Impact of exercise-induced coronary vasomotion on anti-ischemic therapy

Coronary vasomotion has an important role in the regulation of myocardial p erfusion. During dynamic exercise, normal coronary arteries dilate, whereas stenotic arteries constrict. This exercise-induced vasoconstriction has be en associated with the occurrence of myocardial ischemia and has been belie ved to be the result of endothelial dysfunction, with a reduced release or production of EDRF, increased sympathetic stimulation, enhanced platelet ag gregation with release of thromboxane A(2) and serotonin, or a passive coll apse of the disease-free wall segment within the stenosis (the Bernoulli ef fect), or a combination of any of these. More recently, it has been realize d that pharmacological treatment might prevent exercise-induced vasoconstri ction and, thus, reduce myocardial ischemia and the occurrence of angina pe ctoris. Vasodilators such as nitrates, calcium antagonists or alpha-recepto r blockers dilate the coronary arteries and prevent coronary stenosis narro wing during exercise. In contrast, beta-blocking agents are associated with coronary vasoconstriction at rest, but - conversely - can induce coronary vasodilatation during exercise. Pharmacological treatment in patients with stable angina pectoris may impro ve myocardial ischemia by reducing pre- and afterload, myocardial contracti lity, oxygen consumption, and vasomotor tone. However, coronary collateral perfusion can modify these effects by shunting blood from the non-ischemic to the ischemic region (collateral flow) or by shunting blood from the isch emic to the non-ischemic zone (coronary steal phenomenon). Typically, a ste al phenomenon has been reported in patients receiving either dipyridamole o r calcium antagonists, whereas a reversed steal has been described after be ta-blockade, with an increase in contralateral tone shunting blood from the non-ischemic to the ischemic zone (reverse steal phenomenon). Coron Artery Dis 11:363-369 (C) 2000 Lippincott Williams & Wilkins.