title: Prior antiplatelet use and infarct volume in ischemic stroke.
abstract: BACKGROUND
  Conflicting data exist on the role of antiplatelet agents in reducing incident ischemic stroke magnitude, but most prior studies used clinically-assessed neurologic deficit as the index of stroke extent rather than more precise volumetric measurements of infarct size. We assessed the relation of premorbid antiplatelet use to initial diffusion-weighted MRI (DWI) lesion volumes among acute ischemic stroke patients.
  
  
  METHODS
  Consecutive patients presenting within 24 h of ischemic stroke over an 18-month period were studied. DWI lesions were outlined using a semi-automated threshold technique. Subjects were categorized into two groups: antiplatelet (AP) or no antithrombotic (NA). The relationship between prestroke antithrombotic status and DWI infarct volumes was examined using multivariate quantile regression.
  
  
  RESULTS
  One hundred sixty-six individuals met study criteria: 75 AP and 91 NA patients. Median DWI volume was lower in the AP group than in the NA group (1.5 cc vs. 5.4 cc, p=0.031). A multivariable model (adjusting for age, history of transient ischemic attack, admission temperature, admission blood pressure, admission serum glucose, stroke onset to imaging interval, stroke mechanism, premorbid statin and antihypertensive use) demonstrated smaller infarcts in the AP vs. NA group (adjusted volume difference: -1.3 cc, 95% CI=-0.09, -2.5, p=0.037). Prior statin use, no history of TIA, large vessel atherosclerosis and microvascular ischemic disease stroke mechanism were also independently associated with reduced infarct volume.
  
  
  CONCLUSIONS
  Prior antiplatelet treatment is independently associated with reduced cerebral infarct volume among acute ischemic stroke patients. Premorbid statin use, TIA history and stroke mechanism also predict infarct volume in ischemic stroke.
authors.affiliation: Stroke Center, Department of Neurology, University of California, Los Angeles 90095, USA. Ovibes@mednet.ucla.edu
authors.forename: Bruce
authors.initials: B
authors.lastname: Ovbiagele
authors.forename: Brian H
authors.initials: BH
authors.lastname: Buck
authors.forename: David S
authors.initials: DS
authors.lastname: Liebeskind
authors.forename: Sidney
authors.initials: S
authors.lastname: Starkman
authors.forename: Oh Young
authors.initials: OY
authors.lastname: Bang
authors.forename: Latisha K
authors.initials: LK
authors.lastname: Ali
authors.forename: J Pablo
authors.initials: JP
authors.lastname: Villablanca
authors.forename: Noriko
authors.initials: N
authors.lastname: Salamon
authors.forename: Susan W
authors.initials: SW
authors.lastname: Yun
authors.forename: Sandra
authors.initials: S
authors.lastname: Pineda
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Saver
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology; D020520:Brain Infarction / Q000188:drug therapy* / Q000473:pathology* / Q000517:prevention & control; D002545:Brain Ischemia / Q000188:drug therapy* / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D002537:Intracranial Arteriosclerosis / Q000150:complications / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000150:complications / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors