{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,8,25]],"date-time":"2024-08-25T04:35:07Z","timestamp":1724560507635},"reference-count":34,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2015,9,11]],"date-time":"2015-09-11T00:00:00Z","timestamp":1441929600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Dihydropyridine calcium\u2010channel blockers (<jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s) inhibit cytochrome 3A4 and could therefore interfere with the conversion of clopidogrel to its active form. The impact of <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s on the antiplatelet effect of clopidogrel has not been studied with assays directly capturing platelet activation to adenosine diphosphate (<jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>), so far. We therefore sought to investigate platelet activation in response to <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content> by flow cytometry in clopidogrel\u2010treated patients without and with <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Platelet surface P\u2010selectin expression and activated glycoprotein (<jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>) <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a in response to <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content> were determined by flow cytometry in 302 patients on dual antiplatelet therapy with aspirin and clopidogrel after successful angioplasty with stent implantation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Ninety\u2010two patients (30.5%) received <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s. Patients with concomitant <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content> therapy showed significantly higher platelet surface expressions of P\u2010selectin and activated <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a in response to <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content> than patients without <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s (both <jats:italic>P<\/jats:italic>\u00a0\u2264\u00a00.03). Moreover, the fold increase of P\u2010selectin and activated <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a in response to <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content> was significantly more pronounced in patients taking <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s (both <jats:italic>P<\/jats:italic>\u00a0\u2264\u00a00.03). The associations of <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010inducible activated <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a and fold increase of activated <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a after the addition of <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content> with <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content> therapy remained significant after adjustment for differences in patient characteristics and factors that were previously associated with clopidogrel response by multivariate regression analyses (both <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). High levels of <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010inducible P\u2010selectin and activated <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a were seen significantly more frequent in patients with <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s than in patients without <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content> therapy (both <jats:italic>P<\/jats:italic>\u00a0\u2264\u00a00.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Dihydropyridine <jats:styled-content style=\"fixed-case\">CCB<\/jats:styled-content>s attenuate the effect of clopidogrel on <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010inducible platelet activation in patients undergoing angioplasty and stenting for cardiovascular disease.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12138","type":"journal-article","created":{"date-parts":[[2015,5,25]],"date-time":"2015-05-25T21:01:50Z","timestamp":1432587710000},"page":"264-269","source":"Crossref","is-referenced-by-count":12,"title":["Calcium\u2010Channel Blockers Attenuate the Antiplatelet Effect of Clopidogrel"],"prefix":"10.1111","volume":"33","author":[{"given":"Thomas","family":"Gremmel","sequence":"first","affiliation":[{"name":"Department of Internal Medicine II Medical University of Vienna Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Markus","family":"Durstberger","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II Medical University of Vienna Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beate","family":"Eichelberger","sequence":"additional","affiliation":[{"name":"Department of Blood Group Serology and Transfusion Medicine Medical University of 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