Document Detail


Atrial ionic remodeling induced by atrial tachycardia in the presence of congestive heart failure.
MedLine Citation:
PMID:  15381657     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Atrial fibrillation (AF) and congestive heart failure (CHF) produce discrete forms of atrial ionic remodeling. The in vivo effects of atrial tachycardia (AT) remodeling are altered by CHF. This study evaluated underlying mechanisms at the level of ionic remodeling. METHODS AND RESULTS: We studied 4 groups of dogs: (1) unpaced controls (CTLs); (2) CHF caused by 2-week ventricular tachypacing (VTP, 240 bpm); (3) AT (400 bpm x 7 days); and (4) CHF+AT (2-week VTP with AT for the last 7 days). CHF and CHF+AT groups equally increased left atrial pressure. AF duration was increased in all paced groups. Effective refractory period (ERP) was decreased by 42% in AT versus CTL but by only 24% in AT+CHF versus CHF. CHF reduced L-type Ca2+ (I(Ca)), transient-outward (I(to)), and the slow delayed-rectifier (I(Ks)) currents while increasing the Na+-Ca2+ exchanger (I(NCX)) and not affecting the inward-rectifier (I(K1)) current. AT reduced I(to) and I(Ca) while increasing I(K1) and leaving I(Ks) unaltered. The addition of AT to CHF failed to alter I(to), I(Ks), or I(NCX) beyond the effect of CHF alone, decreased I(Ca) slightly compared with CHF alone, but had smaller effects on I(Ca) and I(K1) compared with AT alone. Thus, CHF+AT, as would occur in a CHF patient who develops AF, produced an ionic remodeling pattern different from that of CHF or AT alone and from what would have been predicted from additive effects of CHF and AT. CONCLUSIONS: The presence of CHF alters AT-induced ionic remodeling. Thus, the ionic remodeling caused by cardiac arrhythmias in the presence of cardiac pathology is not necessarily predictable from the effects of either alone, with important potential implications for understanding the pathophysiology of arrhythmias in the diseased heart.
Authors:
Tae-Joon Cha; Joachim R Ehrlich; Liming Zhang; Stanley Nattel
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  110     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-09-21     Completed Date:  2005-06-07     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1520-6     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, Montreal Heart Institute and University of Montreal, Montreal, Quebec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Atrial Fibrillation / complications,  metabolism*
Calcium / metabolism*
Calcium Channels / metabolism*
Calcium Channels, L-Type / metabolism
Cardiac Pacing, Artificial / adverse effects
Catheter Ablation / adverse effects
Dogs
Heart Atria / metabolism*
Heart Block / complications
Heart Failure / complications*
Ion Transport*
Myocytes, Cardiac / metabolism
Patch-Clamp Techniques
Potassium / metabolism*
Potassium Channels / metabolism*
Potassium Channels, Inwardly Rectifying / metabolism
Sodium-Calcium Exchanger / metabolism*
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Calcium Channels, L-Type; 0/Potassium Channels; 0/Potassium Channels, Inwardly Rectifying; 0/Sodium-Calcium Exchanger; 7440-09-7/Potassium; 7440-70-2/Calcium

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


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