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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F14%3A33151320%21RIV15-MSM-15110___
rdf:type
skos:Concept n12:Vysledek
dcterms:description
METHODS: The studied group comprises 124 patients with acute myocardial infarction on dual antiplatelet therapy with acetylsalicylic acid (ASA) and thienopyridines. Antiplatelet therapy was monitored by platelet-rich plasma light transmittance aggregometry (LTA) using the APACT 4004 analyzer (Helena Laboratories) and by whole blood impedance aggregometry (multiple electrode aggregometry [MEA]) using the Multiplate analyzer (Dynabyte). Platelet aggregation was detected after stimulation with arachidonic acid for detection of aspirin resistance and with adenosine diphosphate (ADP) and prostaglandin E1 for detection of thienopyridine resistance. To determine the frequencies of P2Y12 (i-744T}C; rs2046934), P2Y12 (34C}T; rs6785930), COX-1 (-842A}G; rs10306114), GPVI (13254T}C; rs1613662), and GPIbA (5T}C; rs2243093) polymorphisms, DNA of patients with AIM was tested by real-time-polymerase chain reaction and melting curve analysis using the LightCycler 480 analyzer (Roche Diagnostics). RESULTS: The cut-off points used for patients with effective ASA therapy are 25% of aggregated platelets and 220 area under the curve (AUC)/min if LTA or MEA, respectively. The cut-off points used for effective thienopyridine therapy are 45% of aggregated platelets or 298 AUC/min, respectively. Both LTA and MEA found that aspirin and thienopyridine therapies failed in 14.51% and 25.8%, respectively. The data were statistically processed using the SPSS version 15 software (SPSS, Inc.). Associations between receptor mutation status and response to therapy were assessed with Fisher's exact test. The significance level was set at 0.05. METHODS: The studied group comprises 124 patients with acute myocardial infarction on dual antiplatelet therapy with acetylsalicylic acid (ASA) and thienopyridines. Antiplatelet therapy was monitored by platelet-rich plasma light transmittance aggregometry (LTA) using the APACT 4004 analyzer (Helena Laboratories) and by whole blood impedance aggregometry (multiple electrode aggregometry [MEA]) using the Multiplate analyzer (Dynabyte). Platelet aggregation was detected after stimulation with arachidonic acid for detection of aspirin resistance and with adenosine diphosphate (ADP) and prostaglandin E1 for detection of thienopyridine resistance. To determine the frequencies of P2Y12 (i-744T}C; rs2046934), P2Y12 (34C}T; rs6785930), COX-1 (-842A}G; rs10306114), GPVI (13254T}C; rs1613662), and GPIbA (5T}C; rs2243093) polymorphisms, DNA of patients with AIM was tested by real-time-polymerase chain reaction and melting curve analysis using the LightCycler 480 analyzer (Roche Diagnostics). RESULTS: The cut-off points used for patients with effective ASA therapy are 25% of aggregated platelets and 220 area under the curve (AUC)/min if LTA or MEA, respectively. The cut-off points used for effective thienopyridine therapy are 45% of aggregated platelets or 298 AUC/min, respectively. Both LTA and MEA found that aspirin and thienopyridine therapies failed in 14.51% and 25.8%, respectively. The data were statistically processed using the SPSS version 15 software (SPSS, Inc.). Associations between receptor mutation status and response to therapy were assessed with Fisher's exact test. The significance level was set at 0.05.
dcterms:title
Genetic polymorphisms of platelet receptors in patients with acute myocardial infarction and resistance to antiplatelet therapy. Genetic polymorphisms of platelet receptors in patients with acute myocardial infarction and resistance to antiplatelet therapy.
skos:prefLabel
Genetic polymorphisms of platelet receptors in patients with acute myocardial infarction and resistance to antiplatelet therapy. Genetic polymorphisms of platelet receptors in patients with acute myocardial infarction and resistance to antiplatelet therapy.
skos:notation
RIV/61989592:15110/14:33151320!RIV15-MSM-15110___
n6:aktivita
n10:S
n6:aktivity
S
n6:cisloPeriodika
9
n6:dodaniDat
n13:2015
n6:domaciTvurceVysledku
n15:2875020 n15:5534917 n15:1699814
n6:druhVysledku
n8:J
n6:duvernostUdaju
n14:S
n6:entitaPredkladatele
n18:predkladatel
n6:idSjednocenehoVysledku
18099
n6:idVysledku
RIV/61989592:15110/14:33151320
n6:jazykVysledku
n9:eng
n6:klicovaSlova
antiplatelet therapy; acute myocardial infarction; platelet; genetic polymorphisms
n6:klicoveSlovo
n7:genetic%20polymorphisms n7:acute%20myocardial%20infarction n7:platelet n7:antiplatelet%20therapy
n6:kodStatuVydavatele
US - Spojené státy americké
n6:kontrolniKodProRIV
[0DDA9981B664]
n6:nazevZdroje
Genetic Testing and Molecular Biomarkers
n6:obor
n17:FD
n6:pocetDomacichTvurcuVysledku
3
n6:pocetTvurcuVysledku
6
n6:rokUplatneniVysledku
n13:2014
n6:svazekPeriodika
18
n6:tvurceVysledku
Kučerová, Jana Slavík, Luděk Indrák, Karel Úlehlová, Jana Krčová, Věra Václavík, Jan
s:issn
1945-0265
s:numberOfPages
6
n5:doi
10.1089/gtmb.2014.0077
n16:organizacniJednotka
15110