Increased sympathetic nerve activity in pulmonary artery hypertension

This study tested the hypothesis that sympathetic nerve activity is increased in pulmonary artery hypertension (PAH), a rare disease of poor prognosis and incompletely understood pathophysiology. We subsequently explored whether chemoreflex activation contributes to sympathoexcitation in PAH. We mea...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2004-09, Vol.110 (10), p.1308-1312
Main Authors: Velez-Roa, Sonia, Ciarka, Agnieszka, Najem, Boutaina, Vachiery, Jean-Luc, Naeije, Robert, van de Borne, Philippe
Format: Article
Language:English
Subjects:
Calcium Channel Blockers - therapeutic use
Cardiac Catheterization
Cardiac Output, Low - etiology
Catecholamines - blood
Chemoreceptor Cells - drug effects
Chemoreceptor Cells - physiology
Cross-Over Studies
Diuretics - therapeutic use
Double-Blind Method
Dyspnea - etiology
Exercise Tolerance
Female
Heart Rate - drug effects
Humans
Hypertension, Pulmonary - blood
Hypertension, Pulmonary - drug therapy
Hypertension, Pulmonary - physiopathology
Hypertrophy, Right Ventricular - diagnostic imaging
Hypertrophy, Right Ventricular - etiology
Male
Middle Aged
Oximetry
Oxygen - blood
Pericardial Effusion - etiology
Peroneal Nerve - physiopathology
Prostaglandins I - adverse effects
Prostaglandins I - therapeutic use
Severity of Illness Index
Single-Blind Method
Sympathetic Fibers, Postganglionic - physiopathology
Sympathetic Nervous System - physiopathology
Ultrasonography
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Summary:This study tested the hypothesis that sympathetic nerve activity is increased in pulmonary artery hypertension (PAH), a rare disease of poor prognosis and incompletely understood pathophysiology. We subsequently explored whether chemoreflex activation contributes to sympathoexcitation in PAH. We measured muscle sympathetic nerve activity (MSNA) by microneurography, heart rate (HR), and arterial oxygen saturation (Sao(2)) in 17 patients with PAH and 12 control subjects. The patients also underwent cardiac echography, right heart catheterization, and a 6-minute walk test with dyspnea scoring. Circulating catecholamines were determined in 8 of the patients. Chemoreflex deactivation by 100% O(2) was assessed in 14 patients with the use of a randomized, double-blind, placebo-controlled, crossover study design. Compared with the controls, the PAH patients had increased MSNA (67+/-4 versus 40+/-3 bursts per minute; P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.0000140724.90898.d3