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Am J Cardiol. 1996 Dec 1;78(11):1210-4.

Flow-induced vasodilation of the human brachial artery is impaired in patients <40 years of age with coronary artery disease.

Author information

1
Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Abstract

The objective of this study was to determine whether abnormal flow-induced endothelium-dependent vasodilation in the brachial artery identifies young patients with coronary artery disease (CAD). High-resolution ultrasonography was used to measure vascular reactivity in a peripheral conduit vessel, the brachial artery, in 14 young men with CAD and in 11 age-matched, healthy, male volunteers. Endothelium-dependent vasodilation was determined by measuring the change in brachial artery diameter during increases in flow induced by reactive hyperemia. Endothelium-independent vasodilation was assessed by administration of sublingual nitroglycerin. To ascertain whether flow-mediated vasodilation in humans is mediated by endothelium-derived nitric oxide, brachial artery diameter was measured during reactive hyperemia, before and during administration of the nitric oxide synthase antagonist NG-monomethyl-L-arginine (L-NMMA). Brachial artery diameter was also measured during intraarterial infusion of acetylcholine and nitroprusside before and after administration of L-NMMA. Flow-induced vasodilation was less in patients with CAD than in healthy volunteers (1.3 +/- 1.1% vs 6.2 +/- 0.7%, p <0.05). Nitroglycerin increased brachial artery diameter similarly in each subject group (11.3 +/- 1.0% vs 15.8 +/- 1.2%, p =0.05). L-NMMA inhibited flow-mediated vasodilation and the vasodilative response to acetylcholine, but did not affect the response to nitroprusside. It is concluded that abnormal flow-induced endothelium-dependent vasodilation occurs in the brachial artery of young patients with CAD.

PMID:
8960576
DOI:
10.1016/s0002-9149(96)00597-8
[Indexed for MEDLINE]

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