Inhalation of cold air (-20°C) for 4 min provoked angina pectoris in 4 of 17 coronary disease patients at rest, and in 4 of 7 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 min caused no detectable constriction of coronary arteries visualized arteriographically. Thus 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.
CITATION STYLE
Hattenhauer, M., & Neill, W. A. (1975). The effect of cold air inhalation on angina pectoris and myocardial oxygen supply. Circulation, 51(6), 1053–1058. https://doi.org/10.1161/01.cir.51.6.1053
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