Premium
Regional reduction in excitability and connexin 43 expression in areas of conduction disturbance in canine ventricles with chronic rapid pacing and ameroid constrictor
Author(s) -
Falcao Stephanie,
Rousseau Guy,
Vermeulen Michel,
Bouchard Caroline,
Jones Douglas,
Cardinal Rene
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a323-a
Subject(s) - connexin , cardiology , disturbance (geology) , medicine , anatomy , gap junction , biology , microbiology and biotechnology , intracellular , paleontology
It has been suggested that altered connexin43 (Cx43) expression may be associated with reentrant ventricular arrhythmias in chronic myocardial infarction. A similar possibility was investigated in canine hearts without necrotic scar, which were subjected to chronic rapid pacing (CRP) at 240 beats/min for 4 weeks and progressive obliteration of the left coronary circumflex artery (LCx) by an ameroid constrictor. Electrophysiologic alterations identified by mapping the LCx territory (191 unipolar recordings) included activation delay, ST segment potential elevation and reduced maximum negative slope (−dV/dtmax) in the activation complex of unipolar electrograms. The LCx was divided into areas displaying depressed conduction (LCx1: 0.07±0.04 m/s,mean±SD) and milder depression (LCx2: 0.23 ±0.01 m/s). Cx43 measured by Western blot in tissue sampled from LCx1 was significantly reduced (62±63%) but not in LCx2 (39±87%) with reference to the left anterior descending artery territory (100%). Moreover, ‐dV/dtmax was significantly depressed (5.3±3.6 mV/ms) and ST segment potential was significantly elevated (17.7±17 mV) in LCx1 in comparison with LCx2 (10±3.9 mV/ms and −1.1±1.9 mV, respectively). The data indicate that conduction disturbances are induced by reduced Cx43 expression in conjunction with depressed excitability in viable energy‐stressed myocardium. Supported by the Canadian Institutes of Health Research and Quebec Heart Foundation.