title: Preoperative cerebral hemodynamic impairment and reactive oxygen species produced during carotid endarterectomy correlate with development of postoperative cerebral hyperperfusion.
abstract: OBJECTIVE
  The purpose of the present study was to determine whether preoperative cerebral hemodynamic impairment and reactive oxygen species produced during carotid endarterectomy (CEA) correlate with development of postoperative cerebral hyperperfusion.
  
  
  METHODS
  Concentrations of malondialdehyde-modified low-density lipoprotein (MDA-LDL), a biochemical marker of oxidative damage, were measured in serum samples obtained from 90 patients undergoing CEA for ipsilateral ICA stenosis (>70%). Serum samples were obtained from a venous catheter inserted into the ipsilateral jugular bulb before clamping of the internal carotid artery (ICA), 10 minutes after clamping of the ICA, and 5 and 20 minutes after declamping of the ICA. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were also measured using single-photon emission computed-tomography before CEA. In addition, CBF was measured postoperatively.
  
  
  RESULTS
  Hyperperfusion (CBF increase >100% compared with preoperative values) was observed immediately after CEA in 12 patients (13%). Logistic regression analysis demonstrated that reduced preoperative CVR (95% CIs, 1.053 to 1.453; P=0.0097) and an increase in MDA-LDL (calculated as a percentage of the preclamp values) after ICA declamping (95% CIs, 0.862 to 0.980; P=0.0098) were significantly associated with development of postoperative cerebral hyperperfusion among the variables tested. Ten of 11 patients with reduced preoperative CVR and increased MDA-LDL after ICA declamping developed post-CEA hyperperfusion, and 2 of these patients developed cerebral hyperperfusion syndrome.
  
  
  CONCLUSIONS
  Both preoperative cerebral hemodynamic impairment and reactive oxygen species produced during surgery correlate with development of cerebral hyperperfusion after CEA.
authors.affiliation: Department of Neurosurgery, School of Medicine, Iwate Medical University, 19-1 Uchimaru, Morioka, Iwate 020-8505, Japan.
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Suga
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Ogasawara
authors.forename: Hideo
authors.initials: H
authors.lastname: Saito
authors.forename: Nobukazu
authors.initials: N
authors.lastname: Komoribayashi
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Inoue
authors.forename: Yasunari
authors.initials: Y
authors.lastname: Otawara
authors.forename: Akira
authors.initials: A
authors.lastname: Ogawa
mesh_terms: D000328:Adult; D000368:Aged; D002545:Brain Ischemia / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D016893:Carotid Stenosis / Q000601:surgery*; D002560:Cerebrovascular Circulation; D016894:Endarterectomy, Carotid / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007432:Intraoperative Period; D008077:Lipoproteins, LDL / Q000097:blood; D016015:Logistic Models; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D011183:Postoperative Complications / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D011300:Preoperative Care; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000503:physiopathology; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D008077:Lipoproteins, LDL; D017382:Reactive Oxygen Species; D008315:Malondialdehyde