Document Detail


Congestive heart failure: pathophysiologic consequences of neurohormonal activation and the potential for recovery: part I.
MedLine Citation:
PMID:  22030844     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
What begins with a failing heart, unable to sustain adequate renal perfusion and metabolic needs of the tissues it serves becomes a systemic illness whose origins are rooted in neurohormonal activation. This unwanted homeostatic stressor response, an adaptation gone awry, has pathologic consequences. It involves endocrine properties of effector hormones arising from the adrenergic and renin-angiotensin-aldosterone systems. The clinical syndrome congestive heart failure (CHF) has its symptoms and signs rooted in a hormonally mediated salt-avid state. The ensuing salt and water retention includes the expansion of the intravascular space with consequent central and systemic venous congestion that, respectively, involves the heart and lungs, the liver, gut and kidneys and ultimately the extravascular space. Other pathophysiologic outcomes contribute to a proinflammatory CHF phenotype. These include an ongoing adverse remodeling of the failing heart with lost necrotic cardiomyocytes and a consequent replacement fibrosis; wasting of soft tissues and resorption of bone; dyshomeostasis of extra- and intracellular mono- and divalent cations that contributes to the appearance of oxidative stress coupled with compromised antioxidant defenses and an immunostimulatory state with activated lymphocytes and monocytes elaborating proinflammatory cytokines. In this 2-part review, the pathophysiologic consequences associated with neurohormonal activation in CHF will first be reviewed. Next, several lines of evidence are considered that raise the hitherto unfathomable prospect for recovery from CHF, including reverse remodeling of the heart and systemic tissues.
Authors:
Preeti Dube; Karl T Weber
Related Documents :
3511334 - The valsalva maneuver and response revisited.
22166594 - Left atrial global and regional function in patients with paroxysmal atrial fibrillatio...
22652004 - Ventricular hcn channels decrease the repolarization reserve in the hypertrophic heart.
11416534 - Pathophysiology of hypertension in the elderly.
21258154 - Cardiac biomarkers in the diagnosis, prognosis and management of coronary artery diseas...
12408214 - The physiological response in patients with acute myocardial infarction to the administ...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The American journal of the medical sciences     Volume:  342     ISSN:  1538-2990     ISO Abbreviation:  Am. J. Med. Sci.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-10-27     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370506     Medline TA:  Am J Med Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  348-51     Citation Subset:  AIM; IM    
Affiliation:
From the Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, Tennessee.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Late termination of pregnancy for fetal abnormalities: The perspective of Indian lay persons and med...
Next Document:  Gill Remodeling in Crucian Carp during Sustained Exercise and the Effect on Subsequent Swimming Perf...