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.
- Marchant B, Donaldson G, Mridha K. et al. Mechanisms of cold intolerance in patients with angina. J Am Coll Cardiol 1994;23:630-6.
- Hattenhauer M, Neill WA. The effect of cold air inhalation on angina pectoris and myocardial oxygen supply. Circulation 1975;51:1053-1058.
- 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.