title: [The relationship between aspirin resistance and endothelial dysfunction in patients with stable coronary artery disease].
abstract: OBJECTIVE
  Endothelial dysfunction may enhance platelet aggregation despite regular aspirin therapy. We investigated the relationship between aspirin-resistant platelet aggregation and endothelial dysfunction in patients with stable coronary artery disease.
  
  
  METHODS
  The study included 98 patients (60 males, 38 females; mean age 62+/-8 years) receiving medical treatment for stable coronary artery disease. Platelet function assays were performed with the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate cartridges. Aspirin resistance was defined as a closure time of less than 186 seconds with Col/Epi cartridges despite regular aspirin therapy. Endothelial function was assessed via measurement of flow-mediated dilatation by brachial artery ultrasonography.
  
  
  RESULTS
  Twenty patients (20.4%) were found to be aspirin-resistant by the PFA-100. There were no significant differences between patients with and without aspirin resistance with respect to the mean aspirin dose administered and other medications. The mean basal diameter of the brachial artery was 4.11 mm and the mean flow-mediated dilatation (percentage change from basal diameter) was 4.7% in patients with aspirin resistance. The corresponding figures were 4.14 mm and 5.3% in the absence of aspirin resistance (p>0.05).
  
  
  CONCLUSIONS
  In our study, endothelial dysfunction was found in all the patients with stable coronary artery disease, without any association of its presence and severity with aspirin resistance.
authors.affiliation: Department of Cardiology, Istanbul Medical Faculty of Istanbul University, Istanbul, Turkey. bpamukcu@gmail.com
authors.forename: Burak
authors.initials: B
authors.lastname: Pamukçu
authors.forename: Imran
authors.initials: I
authors.lastname: Onür
authors.forename: Hüseyin
authors.initials: H
authors.lastname: Oflaz
authors.forename: Ali
authors.initials: A
authors.lastname: Elitok
authors.forename: Zehra
authors.initials: Z
authors.lastname: Buğra
authors.forename: Yilmaz
authors.initials: Y
authors.lastname: Nişanci
mesh_terms: D001132:Arm / Q000098:blood supply; D001241:Aspirin / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000502:physiology; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D004351:Drug Resistance; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D011673:Pulsatile Flow; D012039:Regional Blood Flow; D018608:Ultrasonography, Doppler
chemical_list: D010975:Platelet Aggregation Inhibitors; D001241:Aspirin