Genetic polymorphisms of platelet receptors in young patients with AIM and resistance to antiplatelet therapy

Česká verze

Authors: J. Úlehlová ¹; L. Slavík ¹; J. Kučerová ¹; V. Krčová ¹; J. Václavík ²; K. Indrák ¹
Authors place of work: Hemato-onkologická klinika LF UP a FN Olomouc, I. interní klinika FN Olomouc ¹
Published in the journal: Transfuze Hematol. dnes,18, 2012, No. 1, p. 14-18.
Category: Souhrnné práce, původní práce, kazuistiky

Summary

The studied group comprises 80 young patients with AIM on dual antiplatelet therapy with acetylsalicylic acid (ASA) and thienopyridines. Antiplatelet therapy was monitored by platelet-rich plasma light transmittance aggregometry using the APACT 4004 analyser (Helena Laboratories, Austria) and by whole blood impedance aggregometry using the Multiplate analyser (Dynabyte, Germany). Platelet aggregation was detected after stimulation with arachidonic acid for the detection of aspirin resistance and with ADP and prostaglandin E1 for the detection of thienopyridine resistance. To determine the frequencies of P2Y12 (i-744T>C; rs2046934), P2Y12 (34C>T; rs6785930) and COX-1 (-842A>G; rs10306114) polymorphisms, DNA of patients with AIM was tested by RT-PCR and melting curve analysis using the LightCycler 480 analyser (Roche Diagnostics, Germany).The cut-offs for patients with effective ASA therapy are 25% of aggregated platelets and 220 AUC/min respectively if LTA or MEA is used. The cut-offs for effective thienopyridine therapy are 45% of aggregated platelets or 298 AUC/min, respectively.The aim of our work was to use the two aforementioned functional laboratory methods to assess both aspirin and thienopyridine resistance and to determine the contribution of platelet receptor genetic polymorphisms to resistance to antiplatelet therapy in AIM.

Key words:
platelet gene polymorphisms, resistance to antiplatelet therapy

Zdroje

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