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Abstract
Aim.In patients with acute coronary syndrome (ACS), to investigate the prevalence of aspirin resistance, its clinical features, prognostic effects, and potential correction.Material and methods.The study included 100 ACS patients receiving aspirin. Aspirin resistance was diagnosed if at Day 7 of aspirin therapy, the level of platelet aggregation (PLA) with arachidonic acid was ≥20%. In addition, a thromboxane A2 (ТхА2) metabolite – 11-dehydro-thromboxane B2 (11DHTxB2), as well as inflammation markers and genetic polymorphisms (sub-unit IIIa – Leu33Pro and cyclooxygenase-2 (COG) genes) were studied.Results.Aspirin resistance was diagnosed in 11% of ACS patients, receiving aspirin in a standard dose of 100 mg/d. The majority of aspirin-resistant patients had ACS with ST segment elevation (STE-ACS). In all aspirin-resistant ndividuals, the resistance was pharmacokinetic. The level of 11DHTxB2, increased at baseline in ACS patients and especially in those with STE-ACS, was reduced during aspirin therapy. The combination of high PLA and high 11DHTxB2 levels was typically associated with true aspirin resistance. In patients with metabolite levels >438 ng/ mmol creatinine, prognosis was significantly worse than in those with lower levels of this parameter. In aspirinresistant patients, the levels of interleukin-6 (IL-6), IL-10, and C-reactive protein (CRP) at baseline and throughout the study were significantly higher than in aspirin-sensitive subjects. There was no significant association between aspirin resistance and Leu33Pro or А842G polymorphisms, while А842G polymorphism was more common in aspirin-resistant patients.Conclusion.In aspirin-resistant patients, the level of ТхА2 metabolite is increased (true resistance). In ACS individuals with high levels of 11DHTxB2, the prognosis was worse. Aspirin resistance could be linked to inflammation activation. There was no consistent association between aspirin resistance and studied genetic polymorphisms.
Highlights
There was no significant association between aspirin resistance and Leu33Pro or А842G polymorphisms, while А842G polymorphism was more common in aspirin-resistant patients
Lepantalo A, Mikkelsson J, Resendiz JC, et al Polymorphisms thromboxan biosynthesis and the risc of myocardial infarction, of COX-1 and GPVI associate with the antiplatelet effect of stroke, or cardiovascular death in patients at high risk for aspirin in coronary artery disease patients
Summary
Исследование агрегации тромбоцитов (АТ) проводилось всем больным исходно, через 7 сут., через 30 сут., а также через 6-8 мес. с момента госпитализации. Для определения уровня 11 дегидро тромбоксана В2 (11ДГТхВ2) образцы мочи собирали при поступлении, а также утреннюю порцию мочи на 7 сут., 30 сут. Мочу помещали в пробирки с консервантом (индометацин 250 мкг) и замораживали при температуре -60°С для серийных определений. Для определения 11ДГТхВ2 были использованы коммерческие наборы производства “Neogen”. Масенко В.П.) Для определения уровня интерлейкина 6 (IL-6), IL-10 использовали иммуноферментные наборы фирмы BenderMedSystems (BMS) в соответствии в инструкцией изготовителя. Количественное определение С-реактивного белка (СРБ) проводилось иммуноферментным методом с использованием набора “Cytoimmune Science” (норма < 2,5-3 мг/л). Дезоксирибонуклеиновую кислоту (ДНК) для генетического исследования выделяли из цельной венозной крови, забранной в пробирку с ЭДТА, стандартным фенол-хлороформным методом. При статистической обработке результатов использовали пакеты прикладных статистических программ STATISTICA v 6.0 для каждой из непрерывных величин приведены в таблицах либо среднее (М) и стандартное отклонение (σ), либо медиана и квартили распределения.
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