Cardiology Unit,
Hammersmith Hospital,
London, UK
Cardiology Unit St Bartholomew's Hospital,
London, UK
To the Editor:
Hasdai et al1 reported that myocardial perfusion
defects are produced in response to acetylcholine
10-4 mol/L IC. However, acetylcholine has dual
effects on coronary artery tone depending on the
intracoronary concentration of acetylcholine and the presence
of coronary atheroma. In normal coronary
arteries, vasodilation, mediated by the endothelial
cells, occurs at low concentrations and vasoconstriction, mediated by a
direct action on the smooth muscle cells, at higher concentrations. In
atheromatous coronary arteries, constriction
and dilation occur at low concentration and only constriction occurs at
high concentrations of acetylcholine.2 3
We have studied the responses of epicardial coronary arteries
to intracoronary infusion of acetylcholine in 15 patients with
normal coronary arteriograms, chest pain, and risk factors for
coronary artery disease.4 In 53% of
patients, there was both constriction and dilation of proximal and
distal segments coexisting not only in different coronary
arteries but also in different segments of the same artery at
10-7 to 10-6 mol/L
acetylcholine. At 10-4 and
10-3 mol/L, the dilatation response was blunted
and constriction predominated.
We also studied the responses of stenotic and
nonstenotic segments to intracoronary infusion of
acetylcholine in 18 patients with coronary artery disease and
stable angina.5 In all the patients and in 90%
to 100% of the stenotic segments, vasoconstriction occurred at
10-5 to 10-3 mol/L
acetylcholine (Figure
Mayo Clinic,
Rochester, Minn
© 1998 American Heart Association, Inc.
Correspondence
Acetylcholine and Endothelial Function
). In particular, in
response to 10-4 mol/L acetylcholine, both the
stenotic segments and the adjacent reference segment
constricted significantly (-26.7±4.3 and -11.4±2.0%, respectively;
Figure) with evidence of myocardial ischemia (ST