Prolongation of atrio-ventricular node conduction in a rabbit model of ischaemic cardiomyopathy: Role of fibrosis and connexin remodelling
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- 作者：Ashley M. Nisbeta ; 1 ; Patrizia Camellitib ; 1 ; p.camelliti@surrey.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Nicola L. Walkera ; Francis L. Burtona ; Stuart M. Cobbea ; Peter Kohlc ; d ; Godfrey L. Smitha ;
- 关键词：AVN ; atrio-ventricular node ; AN ; atrio-nodal ; CHF ; chronic heart failure ; ERPA ; atrial effective refractory period ; ERPAVN ; AVN effective refractory period ; FRPAVN ; AVN functional refractory period ; LV ; left ventricle ; LVD ; left ventricular dysfunction ; MI ; myocardial infarction ; NH ; nodo-Hisian ; O/N ; overnight ; RV ; right ventricle ; RT ; room temperature ; Tact ; activation time
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2016
- 出版时间：May 2016
- 年：2016
- 卷：94
- 期：Complete
- 页码：54-64
- 全文大小：2217 K
文摘
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Chronic myocardial infarction (MI) causes changes in atrio-ventricular node (AVN) function.
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Isolated hearts post-MI show delays in ventricular activation due to slowed conduction via the AVN.
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Isolated AVN preparations demonstrated AVN electrical remodelling post-MI.
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Electrical remodelling is associated with fibrosis and altered expression of connexins in the AVN.
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AVN dysfunction post-MI is caused by localized functional and structural remodelling.