Document Detail

The relationship between aldosterone, oxidative stress, and inflammation in chronic, stable human heart failure.
MedLine Citation:
PMID:  16520260     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Aldosterone antagonists reduce morbidity and mortality in patients with severe heart failure, but the mechanisms responsible are not fully understood. Observations in animal models suggest that elevated levels of aldosterone promote oxidative stress and inflammation in the myocardium. It is unknown if these findings are relevant to heart failure patients who may have much lower aldosterone levels. METHODS AND RESULTS: We therefore examined the relationship of plasma aldosterone levels to markers of oxidative stress, inflammation and matrix turnover in 58 patients with chronic, stable heart failure from systolic dysfunction (LV ejection fraction <0.40) who were not receiving aldosterone antagonists. Chronic, stable heart failure patients had modestly elevated levels of aldosterone. Additionally, these patients had elevated levels of 8-isoprostaglandin F(2alpha), C-reactive protein, soluble intercellular adhesion molecule-1, osteopontin, brain natriuretic peptide, procollagen type III aminoterminal peptide, and tissue inhibitor of metalloproteinase-1. Among these patients with heart failure, aldosterone levels correlated with 8-iso-PGF(2alpha) (P = .003), ICAM-1 (P = .008), and TIMP-1 (P = .006) after adjustment for age, gender, race, diabetes, smoking, heart rate, left ventricular mass, and body mass index. CONCLUSION: In chronic, stable heart failure patients on standard therapy, higher aldosterone levels are associated with systemic evidence of oxidative stress, inflammation, and matrix turnover.
Eugene Kotlyar; Joseph A Vita; Michael R Winter; Eric H Awtry; Deborah A Siwik; John F Keaney; Douglas B Sawyer; L Adrienne Cupples; Wilson S Colucci; Flora Sam
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiac failure     Volume:  12     ISSN:  1532-8414     ISO Abbreviation:  J. Card. Fail.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-03-07     Completed Date:  2006-08-08     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9442138     Medline TA:  J Card Fail     Country:  United States    
Other Details:
Languages:  eng     Pagination:  122-7     Citation Subset:  IM    
Cardiovascular Section, Evans Department of Medicine, Boston University, 88 E. Newton Street D-8, Boston, MA, USA.
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MeSH Terms
Aldosterone / blood*
Biological Markers / blood
C-Reactive Protein / analysis
Dinoprost / analogs & derivatives,  blood
Heart Failure / blood*,  physiopathology*
Intercellular Adhesion Molecule-1 / blood
Middle Aged
Natriuretic Peptide, Brain / blood
Oxidative Stress / physiology*
Peptide Fragments / blood
Procollagen / blood
Sialoglycoproteins / blood
Tissue Inhibitor of Metalloproteinase-1 / blood
Grant Support
Reg. No./Substance:
0/Biological Markers; 0/Peptide Fragments; 0/Procollagen; 0/SPP1 protein, human; 0/Sialoglycoproteins; 0/Tissue Inhibitor of Metalloproteinase-1; 0/procollagen Type III-N-terminal peptide; 106441-73-0/Osteopontin; 114471-18-0/Natriuretic Peptide, Brain; 126547-89-5/Intercellular Adhesion Molecule-1; 27415-26-5/8-epi-prostaglandin F2alpha; 52-39-1/Aldosterone; 551-11-1/Dinoprost; 9007-41-4/C-Reactive Protein

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