"key":"e_1_3_1_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.118.038317"},{"key":"e_1_3_1_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2011.04.017"},{"key":"e_1_3_1_11_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2011.1332"},{"key":"e_1_3_1_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.812636"},{"key":"e_1_3_1_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.80.2.410"},{"key":"e_1_3_1_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2013.01.014"},{"key":"e_1_3_1_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2014.08.056"},{"key":"e_1_3_1_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2008.09.060"},{"key":"e_1_3_1_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2008.03.030"},{"key":"e_1_3_1_18_2","doi-asserted-by":"publisher","DOI":"10.1080\/09537100802351065"},{"key":"e_1_3_1_19_2","first-page":"15","article-title":"Personalized antiplatelet therapy: state of art","volume":"1","author":"Gurbel PA","year":"2012","unstructured":"Gurbel PA, Young\u2010Hoon J, Udaya ST. 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