The effect of cold air inhalation on again pectoris and myocardial oxygen supply

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.