title: Dynamic cerebral autoregulation is compromised acutely following mild ischaemic stroke but not transient ischaemic attack.
abstract: BACKGROUND
  Dynamic cerebral autoregulation (dCA), the process by which the cerebral blood flow (CBF) is normally maintained relatively constant despite fluctuations in beat-to-beat blood pressure (BP), is impaired acutely following major ischaemic stroke. It is uncertain if dCA is impaired acutely after mild ischaemic stroke or transient ischaemic attack (TIA). We assessed dCA in patients acutely and sub-acutely following TIA or mild ischaemic stroke.
  
  
  METHODS
  Nineteen consecutive mild ischaemic stroke patients and 17 consecutive TIA patients underwent recordings of beat-to-beat BP, cerebral blood flow velocity (bilateral transcranial Doppler insonation of the middle cerebral artery) and heart rate a median of 36 h from onset and again a median of 96 h from onset. Dynamic autoregulatory indices (ARI) were then calculated from these data and the results compared to 22 age-, BP- and gender-matched controls.
  
  
  RESULTS
  ARI was significantly reduced in affected hemispheres of mild stroke patients at baseline compared to controls (4.0 +/- 1.7 vs. 5.6 +/- 1.1, p < 0.01) and remained so after adjustment for significant covariates. ARI was significantly reduced in both affected (4.0 +/- 2.7 vs. 5.6 +/- 1.1, p = 0.03) and unaffected hemispheres (4.2 +/- 1.8 vs. 5.6 +/- 1.1, p = 0.01) of mild stroke patients at follow-up compared to controls. However, after adjustment for significant covariates including ipsilateral carotid stenosis these results were not significant. No reduction in ARI was seen in TIA patients.
  
  
  CONCLUSIONS
  The impairment of cerebrovascular haemodynamic control that was observed acutely following mild ischaemic stroke may have implications for the appropriate timing of anti-hypertensive therapy acutely following mild ischaemic stroke. No impairment of cerebrovascular haemodynamic control was seen following TIA.
authors.affiliation: Ageing and Stroke Medicine, Department of Cardiovascular Sciences, University of Leicester, University Hospitals of Leicester NHS Trust, Leicester, UK. era3@le.ac.uk
authors.forename: Emily R
authors.initials: ER
authors.lastname: Atkins
authors.forename: Fiona G
authors.initials: FG
authors.lastname: Brodie
authors.forename: Suzanne E
authors.initials: SE
authors.lastname: Rafelt
authors.forename: Ronney B
authors.initials: RB
authors.lastname: Panerai
authors.forename: Thompson G
authors.initials: TG
authors.lastname: Robinson
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage; D001794:Blood Pressure; D002545:Brain Ischemia / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D054022:Cerebrum / Q000098:blood supply*; D004334:Drug Administration Schedule; D005260:Female; D006339:Heart Rate; D006706:Homeostasis; D006801:Humans; D002546:Ischemic Attack, Transient / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D020521:Stroke / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D000959:Antihypertensive Agents