Circulation, Vol 51, 1053-1058, Copyright © 1975 by American Heart Association
M Hattenhaur and WA Neill
Inhalation of cold air (-20 degrees C) for four minutes provoked angina
pectoris in four of 17 coronary disease patients at rest and in four of
seven of the patients while they were paced at a heart rate level which was
subanginal at room temperature. The cold air did not increase myocardial O2
consumption significantly, and the accompanying changes in systemic
hemodynamic factors known to influence myocardial O2 consumption were
minor. Coronary blood flow determined by the xenon clearance method did not
change significantly. In 18 patients, cold air inhalation for 1 1/2 minutes
caused no detectable constriction of coronary arteries visualized
arteriographically. We conclude that angina pectoris induced by breathing
cold air cannot be explained satisfactorily by a concurrent increase in
myocardial work and O2 consumption. Although neither large coronary artery
constriction nor generalized coronary arteriole constriction seem to be
involved, some other specific effect of cold air inhalation on coronary
vasomotion, perhaps affecting collaterals or coronary blood flow
distribution, is suspected.
ARTICLES
The effect of cold air inhalation on again pectoris and myocardial oxygen supply
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