Dynamic mechanisms in human coronary stenosis.

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Abstract
At the clinical level, coronary stenoses frequently behave as though the obstruction to flow were variable and not as rigidly fixed as previously imagined. Pressure (energy) lost in flow through a stenosis is the primary determinant of its hemodynamic impact. Ischemic episodes occur when pressure distal to the stenosis falls below that needed to perfuse the subendocardium. Three important properties of the stenosis contribute to variation in its pressure loss. First, loss is proportional to the square of stenosis flow. Thus proper distribution of perfusion is doubly vulnerable to conditions such as exercise, anemia, or pharmacologic vasodilation, which ordinarily increase myocardial blood flow. Second, pressure loss is proportional to the inverse fourth power of minimum lumen diameter. As a result, seemingly small changes in diameter are amplified to large changes in stenosis resistance. Third, a compliant arc of normal arterial wall borders part of the lumen in the majority of coronary lesions. This extremely important morphologic feature of stenoses permits transient variation in stenosis lumen diameter in response to drugs or to variation in endogenous vasomotor activity or intraluminal pressure. Although our understanding is incomplete, many of the clinical features of coronary disease and its pharmacologic responses are explained in terms of these stenosis properties and their interaction.