Circulation, Vol 51, 1085-1094, Copyright © 1975 by American Heart Association
KL Gould, K Lipscomb and C Calvert
The degree and effectiveness of compensatory changes in the distal coronary
vascular bed during progressive proximal coronary stenosis have not been
described. In this study, coronary vascular bed resistance and pressure
gradient-flow relationships were determined for 157 different stenoses in
nine opened-chest dogs by measuring coronary flow, aortic pressure, and
coronary pressure distal to a coronary constrictor while flow was varied
from resting to maximal values by the intracoronary injection of Hypaque-M,
75% (previously shown to cause transient, maximal vasodilatation comparable
to ten second occlusion). This approach provided a means of hemodynamically
characterizing coronary stenoses in a standary, experimental manner for
quantitative analysis of different arteries at different flow rates as
found in the intact coronary circulation. The results show that 1) pressure
gradient- flow characteristics or hydraulic resistance of stenoses do not
become abnormal enough to alter normal resting coronary flow nor to elicit
compensatory changes for stenoses up to constriction of approximately 60%
of the diameter, 2) compensatory vasodilatation of the distal coronary
vascular bed maintains near normal resting flow for lesions between 60% and
85% diameter stenosis but adaptive vasodilatation fails to compensate for
the high resistance of lesions greater than 85% diameter stenosis, and 3)
there is vasodilator reserve still present when total coronary artery flow
is reduced below normal by a stenosis. This vasodilator reserve probably
exists in the epicardium since the endocardium is characteristically
underperfused due to the low coronary pressure caused by stenosis and is
therefore likely to be maximally vasodilated with no remaining vasodilator
reserve.
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