Circulation, Vol 74, 1255-1265, Copyright © 1986 by American Heart Association
JC Kaski, F Crea, D Meran, L Rodriguez, L Araujo, S Chierchia, G Davies and A Maseri
It has been shown in different groups of patients with variant angina that
coronary spasm can be reproduced by physiologic maneuvers and pharmacologic
agents. It is not known, however, to what extent different stimuli can
induce spasm in the same patient. To investigate whether coronary arterial
spasm results from specific abnormal agonist- receptor interactions or from
a local nonspecific coronary supersensitivity to different stimuli, 28
patients with vasospastic angina were submitted to a series of diverse
vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine,
hyperventilation, handgrip, cold pressor, and exercise-tests, were carried
out in all 28 patients. In the last 15 patients histamine was also
administered. Spasm was provoked by ergonovine in 96% of patients, by
hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by
the cold pressor and handgrip tests in 11% and 7%, respectively. No
significant differences were found in the responses to provocative tests of
patients with normal coronary arteries or nonsignificant stenoses and those
with significant lesions. In the same individual, spasm was induced by at
least two vasoconstrictive stimuli, although with a different mechanism of
action, in 82% of patients and spasm was induced by three or more stimuli
in 39%. Tests were repeated in at least 23 patients and short-term
reproducibility paralleled sensitivity. These results suggest that in
patients with variant angina, a local nonspecific supersensitivity rather
than an abnormal specific agonist-receptor interaction plays a major role
in the genesis of coronary arterial spasm.
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Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina
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