Document Detail

Innate inflammation in myocardial perfusion and its implication for heart failure.
MedLine Citation:
PMID:  20955433     Owner:  NLM     Status:  MEDLINE    
Heart failure is characterized by a chronic inflammatory status, with high circulating levels of inflammatory cytokines significantly correlated with deterioration of functional capacity, cardiac performance, and coronary flow reserve--the latter occurring even with normal systemic endothelial function. Impaired coronary flow reserve in heart failure is poorly related to systemic inflammation levels and somewhat matched by a reduction in myocardial contractile reserve. Both coronary flow and myocardial functional reserve can be imaged noninvasively and can be useful clinically for disease severity titration, diagnostic anticipation, and prognostic stratification. Coronary microcirculatory dysfunction can be a trigger of disease and a potential target for therapeutic intervention in heart failure patients. Clinical observational studies showed a striking beneficial effect of endogenous adenosine accumulation on symptoms, exercise capacity, and left ventricular function in chronic heart failure, but this needs to be confirmed in prospective randomized large-scale trials.
Eugenio Picano; Maria Aurora Morales; Silvia del Ry; Rosa Sicari
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1207     ISSN:  1749-6632     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-19     Completed Date:  2010-11-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  107-15     Citation Subset:  IM    
Copyright Information:
© 2010 New York Academy of Sciences.
CNR, Institute of Clinical Physiology, Pisa, Italy.
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MeSH Terms
Coronary Circulation
Endothelium, Vascular / immunology,  physiopathology
Heart Failure / immunology*,  physiopathology*
Immunity, Innate*
Inflammation / immunology*
Inflammation Mediators / physiology
Models, Cardiovascular
Reg. No./Substance:
0/Inflammation Mediators

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