Abstract
Studies were performed to evaluate the hemodynamic response of severely stenotic coronary arteries to dilation of the distal coronary bed. A critical stenosis was produced with an adjustable wire snare on the left anterior descending or circumflex arteries of open chest dogs. Coronary flow, distal coronary pressure and aortic pressure were measured. In one group of experiments, coronary arteriolar dilatation was induced by transient occlusion of the artery distal to the stenosis. After the release of a transient occlusion in vessels without a critical stenosis, flow increased (from 33 ± 4 to 85 ± 8 ml/min, P <0.01), distal pressure decreased slightly (from 86 ± 4 to 80 ± 4 mm Hg, P <0.01), and large vessel resistance did not change significantly (from 0.06 ± 0.02 to 0.08 ± 0.03 units). After the release of a transient occlusion in vessels with a critical stenosis, flow decreased (from 23 ± 3 to 12 ± 2 ml/min, P <0.01), distal pressure decreased to persistently low levels (from 63 ± 2 to 29 ± 2 mm Hg, P <0.01), and large vessel resistance increased (from 1.4 ± 0.3 to 6.7 ± 1.8 units, P <0.01). In a separate group of experiments, radio-opaque contrast medium was used to dilate the distal coronary bed. In these studies dilation of the distal coronary bed of arteries with a critical stenosis again resulted in a decrease in coronary blood flow (from 35 ± 4 to 19 ± 3 ml/min, P <0.01), a decrease in distal coronary pressure (from 84 ± 6 to 35 ± 6 mm Hg, P <0.01) and an increase in large arterial resistance (from 1.0 ± 0.2 to 5.5 ± 1.2 units, P <0.02). Therefore, in coronary vessels with severe stenosis, dilation of the distal coronary bed may result in a paradoxical decrease in coronary blood flow.
Original language | English (US) |
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Pages (from-to) | 219-224 |
Number of pages | 6 |
Journal | The American Journal of Cardiology |
Volume | 43 |
Issue number | 2 |
DOIs | |
State | Published - Feb 1979 |
Bibliographical note
Funding Information:From the University of Minnesota, Department of Medicine, Cardiovascular Division, Minneapolis, Minnesota. This work was supported by a Grant-In-Aid from the American Heart Association, Minnesota Affiliate, Minneapolis, Minnesota; and by a Young Investigator Research Award (Grant HL-21298) from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Manuscript.r eceived September 5, 1978, accepted September 6, 1978.