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HYPOXIA HAS been long known to cause a dramatic decrease in resistance in the coronary vascular bed. In the presence of localized ischemia due to coronary artery disease, pronounced reduction of vascular resistance would presumably result in a marked drop in the pressure head in the parent artery, distal to a proximal stenotic lesion. Such reduction in the pressure head conceivably could reduce perfusion in the terminal reaches of that parent vessel. The concept is simple; the hemodynamic possibilities are not. Renewed impetus was given to study of the role of arterial collateral channels by the report that exercise of an arm, in the presence of stenosis at or near the origin of the subclavian artery, could give rise to neurologic symptoms.1 This syndrome, related to an increased reversed flow through the vertebral artery, became known by the catchy title of "subclavian steal." Presumably vascular dilatation in the arm muscles decreases the pressure in the subclavian and vertebral arteries, in turn decreasing the perfusion pressure in the brain stem. Thus blood is "stolen" by the upper extremity, with resulting symptoms of an ischemic brain. It is apparent that the nature of the communications in the circle of Willis is important in the development of the syndrome. The concept of vascular "steal" has become popular, and aortoiliac2 and mesenteric steals3 have been described. For a long time it has been known that, when a coronary artery arises from the pulmonary artery, it may be subject to a low pulmonary artery pressure, inadequate for myocardial perfusion. Brooks4 early pointed this out. Amongst others, Effler and associates5 suggested the term "coronary steal" for this situation, wherein flow is reversed in an anomalous coronary artery connected to the

Inequalities of Myocardial Perfusion in Coronary Artery Disease ("Coronary Steal")