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POINT OF CARE TESTING OF ASPIRIN RESISTANCE IN PATIENTS WITH VASCULAR DISEASE
Author(s) -
Wong Shen,
Ward Christopher M.,
Appleberg Michael,
Lewis David R.
Publication year - 2006
Publication title -
anz journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.426
H-Index - 70
eISSN - 1445-2197
pISSN - 1445-1433
DOI - 10.1111/j.1445-2197.2006.03693.x
Subject(s) - medicine , aspirin , epinephrine , platelet , antiplatelet drug , adenosine diphosphate , gastroenterology , cardiology , clopidogrel , anesthesia , platelet aggregation
  The reported range in rates of aspirin resistance (5.5–60%) may reflect difficulties in studying platelet function and the variety of tests used. This study used a platelet function analyzer (PFA‐100) to prospectively document aspirin resistance in a cohort of patients with arterial disease. Methods:  Patients with internal carotid artery (ICA) stenosis or intermittent claudication (IC) were recruited. Exclusion criteria were contraindications to aspirin, prescription of other medication with known antiplatelet effects or known platelet abnormalities. After prescription of 100 mg aspirin/day for 2 weeks an uncuffed venous blood sample was taken and analysed with the PFA‐100. Aspirin resistance was defined as closure time (CT) less than the upper limit of normal (158 s collagen/epinephrine agonist; 118 s collagen/adenosine diphosphate (ADP) agonist). Results:  Thirty‐three patients with IC and 12 patients with ICA stenosis were recruited ( n  = 45). Median (range) age was 74 years (49–85) and the male to female ratio was 1.5:1. The median (range) CT was >300 (85 to >300) s with collagen/epinephrine and 100 (52 to >300) s with collagen/ADP agonist. Twelve patients (27%) in the collagen/epinephrine group had normal CT despite treatment with 100 mg aspirin, indicating resistance. Of the 33 patients with collagen/epinephrine CT prolonged by aspirin, 10 patients also had prolonged collagen/ADP CT, suggesting excessive platelet inhibition. Conclusion:  A significant proportion of patients taking aspirin do not show laboratory evidence of platelet inhibition and may not be protected from atherothrombotic events. The PFA‐100 appears to be a useful tool to screen for both aspirin resistance and excessive aspirin mediated platelet inhibition.

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