A. Hamabe et al., Impaired endothelium-dependent vasodilation in the brachial artery in variant angina pectoris and the affect of intravenous administration of vitaminC, AM J CARD, 87(10), 2001, pp. 1154-1159
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Endothelial dysfunction in the coronary artery contributes to the pathogene
sis of variant angina, and endothelial dysfunction in variant angina may be
associated with increased oxidant stress in the systemic arteries. We inve
stigated whether endothelial dysfunction exists in the peripheral artery in
patients with variant angina, and also examined the effect of vitamin C, a
n antioxidant, on endothelium-dependent vasodilation. Using high-resolution
ultrasound, both the flow-mediated vasodilation (FMD, endothelium-dependen
t vasodilation) and sublingual nitroglycerin-induced vasodilation (NTG-D, e
ndothelium-independent vasodilation) in the brachial artery were measured i
n 28 patients with variant angina and 24 control subjects who had normal co
ronary arteries. FMD was significantly impaired in patients with variant an
gina compared with control subjects (1.8 +/- 2.2% vs 6.4 +/- 4.9%, p <0.001
). FMD and NTG-D before and after intravenous administration of either vita
min C or placebo were measured in 17 patients with variant angina. FMD sign
ificantly improved after the administration of vitamin C (from 2.2 +/- 2.4%
to 4.5 +/- 1.6%, P <0.01), but not after administration of the placebo (fr
om 2.0 +/- 2.6% to 1.7 +/- 1.9%). The improved FMD due to vitamin C in pati
ents with variant angina, however, was not significantly different from tha
t in the control subjects. NTG-D was not significantly different between pa
tients with variant angina and control subjects (14.0 +/- 7.8% vs 13.6 +/-
5.0%) and it was also not affected by vitamin C. In conclusion: (1) FMD in
the brachial artery is impaired in patients with variant angina, and (2) th
e acute administration of the antioxidant, vitamin C, was observed to rever
se this endothelial dysfunction. These findings support the theory that the
systemic inactivation of nitric oxide due to oxidative stress might exist
in patients with variant angina. (C)2001 by Excerpta Medica, Inc.