title: Impact of exercise-induced coronary vasomotion on anti-ischemic therapy.
abstract: Coronary vasomotion has an important role in the regulation of myocardial perfusion. During dynamic exercise, normal coronary arteries dilate, whereas stenotic arteries constrict. This exercise-induced vasoconstriction has been associated with the occurrence of myocardial ischemia and has been believed to be the result of endothelial dysfunction, with a reduced release or production of EDRF, increased sympathetic stimulation, enhanced platelet aggregation with release of thromboxane A2 and serotonin, or a passive collapse of the disease-free wall segment within the stenosis (the Bernoulli effect), or a combination of any of these. More recently, it has been realized that pharmacological treatment might prevent exercise-induced vasoconstriction and, thus, reduce myocardial ischemia and the occurrence of angina pectoris. Vasodilators such as nitrates, calcium antagonists or alpha-receptor blockers dilate the coronary arteries and prevent coronary stenosis narrowing 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 improve myocardial ischemia by reducing pre- and afterload, myocardial contractility, 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 ischemic to the non-ischemic zone (coronary steal phenomenon). Typically, a steal phenomenon has been reported in patients receiving either dipyridamole or calcium antagonists, whereas a reversed steal has been described after beta-blockade, with an increase in contralateral tone shunting blood from the non-ischemic to the ischemic zone (reverse steal phenomenon).
authors.affiliation: Cardiovascular Center, University Hospital, Zurich, Switzerland. Philipp.Kaufmann@dmr.usz.ch
authors.forename: P A
authors.initials: PA
authors.lastname: Kaufmann
authors.forename: L
authors.initials: L
authors.lastname: Mandinov
authors.forename: C
authors.initials: C
authors.lastname: Seiler
authors.forename: O M
authors.initials: OM
authors.lastname: Hess
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000787:Angina Pectoris / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003097:Collateral Circulation / Q000187:drug effects / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009566:Nitrates / Q000494:pharmacology*; D014666:Vasomotor System / Q000187:drug effects*
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D009566:Nitrates