title: Metabolic syndrome and cerebral vasomotor reactivity.
abstract: OBJECTIVE
  Metabolic syndrome has been proposed as a risk factor for stroke and transient ischaemic attack. One pathophysiological mechanism could be impairment of endothelial function. Thus, we hypothesized that cerebral vasomotor reactivity would be decreased in patients with metabolic syndrome, compared to patients without metabolic syndrome.
  
  
  METHODS
  In this retrospective analysis, 83 consecutive patients (aged 59.19 ± 15.98; 33 women) underwent Doppler examination for carotid artery disease including bi-hemispherical vasomotor reactivity assessment using transcranial Doppler monitoring. Vasomotor reactivity data were analyzed from the hemisphere with no or low-grade carotid stenosis (<40%). Cerebral vasomotor reactivity was calculated as percent increase in mean flow velocity per mmHg pCO(2) during 2 min of 5% CO(2) inhalation delivered by anesthesia mask (normal if ≥ 2%/mmHg). Univariate and multivariable linear regression models were used to determine factors, including metabolic syndrome, that were independently associated with pathologic vasomotor reactivity.
  
  
  RESULTS
  After adjusting for the presence of contralateral carotid stenosis and ipsilateral stroke in the multivariable model, metabolic syndrome was independently associated with lower vasomotor reactivity values (2.27 ± 1.24% vs. 2.68 ± 1.37; ß = -0.258, P = 0.033). In this model, there was no association of cerebral vasomotor reactivity with age, gender, race, cardiac disease, current statin therapy, or small vessel disease.
  
  
  CONCLUSIONS
  Our findings suggest that impaired cerebral vasomotor reactivity may be a mediator of stroke in patients with metabolic syndrome, a syndrome affecting a significant and growing proportion of the population. A prospective longitudinal study is warranted to study the cerebral haemodynamic effect of metabolic syndrome.
authors.affiliation: Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA. sgiannop@uoi.gr
authors.forename: S
authors.initials: S
authors.lastname: Giannopoulos
authors.forename: B
authors.initials: B
authors.lastname: Boden-Albala
authors.forename: J H
authors.initials: JH
authors.lastname: Choi
authors.forename: E
authors.initials: E
authors.lastname: Carrera
authors.forename: M
authors.initials: M
authors.lastname: Doyle
authors.forename: T
authors.initials: T
authors.lastname: Perez
authors.forename: R S
authors.initials: RS
authors.lastname: Marshall
mesh_terms: D001921:Brain / Q000098:blood supply*; D002561:Cerebrovascular Disorders / Q000150:complications / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D017585:Ultrasonography, Doppler, Transcranial / Q000379:methods; D014666:Vasomotor System / Q000503:physiopathology*