Vitamin C attenuates abnormal vasomotor reactivity in spasm coronary arteries in patients with coronary spastic angina.
OBJECTIVE
This study sought to examine effect of vitamin C, an antioxidant, on the abnormal vasomotor reactivity in spasm coronary arteries.


BACKGROUND
Oxygen free radicals generated in the arterial walls have been shown to cause endothelial vasomotor dysfunction.


METHODS
Responses of the epicardial arterial diameters of the left coronary arteries to the intracoronary infusion of acetylcholine (ACh) (10 and 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of vitamin C (10 mg/min) or saline as a placebo in 32 patients with coronary spastic angina and in 34 control subjects.


RESULTS
Vitamin C infusion suppressed the constrictor response of the epicardial diameter to ACh in spasm coronary arteries but had no significant effect in the control coronary arteries (percent change in distal diameter in response to 10 microg/min of ACh [constriction (-), dilation (+), mean +/- SEM] before vitamin C: -8.2 +/- 2.9% in spasm arteries, +8.4 +/- 2.9%* in control arteries; during vitamin C: +0.2 +/- 3.8%* in spasm arteries, +7.2 +/- 1.3%* in control arteries [*p < 0.01 vs. spasm arteries before vitamin CI). The coronary sinus-arterial difference in plasma thiobarbituric acid reactive substances during ACh infusion, an indicator of lipid peroxidation in coronary circulation, was higher in patients with coronary spastic angina than in control subjects (p < 0.01) but was suppressed in patients with coronary spastic angina to comparable levels in control subjects by combined infusion of vitamin C. Saline infusion had no effect.


CONCLUSIONS
The results indicate that vitamin C attenuates vasomotor dysfunction in epicardial coronary arteries in patients with coronary spastic angina. Oxygen free radicals may at least in part play a role in the abnormal coronary vasomotor reactivity in response to ACh in spasm coronary arteries.
Kugiyama
K
K
Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan. kiyo@gpo.kumamoto-u.ac.jp
Motoyama
T
T
Hirashima
O
O
Ohgushi
M
M
Soejima
H
H
Misumi
K
K
Kawano
H
H
Miyao
Y
Y
Yoshimura
M
M
Ogawa
H
H
Matsumura
T
T
Sugiyama
S
S
Yasue
H
H
D000109:Acetylcholine; D000328:Adult; D000368:Aged; D000788:Angina Pectoris, Variant / Q000503:physiopathology*; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D017023:Coronary Angiography; D003329:Coronary Vasospasm / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007261:Infusions, Intra-Arterial; D008297:Male; D008875:Middle Aged; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology
D000975:Antioxidants; D017382:Reactive Oxygen Species; D000109:Acetylcholine; D001205:Ascorbic Acid