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Research Article Free access | 10.1172/JCI107280
Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and the Veterans Administration Hospital, Iowa City, Iowa 52240
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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and the Veterans Administration Hospital, Iowa City, Iowa 52240
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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and the Veterans Administration Hospital, Iowa City, Iowa 52240
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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and the Veterans Administration Hospital, Iowa City, Iowa 52240
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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and the Veterans Administration Hospital, Iowa City, Iowa 52240
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Published May 1, 1973 - More info
We tested the hypothesis that the normal forearm vasoconstrictor response to leg exercise is inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. Forearm vascular responses to supine leg exercise were measured in 10 patients with aortic stenosis and in 2 control groups of 6 patients with mitral stenosis and 5 patients without valvular heart disease.
Forearm vasoconstriction occurred during exercise in the control groups. In contrast, forearm blood flow increased and forearm vascular resistance did not change in patients with aortic stenosis. In six patients with aortic stenosis and a history of exertional syncope, forearm vasodilatation occurred during the second minute of leg exercise. Inhibition or reversal of forearm vasoconstrictor responses in aortic stenosis was asscociated with significant increases in left ventricular pressure.
In three patients with aortic stenosis and exertional syncope, forearm vasodilator responses to exercise changed to vasoconstrictor responses after aortic valve replacement.
The results indicate that forearm vasoconstrictor responses to leg exercise are inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. The observations suggest that reflex vasodilatation resulting from activation of left ventricular baroreceptors may contribute to exertional syncope in patients with aortic stenosis.