Although it is well known that exposure to cold can provoke AP in some patients with coronary artery disease¹, a unifying mechanism for its explanation has yet to be found.

One study involving subjects with exertional AP who inhaled cold air (-20 C°) during cardiac catheterization found no evidence of reactive constriction of large coronary arteries², while another study involving patients with >50% coronary stenosis undergoing cold pressor test ( placing patient’s hand and forearm in ice water for 90 seconds), demonstrated a 39% decrease in coronary blood flow³.  

 Another experiment involving patients undergoing exercise treadmill testing at 6 and 25 C° found an increase in serum norepinephrine levels, increase in blood pressure and an increase in myocardial oxygen demand in all subjects on exposure to cold air³.  It concluded that compared to patients without cold-induced AP, patients with cold-induced AP may not have a reflex decrease in their heart rate, possibly due to a baroreceptor dysfunction. 

References

1. Marchant B, Donaldson G, Mridha K. et al. Mechanisms of cold intolerance in patients with angina. J Am Coll Cardiol 1994;23:630-6.
2. Hattenhauer M, Neill WA. The effect of cold air inhalation on angina pectoris and myocardial oxygen supply. Circulation 1975;51:1053-1058.
3. Nabel EG, Ganz P, Gordon JB, et al. Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. Circulation 1988;77:43-52.