Impaired endothelial function of forearm resistance arteries in CADASIL patients

Anna Stenborg1, Hannu Kalimo, Matti Viitanen

  • 1Department of Medical Sciences, University and University Hospital of Uppsala, Sweden. anna.stenborg@akademiska.se

Stroke
|September 1, 2007
PubMed

Insights

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) patients show impaired endothelium-dependent vasodilation in forearm resistance arteries. This dysfunction was not observed in conduit arteries, suggesting a specific vascular defect in CADASIL.

Area of Science:

  • Vascular Biology
  • Neurology
  • Genetics

Background:

  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic disorder causing stroke and dementia.
  • Previous studies in CADASIL patients on vasoreactivity have yielded inconclusive results.

Purpose of the Study:

  • To investigate peripheral endothelium-dependent vasodilation in CADASIL patients.
  • To compare vasodilation in resistance and conduit arteries in CADASIL patients.

Main Methods:

  • Forearm blood flow using venous occlusion plethysmography with intraarterial infusions of acetylcholine and sodium nitroprusside.
  • Ultrasound assessment of flow-mediated dilation (FMD) in the brachial artery.
  • Pulse wave analysis before and after terbutaline administration.

Main Results:

  • CADASIL patients exhibited reduced basal and stimulated forearm blood flow.
  • Impaired endothelium-dependent vasodilation was observed in forearm resistance arteries of CADASIL patients.
  • No significant reduction in endothelium-dependent vasodilation was detected in the conduit brachial artery using FMD or pulse wave methods.

Conclusions:

  • Endothelium-dependent vasodilation is specifically impaired in the resistance arteries of CADASIL patients.
  • Conduit artery function remains unaffected in CADASIL patients.
  • Findings highlight a localized vascular defect in small cerebral arteries in CADASIL.
Abstract

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