Document Detail

Cycle length dependence of the electrophysiological effects of increased load on the myocardium.
MedLine Citation:
PMID:  8790056     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Mechanoelectric feedback, the process by which changes in mechanical activity change the electrophysiology of the myocardium, has been linked to the genesis of arrhythmias. We investigated possible arrhythmogenic mechanisms by measuring changes in steady-state action potential duration and, more particularly, electrical restitution on a transiently applied load change, because action potential recovery may provide clues to arrhythmogenesis. METHODS AND RESULTS: Pigs were anesthetized and their hearts exposed. A snare was placed around the aorta, and the right atrium was paced. Ventricular pressure, monophasic action potential, and segment motion were recorded from the left ventricle. The action potential duration was measured before and during transient aortic occlusion. Electrical restitution curves were constructed from the records obtained during normal loading or during transient aortic occlusion. The degree of shortening of action potential duration on aortic occlusion decreased with decreases in the steady-state beat-to-beat interval (P = .0008). Control restitution curves had the typical configuration, with a rapid initial, usually monotonic, rise toward a plateau. Some curves showed a marginal "supernormal" section. Increased load reduced the action potential duration at the plateau of the restitution curve (9.4 ms, P < .0001) but increased the action potential duration at the start of the restitution curve (8.7 ms, P = .03). Increased loading increased the maximum slope of the electrical restitution curve by 32 ms/100 ms (P = .04). Increased load also increased the supernormal period of the electrical restitution curves. CONCLUSIONS: Mechanoelectric feedback produces changes in rate-dependent electrophysiology, which could favor a matrix conducive to arrhythmogenesis.
S M Horner; D J Dick; C F Murphy; M J Lab
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  94     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1996 Sep 
Date Detail:
Created Date:  1996-10-17     Completed Date:  1996-10-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1131-6     Citation Subset:  AIM; IM; S    
British Heart Foundation Cardiac Arrhythmia Research Group, Department of Physiology, Charing Cross and Westminster Medical School, London, UK.
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MeSH Terms
Action Potentials
Arrhythmias, Cardiac / etiology
Heart / physiology*

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