{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T12:27:50Z","timestamp":1753878470032,"version":"3.41.2"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2022,5,16]],"date-time":"2022-05-16T00:00:00Z","timestamp":1652659200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100005788","name":"Medizinische Universit\u00e4t Wien","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005788","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabet Med"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Antiplatelet therapy is a cornerstone in the secondary prevention of ischemic events following percutaneous coronary intervention (PCI). The new P2Y<jats:sub>12<\/jats:sub> receptor inhibitors prasugrel and ticagrelor have been shown to improve patients' outcomes. Whether or not these drugs have equal efficacy in individuals with or without diabetes is disputed. Furthermore, platelets can be activated by thrombin, which is, at least in part, independent of P2Y<jats:sub>12<\/jats:sub>\u2010mediated platelet activation. Protease\u2010activated receptor (PAR)\u20101 and \u22124 are thrombin receptors on human platelets. We sought to compare the in vitro efficacy of prasugrel (<jats:italic>n<\/jats:italic>\u00a0=\u00a0121) and ticagrelor (<jats:italic>n<\/jats:italic>\u00a0=\u00a099) to inhibit PAR\u2010mediated platelet aggregation in individuals with type 2 diabetes (prasugrel <jats:italic>n<\/jats:italic>\u00a0=\u00a026, ticagrelor <jats:italic>n<\/jats:italic>\u00a0=\u00a029).<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>We compared P2Y<jats:sub>12<\/jats:sub>\u2010, PAR\u20101\u2010 and PAR\u20104\u2010mediated platelet aggregation as assessed by multiple electrode platelet aggregometry between prasugrel\u2010 and ticagrelor\u2010treated patients without and with type 2 diabetes who underwent acute PCI.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Overall, there were no differences of P2Y<jats:sub>12<\/jats:sub>\u2010, PAR\u20101\u2010 and PAR\u20104\u2010mediated platelet aggregation between prasugrel\u2010 and ticagrelor\u2010treated patients. However, both drugs inhibited P2Y<jats:sub>12<\/jats:sub>\u2010mediated platelet aggregation stronger, and thereby to a similar extent in patients with type 2 diabetes than in those without diabetes. There was no correlation between either P2Y<jats:sub>12<\/jats:sub>\u2010, or PAR\u20101\u2010 or PAR\u20104\u2010mediated platelet aggregation and levels of HbA1c or the body mass index (BMI). However, we observed patients with high residual platelet reactivity in response to PAR\u20101 and PAR\u20104 stimulation in all cohorts.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Prasugrel and ticagrelor inhibit P2Y<jats:sub>12<\/jats:sub>\u2010 and PAR\u2010mediated platelet aggregation in individuals with diabetes to a similar extent, irrespective of HbA<jats:sub>1c<\/jats:sub> levels and BMI.<\/jats:p><\/jats:sec>","DOI":"10.1111\/dme.14868","type":"journal-article","created":{"date-parts":[[2022,5,6]],"date-time":"2022-05-06T08:33:35Z","timestamp":1651826015000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Protease\u2010activated receptor\u2010mediated platelet aggregation in patients with type 2 diabetes on potent <scp>P2Y<\/scp><sub>12<\/sub> inhibitors"],"prefix":"10.1111","volume":"39","author":[{"given":"Benjamin","family":"Panzer","sequence":"first","affiliation":[{"name":"Department of Internal Medicine II Medical University of Vienna  Vienna Austria"},{"name":"Sigmund Freud University, Medical School  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patricia P.","family":"Wadowski","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II Medical University of Vienna  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kurt","family":"Huber","sequence":"additional","affiliation":[{"name":"Sigmund Freud University, Medical School  Vienna Austria"},{"name":"3rd Department of Medicine Cardiology and Intensive Care Medicine, Wilhelminen Hospital  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon","family":"Panzer","sequence":"additional","affiliation":[{"name":"Department of Blood Group Serology and Transfusion Medicine Medical University of Vienna  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Gremmel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II Medical University of Vienna  Vienna Austria"},{"name":"Institute of Antithrombotic Therapy in Cardiovascular Disease Karl Landsteiner Society  St. P\u00f6lten Austria"},{"name":"Department of Internal Medicine I Cardiology and Intensive Care Medicine, Landesklinikum Mistelbach\u2010G\u00e4nserndorf  Mistelbach 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