title: Antiplatelet therapy contributes to acute deterioration of intracerebral hemorrhage.
abstract: OBJECTIVE
  The purpose of this study was to examine the effect of antiplatelet therapy on the initial severity and the acute outcome of intracerebral hemorrhage (ICH).
  
  
  METHODS
  The authors reviewed records of 251 consecutive patients hospitalized in their cerebrovascular center within 24 hours after onset of ICH.
  
  
  RESULTS
  Fifty-seven patients (23%) had development of ICH during oral antiplatelet therapy. The major indication for antiplatelet therapy was the prevention of stroke recurrence (63%). As compared with patients without antiplatelet therapy, those who received antiplatelet therapy more frequently were aged 70 years or older (60% vs 35%; p < 0.001), had previous symptomatic ischemic stroke (54% vs 7%; p < 0.0001), had diabetes mellitus (26% vs 15%; p < 0.05), and had heart disease (32% vs 8%; p < 0.0001). Antiplatelet therapy was predictive of an increase in the hematoma volume by more than 40% on the second hospital day (hematoma enlargement, odds ratio [OR] 7.67, 95% CI 1.62 to 36.4) and the need for emergent surgical evacuation of the hematoma (OR 3.10, 95% CI 1.18 to 8.15). Antiplatelet therapy was an independent predictor for the occurrence of any of hematoma enlargement, emergent death, or evacuation surgery, which suggests that clinical deterioration occurs into the second hospital day (OR 7.45, 95% CI 2.46 to 22.5).
  
  
  CONCLUSIONS
  Antiplatelet therapy seems to contribute to the acute clinical deterioration of intracerebral hemorrhage.
authors.affiliation: Department of Cerebrovascular Disease, Cerebrovascular Center and Clinical Research Institute, National Kyushu Medical Center, 1-8-1 Jigyohama, Fukuoka 810-8563, Japan. toyoda@hsp.ncvc.go.jp
authors.forename: K
authors.initials: K
authors.lastname: Toyoda
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: K
authors.initials: K
authors.lastname: Minematsu
authors.forename: M
authors.initials: M
authors.lastname: Kamouchi
authors.forename: S
authors.initials: S
authors.lastname: Fujimoto
authors.forename: S
authors.initials: S
authors.lastname: Ibayashi
authors.forename: T
authors.initials: T
authors.lastname: Inoue
mesh_terms: D000284:Administration, Oral; D000368:Aged; D001241:Aspirin / Q000008:administration & dosage / Q000009:adverse effects; D002545:Brain Ischemia / Q000188:drug therapy* / Q000517:prevention & control; D015984:Causality; D002536:Cerebral Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000139:chemically induced* / Q000401:mortality* / Q000503:physiopathology; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000517:prevention & control; D002561:Cerebrovascular Disorders / Q000188:drug therapy* / Q000517:prevention & control; D002648:Child; D018450:Disease Progression; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D012189:Retrospective Studies; D012307:Risk Factors; D055502:Secondary Prevention
chemical_list: D010975:Platelet Aggregation Inhibitors; D001241:Aspirin