Circulation, Vol 79, 287-291, Copyright © 1989 by American Heart Association
SW Werns, JA Walton, HH Hsia, EG Nabel, ML Sanz and B Pitt
Acetylcholine causes endothelium-dependent dilation of normal arteries in
most animal species. The effect of acetylcholine on normal human coronary
arteries is controversial. Pathologic studies and epicardial
echocardiography have shown that diffuse atherosclerosis is often present
despite angiographic evidence of discrete coronary artery disease (CAD).
Therefore, we postulated that acetylcholine would cause vasoconstriction of
coronary arteries that are angiographically normal in patients with CAD.
Coronary artery diameter, measured by automated quantification of digitized
cineangiograms, was determined before and after the intracoronary infusion
of 0.2 mM acetylcholine at 0.8-1.6 ml/min. The diameter of stenotic or
irregular segments of six atherosclerotic coronary arteries decreased from
1.80 +/- 0.42 mm before acetylcholine to 1.26 +/- 0.46 mm after
acetylcholine (p = 0.0025). Acetylcholine had a significantly different
effect on the diameter of two groups of coronary arteries that are
angiographically normal. Acetylcholine caused a 0.16 +/- 0.09-mm increase
in the diameter of 14 normal coronary arteries in patients without CAD,
whereas it caused a 0.26 +/- 0.12-mm decrease in the diameter of 14 normal
coronary arteries in patients with CAD (p less than 0.01). Thus, the normal
response to intracoronary acetylcholine is vasodilation, suggesting that
endothelium-derived relaxing factor is released from normal human coronary
endothelium. The vasoconstrictive effect of acetylcholine in the
angiographically normal coronary arteries of patients with CAD suggests the
presence of a diffuse abnormality of endothelial function.
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Evidence of endothelial dysfunction in angiographically normal coronary arteries of patients with coronary artery disease
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
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