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Platelet reactivity patterns in patients treated with dual antiplatelet therapy
Aim The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS). Design In this multicentre prospective obser...
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Published in: | European journal of clinical investigation 2019-06, Vol.49 (6), p.e13102-n/a |
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container_start_page | e13102 |
container_title | European journal of clinical investigation |
container_volume | 49 |
creator | Winter, Max‐Paul Schneeweiss, Theresia Cremer, Rolf Biesinger, Benedikt Hengstenberg, Christian Prüller, Florian Wallner, Markus Kolesnik, Ewald Lewinski, Dirk Lang, Irene M. Siller‐Matula, Jolanta M. |
description | Aim
The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS).
Design
In this multicentre prospective observational study, 492 patients with ACS were enrolled. Platelet aggregation was determined by multiple electrode aggregometry after stimulation with adenosine diphosphate (ADP) or arachidonic acid (AA) as agonists in the maintenance phase of treatment with prasugrel or ticagrelor.
Results
Age emerged as the strongest variable influencing aspirin response status: The mean AA‐induced platelet aggregation in patients 49 years (13.1 U vs 8.8 U; P = 0.011). The second strongest discriminator of aspirin response was sex: Male patients had a 40% higher AA‐induced platelet aggregation values than female patients (9.5 U vs 6.8 U; P = 0.026). Platelet count emerged as the only variable influencing ADP antagonists response status showing that patients with platelet count >320 g/L displayed higher ADP‐induced platelet aggregation. About 12% of patients had high on‐treatment platelet reactivity (HTPR) to aspirin, 3% and 4% a HTPR to prasugrel and ticagrelor, respectively, and only 2% displayed HTPR to dual antiplatelet therapy.
Conclusion
When potent platelet inhibitors as prasugrel and ticagrelor are administered with aspirin, HTPR to DAPT plays only a marginal role. |
doi_str_mv | 10.1111/eci.13102 |
format | article |
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The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS).
Design
In this multicentre prospective observational study, 492 patients with ACS were enrolled. Platelet aggregation was determined by multiple electrode aggregometry after stimulation with adenosine diphosphate (ADP) or arachidonic acid (AA) as agonists in the maintenance phase of treatment with prasugrel or ticagrelor.
Results
Age emerged as the strongest variable influencing aspirin response status: The mean AA‐induced platelet aggregation in patients <49 years of age was 49% higher than in those >49 years (13.1 U vs 8.8 U; P = 0.011). The second strongest discriminator of aspirin response was sex: Male patients had a 40% higher AA‐induced platelet aggregation values than female patients (9.5 U vs 6.8 U; P = 0.026). Platelet count emerged as the only variable influencing ADP antagonists response status showing that patients with platelet count >320 g/L displayed higher ADP‐induced platelet aggregation. About 12% of patients had high on‐treatment platelet reactivity (HTPR) to aspirin, 3% and 4% a HTPR to prasugrel and ticagrelor, respectively, and only 2% displayed HTPR to dual antiplatelet therapy.
Conclusion
When potent platelet inhibitors as prasugrel and ticagrelor are administered with aspirin, HTPR to DAPT plays only a marginal role.</description><identifier>ISSN: 0014-2972</identifier><identifier>ISSN: 1365-2362</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/eci.13102</identifier><identifier>PMID: 30882911</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>ACS ; Adenosine ; Adenosine diphosphate ; Agglomeration ; Antagonists ; Arachidonic acid ; Aspirin ; Discriminators ; HTPR ; LTPR ; MEA ; Original ; Platelet aggregation ; platelets ; prasugrel ; Reactivity ; Therapy ; ticagrelor</subject><ispartof>European journal of clinical investigation, 2019-06, Vol.49 (6), p.e13102-n/a</ispartof><rights>2019 The Authors. published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation</rights><rights>2019 The Authors. European Journal of Clinical Investigation published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation.</rights><rights>2019. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4432-400967b357480aae82df957ae0c83e824c0185135bf9a4d530169d882cbacfd83</citedby><cites>FETCH-LOGICAL-c4432-400967b357480aae82df957ae0c83e824c0185135bf9a4d530169d882cbacfd83</cites><orcidid>0000-0002-2945-9742</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30882911$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Winter, Max‐Paul</creatorcontrib><creatorcontrib>Schneeweiss, Theresia</creatorcontrib><creatorcontrib>Cremer, Rolf</creatorcontrib><creatorcontrib>Biesinger, Benedikt</creatorcontrib><creatorcontrib>Hengstenberg, Christian</creatorcontrib><creatorcontrib>Prüller, Florian</creatorcontrib><creatorcontrib>Wallner, Markus</creatorcontrib><creatorcontrib>Kolesnik, Ewald</creatorcontrib><creatorcontrib>Lewinski, Dirk</creatorcontrib><creatorcontrib>Lang, Irene M.</creatorcontrib><creatorcontrib>Siller‐Matula, Jolanta M.</creatorcontrib><title>Platelet reactivity patterns in patients treated with dual antiplatelet therapy</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Aim
The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS).
