Circulation, Vol 75, 577-582, Copyright © 1987 by American Heart Association
D Hackett, S Larkin, S Chierchia, G Davies, JC Kaski and A Maseri
To investigate whether ergonovine acts directly on coronary arteries or via
remote neurohumoral reflexes, we administered small titrated increments of
intracoronary ergonovine up to a maximum cumulative dose of 50 micrograms
to 15 patients. In six patients with variant angina (group 1), ischemic
electrocardiographic ST changes, angina, and localized coronary spasm
(local coronary diameter reduction of 87.8 +/- 18.9% [mean +/- SD])
followed after 6 to 50 micrograms (mean 20.7) cumulative intracoronary
ergonovine. In nine patients with atypical chest pain, normal baseline
coronary arteriograms, and no evidence of variant angina (group 2), there
was no ischemic ST segment change or localized coronary spasm after 6 to 50
micrograms (mean 31.6) intracoronary ergonovine. Coronary diameter of
proximal vessels of patients in group 2 was reduced by 16.2 +/- 6.5% and
did not differ from the response of nonspastic vessels of comparable size
of group 1 (20.5 +/- 13.8%; p = .7). There was no significant difference in
the median effective dose values in the dose-response curves of the spastic
and nonspastic segments between groups 1 and 2. Ergonovine causes coronary
spasm by a direct local effect, which seems to be caused by localized
arterial hyperreactivity rather than supersensitivity. Intracoronary
delivery may be safer than intravenous administration because negligible
drug recirculation may prevent perpetuation of spasm and selective coronary
administration can avoid branches with critical stenoses.
ARTICLES
Induction of coronary artery spasm by a direct local action of ergonovine
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