This Article Full Text Full Text (PDF) All Versions of this Article: 38/10/2692    most recent STROKEAHA.107.490029v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Stenborg, A. Articles by Lind, L. Search for Related Content PubMed PubMed Citation Articles by Stenborg, A. Articles by Lind, L. Related Collections Endothelium/vascular type/nitric oxide

(Stroke. 2007;38:2692.)
© 2007 American Heart Association, Inc.

Original Contributions

Impaired Endothelial Function of Forearm Resistance Arteries in CADASIL Patients

Anna Stenborg, MD; Hannu Kalimo, PhD, MD; Matti Viitanen, PhD, MD; Andreas Terent, PhD, MD Lars Lind, PhD, MD

From the Departments of Medical Sciences (A.S., A.T., L.L.) and Pathology (H.K.), University and University Hospital of Uppsala, Sweden; the Departments of Pathology, Universities and University Hospitals of Helsinki (H.K.) and Turku (H.K.), Finland, Departments of Geriatrics of Karolinska Institutet (M.V.) and University Hospital Huddinge, Stockholm, Sweden; and the University of Turku (M.V.), and City and University Hospitals of Turku, Finland.

Correspondence to Anna Stenborg, Ingång 40 Akademiska sjukhuset, 75185 Uppsala, Sweden. E-mail anna.stenborg{at}akademiska.se

Background and Purpose— Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary arteriopathy, which mainly involves the brain causing stroke and dementia. Mice expressing the mutated protein display early dysfunction in vasoreactivity in resistance arteries, but studies of patients have been inconclusive so far.

Methods— We examined peripheral endothelium-dependent vasodilatation in 10 CADASIL-patients and 20 controls using 3 methods: venous occlusion plethysmography of forearm blood flow with intraarterial acetylcholine and sodium nitroprusside infusions for evaluation of resistance arteries, ultrasound with flow mediated vasodilatation (FMD) of the brachial artery for evaluation of a conduit artery, and the pulse wave method with measurements before and after terbutaline for evaluation of systemic endothelium-dependent vasodilation.

Results— The CADASIL patients displayed reductions in both basal (P=0.034) and stimulated blood flow (P=0.023 for the highest dose of acetylcholine) and an impaired endothelium-dependent vasodilation when investigated in forearm resistance arteries (P=0.019). The FMD and the pulse wave method did not show any reduction in endothelium-dependent vasodilation in the patients.

Conclusions— Endothelium-dependent vasodilation was impaired in resistance arteries, but not in a conduit artery, in the forearm of CADASIL patients.

Key Words: CADASIL syndrome • endothelium • vasodilation