Design
In this multicentre prospective observational study, 492 patients with ACS were enrolled. Platelet aggregation was determined by multiple electrode aggregometry after stimulation with adenosine diphosphate (ADP) or arachidonic acid (AA) as agonists in the maintenance phase of treatment with prasugrel or ticagrelor.
Results
Age emerged as the strongest variable influencing aspirin response status: The mean AA‐induced platelet aggregation in patients <49 years of age was 49% higher than in those >49 years (13.1 U vs 8.8 U; P = 0.011). The second strongest discriminator of aspirin response was sex: Male patients had a 40% higher AA‐induced platelet aggregation values than female patients (9.5 U vs 6.8 U; P = 0.026). Platelet count emerged as the only variable influencing ADP antagonists response status showing that patients with platelet count >320 g/L displayed higher ADP‐induced platelet aggregation. About 12% of patients had high on‐treatment platelet reactivity (HTPR) to aspirin, 3% and 4% a HTPR to prasugrel and ticagrelor, respectively, and only 2% displayed HTPR to dual antiplatelet therapy.
Conclusion
When potent platelet inhibitors as prasugrel and ticagrelor are administered with aspirin, HTPR to DAPT plays only a marginal role.</description><subject>ACS</subject><subject>Adenosine</subject><subject>Adenosine diphosphate</subject><subject>Agglomeration</subject><subject>Antagonists</subject><subject>Arachidonic acid</subject><subject>Aspirin</subject><subject>Discriminators</subject><subject>HTPR</subject><subject>LTPR</subject><subject>MEA</subject><subject>Original</subject><subject>Platelet aggregation</subject><subject>platelets</subject><subject>prasugrel</subject><subject>Reactivity</subject><subject>Therapy</subject><subject>ticagrelor</subject><issn>0014-2972</issn><issn>1365-2362</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNp1kU1LAzEURYMoWqsL_4AMuNHF1JdkPjIbQUr9AEEXug5p5o1Nmc6MSaal_97YqqhgNskjJ4cbLiEnFEY0rEvUZkQ5BbZDBpRnacx4xnbJAIAmMStydkAOnZsDgKCc7ZMDDkKwgtIBeXyqlccafWRRaW-Wxq-jTnmPtnGRaT7OBhvvIh8Aj2W0Mn4Wlb2qI9V403099zO0qlsfkb1K1Q6PP_chebmZPI_v4ofH2_vx9UOsk4SzOAEosnzK0zwRoBQKVlZFmisELXiYEg1UpJSn06pQSZlyoFlRhtB6qnRVCj4kV1tv108XWOoQ0apadtYslF3LVhn5-6YxM_naLmWWFjwXLAjOPwW2fevRebkwTmNdqwbb3klGC55BxgECevYHnbe9bcL3JGOc8hzYRnixpbRtnbNYfYehID9qkqEmuakpsKc_03-TX70E4HILrEyN6_9NcjK-3yrfATBSnJs</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Winter, Max‐Paul</creator><creator>Schneeweiss, Theresia</creator><creator>Cremer, Rolf</creator><creator>Biesinger, Benedikt</creator><creator>Hengstenberg, Christian</creator><creator>Prüller, Florian</creator><creator>Wallner, Markus</creator><creator>Kolesnik, Ewald</creator><creator>Lewinski, Dirk</creator><creator>Lang, Irene M.</creator><creator>Siller‐Matula, Jolanta M.</creator><general>Blackwell Publishing Ltd</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2945-9742</orcidid></search><sort><creationdate>201906</creationdate><title>Platelet reactivity patterns in patients treated with dual antiplatelet therapy</title><author>Winter, Max‐Paul ; Schneeweiss, Theresia ; Cremer, Rolf ; Biesinger, Benedikt ; Hengstenberg, Christian ; Prüller, Florian ; Wallner, Markus ; Kolesnik, Ewald ; Lewinski, Dirk ; Lang, Irene M. ; Siller‐Matula, Jolanta M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4432-400967b357480aae82df957ae0c83e824c0185135bf9a4d530169d882cbacfd83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>ACS</topic><topic>Adenosine</topic><topic>Adenosine diphosphate</topic><topic>Agglomeration</topic><topic>Antagonists</topic><topic>Arachidonic