title: Aspirin responsiveness in acute brain ischaemia: association with stroke severity and clinical outcome.
abstract: OBJECTIVE
  Platelets play a critical role in the pathogenesis of acute brain ischaemia. We studied the association between the degree of inhibition of platelet function by aspirin (ASA) and the severity and outcome of acute brain ischaemia.
  
  
  METHODS
  Platelet responsiveness to ASA was assessed in patients with acute brain ischaemia, treated with ASA since hospital admission. The degree of ASA responsiveness was assessed by optical aggregometry and categorized into patients with good response, partial response and complete unresponsiveness to ASA (good responders, partial responders and non-responders, respectively). An additional evaluation of responsiveness to ASA was performed by Impact-R (cone and platelet analyzer). Patients underwent serial clinical assessment during hospitalization, at discharge and during follow-up.
  
  
  RESULTS
  Among 105 patients (mean age 63 +/- 12 years; 66% men), impaired ASA responsiveness at baseline as assessed by aggregometry was associated with increased stroke severity at baseline, unfavourable clinical course, and poor functional outcome during follow-up (p < 0.05 for all). Age-adjusted odds ratios in non-responders compared to good responders were 9.8 for severe stroke on admission (95% CI 2.8-34.9), 3.1 for lack of early clinical improvement (95% CI 1.1-8.8) and 8.6 for poor functional outcome during follow-up (95% CI 2.4-30.4). Less robust trends were observed with the Impact-R.
  
  
  CONCLUSIONS
  Impaired responsiveness to ASA in acute brain ischaemia is common and is associated with worse neurological deficits at stroke onset, early clinical deterioration and poorer functional outcome. The clinical significance of these findings requires further evaluation in larger longitudinal studies.
authors.affiliation: Stroke Center, Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.
authors.forename: Y
authors.initials: Y
authors.lastname: Schwammenthal
authors.forename: R
authors.initials: R
authors.lastname: Tsabari
authors.forename: B
authors.initials: B
authors.lastname: Shenkman
authors.forename: R
authors.initials: R
authors.lastname: Schwartz
authors.forename: S
authors.initials: S
authors.lastname: Matetzky
authors.forename: A
authors.initials: A
authors.lastname: Lubetsky
authors.forename: D
authors.initials: D
authors.lastname: Orion
authors.forename: S
authors.initials: S
authors.lastname: Israeli-Korn
authors.forename: J
authors.initials: J
authors.lastname: Chapman
authors.forename: N
authors.initials: N
authors.lastname: Savion
authors.forename: D
authors.initials: D
authors.lastname: Varon
authors.forename: D
authors.initials: D
authors.lastname: Tanne
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D012720:Severity of Illness Index; D020521:Stroke / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D001241:Aspirin