Document Detail

Increased sympathetic nerve activity in pulmonary artery hypertension.
MedLine Citation:
PMID:  15337703     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: 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. METHODS AND RESULTS: 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<0.0001) and HR (82+/-4 versus 68+/-3 bpm; P=0.02). MSNA in the PAH patients was correlated with HR (r=0.64, P=0.006), Sao(2) (r=-0.53, P=0.03), the presence of pericardial effusion (r=0.51, P=0.046), and NYHA class (r=0.52, P=0.033). The PAH patients treated with prostacyclin derivatives had higher MSNA (P=0.009), lower Sao(2) (P=0.01), faster HR (P=0.003), and worse NYHA class (P=0.04). Plasma catecholamines were normal. Peripheral chemoreflex deactivation with hyperoxia increased Sao(2) (91.7+/-1% to 98.4+/-0.2%; P<0.0001) and decreased MSNA (67+/-5 to 60+/-4 bursts per minute; P=0.0015), thereby correcting approximately one fourth of the difference between PAH patients and controls. CONCLUSIONS: We report for the first time direct evidence of increased sympathetic nerve traffic in advanced PAH. Sympathetic hyperactivity in PAH is partially chemoreflex mediated and may be related to disease severity.
Sonia Velez-Roa; Agnieszka Ciarka; Boutaina Najem; Jean-Luc Vachiery; Robert Naeije; Philippe van de Borne
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2004-08-30
Journal Detail:
Title:  Circulation     Volume:  110     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-09-08     Completed Date:  2006-04-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1308-12     Citation Subset:  AIM; IM    
Department of Cardiology, Erasme University Hospital, Brussels, Belgium.
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MeSH Terms
Calcium Channel Blockers / therapeutic use
Cardiac Output, Low / etiology
Catecholamines / blood
Chemoreceptor Cells / drug effects,  physiology*
Cross-Over Studies
Diuretics / therapeutic use
Double-Blind Method
Dyspnea / etiology
Exercise Tolerance
Heart Catheterization
Heart Rate / drug effects
Hypertension, Pulmonary / blood,  drug therapy,  physiopathology*
Hypertrophy, Right Ventricular / etiology,  ultrasonography
Middle Aged
Oxygen / blood,  diagnostic use
Pericardial Effusion / etiology
Peroneal Nerve / physiopathology
Prostaglandins I / adverse effects,  therapeutic use
Severity of Illness Index
Single-Blind Method
Sympathetic Fibers, Postganglionic / physiopathology
Sympathetic Nervous System / physiopathology*
Reg. No./Substance:
0/Calcium Channel Blockers; 0/Catecholamines; 0/Diuretics; 0/Prostaglandins I; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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