Document Detail

Relation of cardiac sympathetic innervation to proinflammatory cytokine levels in patients with heart failure secondary to idiopathic dilated cardiomyopathy.
MedLine Citation:
PMID:  12745101     Owner:  NLM     Status:  MEDLINE    
Experimental studies have shown that cytokine production by the heart may be regulated by sympathetic nervous system stimulation of cardiac beta-adrenergic receptors. Proinflammatory cytokine levels are increased in heart failure, whereas cardiac fixation of 123-I-metaiodobenzylguanidine (MIBG) has been used to study myocardial adrenergic innervation. This study was designed to assess the relation between cardiac MIBG uptake and circulating levels of proinflammatory cytokines in patients with idiopathic dilated cardiomyopathy (IDC). Forty-seven patients (12 women; mean age 56.5 +/- 9 years) with angiographically proved IDC, in New York Heart Association functional classes II to III, and who had left ventricular ejection fraction 30.6 +/- 9.5%, and 20 healthy controls were studied with planar MIBG. The early (10 minutes) and late (4 hours) heart to mediastinum uptake ratio and washout were calculated. Circulating plasma levels of interleukins (IL)-1 and IL-6, tumor necrosis factor-alpha, and solube receptors of TNF (sTNFR) I and II were measured. The patient group had significantly lower values of MIBG uptake at 10 minutes (p <0.001) and 4 hours (p <0.001) and higher washout (p <0.001) than the controls. Late MIBG uptake was significantly correlated with New York Heart Association class (r = -0.42, p = 0.02), left ventricular ejection fraction (r = 0.34, p = 0.01), left ventricular systolic wall stress (r = -0.40, p = 0.05), oxygen consumption at peak exercise (r = 0.32, p = 0.03), IL-1 (r = -0.55, p <0.001), TNF (r = -0.33, p = 0.02), and sTNFRII (r = -0.44, p = 0.001). Multivariate linear regression analysis revealed that MIBG at 4 hours was independently associated with IL-1 levels (p <0.001). Thus, reduced cardiac sympathetic innervation in heart failure is associated with elevated levels of inflammatory cytokines, suggesting that it has a potential inflammatory effect via modulation of the cardiac production of these cytokines.
Fragiskos I Parthenakis; Alexandros Patrianakos; Vasilis Prassopoulos; Evangelos Papadimitriou; Dragana Nikitovic; Nikos S Karkavitsas; Panos E Vardas
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  The American journal of cardiology     Volume:  91     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-05-14     Completed Date:  2003-06-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1190-4     Citation Subset:  AIM; IM    
Cardiology Department, University Hospital of Heraklion, Crete, Greece.
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MeSH Terms
3-Iodobenzylguanidine / pharmacokinetics
Cytokines / blood*
Enzyme-Linked Immunosorbent Assay
Heart / innervation*
Heart Failure / blood*,  physiopathology*
Interleukin-1 / blood
Interleukin-6 / blood
Middle Aged
Oxygen Consumption / physiology
Radiopharmaceuticals / pharmacokinetics
Receptors, Tumor Necrosis Factor / blood
Regression Analysis
Sympathetic Nervous System / physiology*
Tumor Necrosis Factor-alpha / analysis
Ventricular Function, Left / physiology
Reg. No./Substance:
0/Cytokines; 0/Interleukin-1; 0/Interleukin-6; 0/Radiopharmaceuticals; 0/Receptors, Tumor Necrosis Factor; 0/Tumor Necrosis Factor-alpha; 77679-27-7/3-Iodobenzylguanidine

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