acid</topic><topic>Aspirin</topic><topic>Discriminators</topic><topic>HTPR</topic><topic>LTPR</topic><topic>MEA</topic><topic>Original</topic><topic>Platelet aggregation</topic><topic>platelets</topic><topic>prasugrel</topic><topic>Reactivity</topic><topic>Therapy</topic><topic>ticagrelor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Winter, Max‐Paul</creatorcontrib><creatorcontrib>Schneeweiss, Theresia</creatorcontrib><creatorcontrib>Cremer, Rolf</creatorcontrib><creatorcontrib>Biesinger, Benedikt</creatorcontrib><creatorcontrib>Hengstenberg, Christian</creatorcontrib><creatorcontrib>Prüller, Florian</creatorcontrib><creatorcontrib>Wallner, Markus</creatorcontrib><creatorcontrib>Kolesnik, Ewald</creatorcontrib><creatorcontrib>Lewinski, Dirk</creatorcontrib><creatorcontrib>Lang, Irene M.</creatorcontrib><creatorcontrib>Siller‐Matula, Jolanta M.</creatorcontrib><collection>Wiley Open Access</collection><collection>Wiley Online Library</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Winter, Max‐Paul</au><au>Schneeweiss, Theresia</au><au>Cremer, Rolf</au><au>Biesinger, Benedikt</au><au>Hengstenberg, Christian</au><au>Prüller, Florian</au><au>Wallner, Markus</au><au>Kolesnik, Ewald</au><au>Lewinski, Dirk</au><au>Lang, Irene M.</au><au>Siller‐Matula, Jolanta M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet reactivity patterns in patients treated with dual antiplatelet therapy</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2019-06</date><risdate>2019</risdate><volume>49</volume><issue>6</issue><spage>e13102</spage><epage>n/a</epage><pages>e13102-n/a</pages><issn>0014-2972</issn><issn>1365-2362</issn><eissn>1365-2362</eissn><abstract>Aim
The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS).
Design
In this multicentre prospective observational study, 492 patients with ACS were enrolled. Platelet aggregation was determined by multiple electrode aggregometry after stimulation with adenosine diphosphate (ADP) or arachidonic acid (AA) as agonists in the maintenance phase of treatment with prasugrel or ticagrelor.
Results
Age emerged as the strongest variable influencing aspirin response status: The mean AA‐induced platelet aggregation in patients <49 years of age was 49% higher than in those >49 years (13.1 U vs 8.8 U; P = 0.011). The second strongest discriminator of aspirin response was sex: Male patients had a 40% higher AA‐induced platelet aggregation values than female patients (9.5 U vs 6.8 U; P = 0.026). Platelet count emerged as the only variable influencing ADP antagonists response status showing that patients with platelet count >320 g/L displayed higher ADP‐induced platelet aggregation. About 12% of patients had high on‐treatment platelet reactivity (HTPR) to aspirin, 3% and 4% a HTPR to prasugrel and ticagrelor, respectively, and only 2% displayed HTPR to dual antiplatelet therapy.
Conclusion
When potent platelet inhibitors as prasugrel and ticagrelor are administered with aspirin, HTPR to DAPT plays only a marginal role.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>30882911</pmid><doi>10.1111/eci.13102</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2945-9742</orcidid><oa>free_for_read</oa></addata></record> |
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source | Wiley-Blackwell Read & Publish Collection |
subjects | ACS Adenosine Adenosine diphosphate Agglomeration Antagonists Arachidonic acid Aspirin Discriminators HTPR LTPR MEA Original Platelet aggregation platelets prasugrel Reactivity Therapy ticagrelor |
title | Platelet reactivity patterns in patients treated with dual antiplatelet therapy |
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