Exercise-induced decrease in flow through stenotic coronary arteries in the dog

Jeffrey S. Schwartz, Bruce Tockman, Jay N Cohn, Robert J Bache

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8 Scopus citations


In the presence of a coronary stenosis, it is generally believed that exercise-induced ischemia is caused by an inadequate increase in coronary blood flow. This study was carried out to test the hypothesis that, in the presence of a critical coronary stenosis, exercise would result in a decrease in flow across the stenosis. Five dogs were chronically instrumented with a flow probe and a wire snare occluder on the circumflex coronary artery and with catheters in the left atrium, left ventricle, and aorta. Four dogs also had a catheter in the circumflex coronary artery distal to the occluder. Measurements were recorded with the animals resting quietly and then during moderate exercise. In the absence of a stenosis, circumflex flow increased with exercise. In 13 experiments in which a severe stenosis was produced in the circumflex coronary artery, the changes from rest to exercise were as follows: heart rate from 102 ± 7 to 151 ± 12 beats/min (p < 0.001 ), mean aortic pressure from 103 ± 4 to 107 ± 3 mm Hg (difference not significant), distal circumflex pressure from 71 ± 5 to 36 ± 2 mm Hg (p < 0.001), the pressure gradient across the stenosis from 32 ± 4 to 71 ± 3 mm Hg (p < 0.001), stenosis resistance from 2.3 × 0.7 to 13.9 ± 3.9 units (p < 0.01), and flow through the stenotic artery from 29 ± 4 to 10 ± 3 ml/min (p < 0.001). Left ventricular filling pressure increased from 9 ± 1 to 15 ± 1 mm Hg (p < 0.01). The decrease in intraluminal pressure distal to the stenosis and thus in the stenosis itself may have resulted in passive narrowing of the stenotic segment, which may have caused the decrease in flow. Exercise, therefore, may result in a decrease in flow through a stenotic coronary artery.

Original languageEnglish (US)
Pages (from-to)1409-1413
Number of pages5
JournalThe American Journal of Cardiology
Issue number6
StatePublished - Dec 1982

Bibliographical note

Funding Information:
From the Department of Medicine, Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minnesota. This study was supported by Young Investigator Research Award Grant HL-21298 and by Grant HL-20598 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, and by a Grant-in-Aid from the American Heart Association, Dallas, Texas, with funds contributed in part by the American Heart Association, Minnesota Affiliate, Minneapolis, Minnesota. Manuscript received April 13, 1982, accepted June 9, 1982. Address for reprints: Jeffrey S. Schwartz, MD, Department of Medicine, Box 258, Mayo Memorial Building, University of Minnesota Hospitals, Minneapolis, Minnesota 55455.


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