Gallagher K P
Seaweed Canyon Laboratory, School of Medicine, University of California, La Jolla.
Basic Res Cardiol. 1990;85 Suppl 1:145-55. doi: 10.1007/978-3-662-11038-6_12.
Transmural coronary steal describes the phenomenon that can occur when coronary narrowing is severe enough to eliminate or nearly eliminate vasodilator reserve in the subendocardial layers. Because blood flow in a maximally vasodilated vascular bed is linearly dependent on perfusion pressure, additional reductions in perfusion pressure will decrease subendocardial blood flow. The subepicardial layers, operating on a different autoregulatory pressure-flow curve, may have vasodilator reserve available and display normal or even elevated blood flow when the subendocardium has reduced perfusion. Therefore, it appears as if subendocardial blood flow has been "stolen" by the subepicardial layers. Blood flow is not actually stolen but redistributed distal to a flow-limiting stenosis and the redistribution tends to favor the subepicardium because it can autoregulate to a lower pressure than the subendocardium. Physiologic interventions such as exercise can alter myocardial oxygen requirements substantially. Vasodilator reserve will be utilized in those parts of the myocardium that have it available, in order to meet the augmented myocardial flow requirements associated with exercise. In poststenotic myocardium, however, decreased vascular resistance in subepicardial layers may reduce poststenotic perfusion pressure which will lead, in turn, to a decrease in blood flow to the subendocardial layers if they are maximally vasodilated. Because transmural systolic function (measured as wall thickening, for example) is largely dominated by changes in subendocardial perfusion, transmural steal during exercise may aggravate the level of dysfunction that occurs by augmenting the subendocardial flow deficit.
