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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F14%3A33151350%21RIV15-MSM-15110___
rdf:type
skos:Concept n18:Vysledek
dcterms:description
Backround: Antiaggregation therapy is still the most frequently used approach to prevent thrombotic events in cardiovascular diseases. It has a good clinical effect but increasing evidence shows high residual platelet aggregation activity in a number of patients. Laboratory methods only allow us to detect clopidogrel %22non-responders%22 or %22low responders%22. Recent methods are based on monitoring residual platelet aggregation activity (aggregation methods) or detecting the number of free epitopes for binding a specific monoclonal antibody such as vasodilator-stimulated phosphoprotein phosphorylation (VASP). Methods: The aims of our study were comparison light transmission aggregometry (LTA) and multiple electrode platelet aggregometry (MEA) with induction by ADP in concentrations of 20 mýmol/L with or without prostaglandin E1 (PGE1) for monitoring clopidogrel resistance. Results: In the group of 84 patients with cardiovascular disease (CAD) studied, an impaired individual response to clopidogrel therapy was found 11.9% and 10.7% of the patients using MEA and LTA, respectively, induced by ADP with PGE1. The LTA and MEA methods with induction by ADP with PGE1 and without PGE1 were statistically compared using Spearman's nonparametric correlation analysis. Both methods with using PGE1 showed a positive significant correlation (p = 0.003) in contrast with the results without PGE1 with a no significant correlation (p = 0.732). Conclusions: The sensitivity for detecting clopidogrel resistance correlates well with other data in the literature suggesting that there are 5% - 30% clopidogrel low-responders depending on the type of platelet function assay used and the criteria for defining a low-responder [16-18]. These results favor implementation of the ADP test with PGE1 by MEA specifically for identification of low-responders to clopidogrel. Backround: Antiaggregation therapy is still the most frequently used approach to prevent thrombotic events in cardiovascular diseases. It has a good clinical effect but increasing evidence shows high residual platelet aggregation activity in a number of patients. Laboratory methods only allow us to detect clopidogrel %22non-responders%22 or %22low responders%22. Recent methods are based on monitoring residual platelet aggregation activity (aggregation methods) or detecting the number of free epitopes for binding a specific monoclonal antibody such as vasodilator-stimulated phosphoprotein phosphorylation (VASP). Methods: The aims of our study were comparison light transmission aggregometry (LTA) and multiple electrode platelet aggregometry (MEA) with induction by ADP in concentrations of 20 mýmol/L with or without prostaglandin E1 (PGE1) for monitoring clopidogrel resistance. Results: In the group of 84 patients with cardiovascular disease (CAD) studied, an impaired individual response to clopidogrel therapy was found 11.9% and 10.7% of the patients using MEA and LTA, respectively, induced by ADP with PGE1. The LTA and MEA methods with induction by ADP with PGE1 and without PGE1 were statistically compared using Spearman's nonparametric correlation analysis. Both methods with using PGE1 showed a positive significant correlation (p = 0.003) in contrast with the results without PGE1 with a no significant correlation (p = 0.732). Conclusions: The sensitivity for detecting clopidogrel resistance correlates well with other data in the literature suggesting that there are 5% - 30% clopidogrel low-responders depending on the type of platelet function assay used and the criteria for defining a low-responder [16-18]. These results favor implementation of the ADP test with PGE1 by MEA specifically for identification of low-responders to clopidogrel.
dcterms:title
Detection of Clopidogrel Resistance Using ADP Induced Aggregometry with Specific Inhibitor PGE1 Detection of Clopidogrel Resistance Using ADP Induced Aggregometry with Specific Inhibitor PGE1
skos:prefLabel
Detection of Clopidogrel Resistance Using ADP Induced Aggregometry with Specific Inhibitor PGE1 Detection of Clopidogrel Resistance Using ADP Induced Aggregometry with Specific Inhibitor PGE1
skos:notation
RIV/61989592:15110/14:33151350!RIV15-MSM-15110___
n3:aktivita
n8:S
n3:aktivity
S
n3:cisloPeriodika
9
n3:dodaniDat
n15:2015
n3:domaciTvurceVysledku
n11:4157311 n11:7451113 n11:2875020 n11:3461904
n3:druhVysledku
n6:J
n3:duvernostUdaju
n4:S
n3:entitaPredkladatele
n17:predkladatel
n3:idSjednocenehoVysledku
10600
n3:idVysledku
RIV/61989592:15110/14:33151350
n3:jazykVysledku
n12:eng
n3:klicovaSlova
multiple electrode aggregometry; resistance; functional test for detection clopidogrel; clopidogrel
n3:klicoveSlovo
n5:functional%20test%20for%20detection%20clopidogrel n5:clopidogrel n5:resistance n5:multiple%20electrode%20aggregometry
n3:kodStatuVydavatele
DE - Spolková republika Německo
n3:kontrolniKodProRIV
[BC0F7FFF2D84]
n3:nazevZdroje
Clinical Laboratory
n3:obor
n13:FD
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
8
n3:rokUplatneniVysledku
n15:2014
n3:svazekPeriodika
60
n3:tvurceVysledku
Slavík, Luděk Indráková, Jarmila Krčová, Věra Galuszka, Jan Indrák, Karel Úlehlová, Jana Hluší, Antonín Hutyra, Martin
n3:wos
000342857900007
s:issn
1433-6510
s:numberOfPages
6
n16:doi
10.7754/Clin.Lab.2013.131004
n14:organizacniJednotka
15110