title: Impairment of endothelial function in patients with spontaneous cervical artery dissection: evidence for a general arterial wall disease.
abstract: OBJECTIVE
  Cervical artery dissection (CAD) accounts for 10-20% of ischemic strokes in young adults. Although trauma and preexisting disorders of the arterial wall are the main predisposing factors, most CADs are considered 'spontaneous'. We hypothesized that CAD could originate in systemic vascular disease bound to the intima-media interface without clinical signs. If this hypothesis is true, endothelium-dependent vasodilation would be impaired in response to a physiological stimulus such as an increase in blood flow.
  
  
  METHODS
  Flow-mediated arterial dilation was studied in 65 consecutive patients with spontaneous CAD: 26 with carotid artery dissection (ICAD), and 39 with vertebral artery dissection (VAD). CAD patients with vascular risk factors, trivial or obvious cervical trauma, or connective tissue disease were excluded. Twenty-three patients with ischemic stroke of unknown cause were included as controls. Using high-resolution ultrasonography, brachial artery diameter was measured at rest, during post-ischemic hyperemia (flow-mediated endothelium-dependent dilation), and after sublingual glyceryl trinitrate spray (endothelium-independent dilation).
  
  
  RESULTS
  The mean +/- SD values of the flow-mediated vasodilation index were 5.7 +/- 6.2% in ICAD, 5.0 +/- 9.3% in VAD and 13.2 +/- 6.5% in controls (p < 0.0005), without any difference between ICAD and VAD. Endothelium-independent dilation mean values were 21.5 +/- 9.5% in ICAD, 25.1 +/- 12.5% in VAD, and 20.8 +/- 8.4% in controls, without a significant difference between groups (p = 0.49).
  
  
  CONCLUSIONS
  These results give evidence of impaired endothelium-dependent vasodilation in CAD patients that is not the result of stroke, and suggest that an underlying abnormality of the arterial wall layers may predispose to CAD.
authors.affiliation: Department of Neurology, Lille University Hospital, France. clucas@chru-lille.fr
authors.forename: C
authors.initials: C
authors.lastname: Lucas
authors.forename: J L
authors.initials: JL
authors.lastname: Lecroart
authors.forename: C
authors.initials: C
authors.lastname: Gautier
authors.forename: X
authors.initials: X
authors.lastname: Leclerc
authors.forename: M
authors.initials: M
authors.lastname: Dauzat
authors.forename: D
authors.initials: D
authors.lastname: Leys
authors.forename: G
authors.initials: G
authors.lastname: Deklunder
mesh_terms: D000328:Adult; D001916:Brachial Artery; D020215:Carotid Artery, Internal, Dissection / Q000453:epidemiology* / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D020030:Nitric Oxide Donors; D012307:Risk Factors; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D020217:Vertebral Artery Dissection / Q000453:epidemiology* / Q000503:physiopathology*
chemical_list: D020030:Nitric Oxide Donors