Document Detail


Biochemical and electrophysiological alterations underlying ventricular arrhythmias in the failing heart.
MedLine Citation:
PMID:  7713105     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our understanding of the electrophysiological and biochemical mechanisms underlying malignant ventricular arrhythmias in the setting of heart failure has been limited, in large part because of the lack of experimental preparations of heart failure that demonstrate spontaneously occurring ventricular arrhythmias. Recent 3-dimensional cardiac mapping studies in experimental preparations of heart failure, as well as the failing human heart, have demonstrated that focal non-reentrant mechanisms may underlie ventricular tachycardia occurring spontaneously or induced by programmed electrical stimulation. This non-reentrant activation may be due to triggered activity arising from delayed after depolarization. Alterations of calcium homeostasis in the failing heart involving a number of ionic channels and membrane transporters may contribute to increased levels of intracellular calcium and the activation of a transient inward current. Modulation of calcium flux by alpha- and beta-adrenergic stimulation may impact significantly on development of arrhythmias in the failing heart. Activation of the renin-angiotensin system and the generation of free radicals may also contribute. A thorough understanding of the underlying electrophysiological and biochemical alterations responsible for arrhythmogenesis in the failing heart will be critical for the development of therapeutic agents to prevent sudden death in patients with congestive heart failure.
Authors:
S M Pogwizd; P B Corr
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  European heart journal     Volume:  15 Suppl D     ISSN:  0195-668X     ISO Abbreviation:  Eur. Heart J.     Publication Date:  1994 Dec 
Date Detail:
Created Date:  1995-05-17     Completed Date:  1995-05-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8006263     Medline TA:  Eur Heart J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  145-54     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / physiology*
Calcium Channels / physiology
Death, Sudden, Cardiac / etiology,  prevention & control
Electrocardiography*
Free Radicals
Heart Failure / physiopathology*
Humans
Receptors, Adrenergic, alpha / physiology
Renin-Angiotensin System / physiology
Sympathetic Nervous System / physiopathology*
Tachycardia, Ventricular / physiopathology*
Grant Support
ID/Acronym/Agency:
HL-17646/HL/NHLBI NIH HHS; HL-28995/HL/NHLBI NIH HHS; HL-46929/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Free Radicals; 0/Receptors, Adrenergic, alpha; 7440-70-2/Calcium

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


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