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This Article Full Text Full Text (PDF) All Versions of this Article: 580/3/895    most recent jphysiol.2006.120659v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chou, C.-C. Articles by Chen, P.-S. Search for Related Content PubMed PubMed Citation Articles by Chou, C.-C. Articles by Chen, P.-S. Related Collections Cardiovascular

¹ Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center
² Division of Anatomical Pathology, Department of Pathology
³ Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
⁴ Second Section of Cardiology, Department of Medicine, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan

We hypothesize that remodelling of action potential and intracellular calcium (Ca_i) dynamics in the peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction setting. To test this hypothesis, we performed simultaneous optical mapping of Ca_i and membrane potential (V_m) in the left ventricle in 15 rabbit hearts with myocardial infarction for 1 week. Ventricular premature beats frequently originated from the peri-infarct zone, and 37% showed elevation of Ca_i prior to V_m depolarization, suggesting reverse excitation–contraction coupling as their aetiology. During electrically induced ventricular fibrillation, the highest dominant frequency was in the peri-infarct zone in 61 of 70 episodes. The site of highest dominant frequency had steeper action potential duration restitution and was more susceptible to pacing-induced Ca_i alternans than sites remote from infarct. Wavebreaks during ventricular fibrillation tended to occur at sites of persistently elevated Ca_i. Infusion of propranolol flattened action potential duration restitution, reduced wavebreaks and converted ventricular fibrillation to ventricular tachycardia. We conclude that in the subacute phase of myocardial infarction, the peri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable Ca_i dynamics. These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks during ventricular fibrillation. Whereas increased tissue heterogeneity after subacute myocardial infarction creates a highly arrhythmogenic substrate, dynamic action potential and Ca_i cycling remodelling also contribute to the initiation and maintenance of ventricular fibrillation in this setting.

(Received 8 September 2006; accepted after revision 30 January 2007; first published online 1 February 2007)
Corresponding author P-S. Chen: Krannert institute of Cardiology, 1801 North Senate Avenue, Indianapolis, IN, 46202, USA. Email: chenpp{at}iupui.edu

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