Circulation, Vol 70, 917-922, Copyright © 1984 by American Heart Association
BG Brown, EL Bolson and HT Dodge
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.
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