Akademik Veri Yönetim Sistemi
BLOOD COAGULATION & FIBRINOLYSIS, cilt.21, sa.1, ss.53-56, 2010 (SCI-Expanded)
Genetic polymorphisms may affect platelets' responses to the antiplatelet therapy. Our aim was to determine the role of genetic polymorphisms on aspirin resistance in patients with coronary heart disease (CHD). A total of 126 consecutive patients (35-85 years old, 32% women) with chronic stable CHD was enrolled in the study. Platelet function assays were realized by the platelet function analyzer (PFA)-100 with Collagen and epinephrine (Col/Epi) and collagen and adenosine diphospate (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time of less than 186 s with Col/Epi cartridges despite regular aspirin therapy. Factor V, prothrombin, factor XIII, beta-fibrinogen, plasminogen activator inhibitor I (PAI-1), glycoprotein Ilia, methylene tetrahydrofolate reductase, ACE and ApoB gene polymophisms were determined by three consecutive steps: isolation and amplification of DNA and reverse hybridization. We determined that 30 patients (23.8%) had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 74 +/- 12 s (51-104s). Ten of the 30 patients with aspirin resistance were women (33.3%). Genetic polymorphisms were determined in 30 aspirin-resistant and 17 aspirin-sensitive patients. No statistically significant relationship was determined between aspirin resistance and the genetic panel. In our study we did not determine a significant relationship between the aspirin resistance and factor V, prothrombin, factor XIII, beta-fibrinogen, PAI-1, glycoprotein Ilia, methylene tetrahydrofolate reductase, ACE and ApoB gene polymophisms. Blood Coagul Fibrinolysis 21:53-56 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.