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Prolongation of atrio-ventricular node conduction in a rabbit model of ischaemic cardiomyopathy: Role of fibrosis and connexin remodelling.

Nisbet, AM, Camelliti, P, Walker, NL, Burton, FL, Cobbe, SM, Kohl, P and Smith, GL (2016) Prolongation of atrio-ventricular node conduction in a rabbit model of ischaemic cardiomyopathy: Role of fibrosis and connexin remodelling. Journal of molecular and cellular cardiology, 94. pp. 54-64.

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Abstract

Conduction abnormalities are frequently associated with cardiac disease, though the mechanisms underlying the commonly associated increases in PQ interval are not known. This study uses a chronic left ventricular (LV) apex myocardial infarction (MI) model in the rabbit to create significant left ventricular dysfunction (LVD) 8weeks post-MI. In vivo studies established that PQ interval increases by approximately 7ms (10%) with no significant change in average heart rate. Optical mapping of isolated Langendorff perfused rabbit hearts recapitulated this result; time to earliest activation of the LV was increased by 14ms (16%) in the LVD group. Intra-atrial and LV transmural conduction times were not altered in the LVD group. Isolated AVN preparations from the LVD group demonstrated a significantly longer conduction time (by approximately 20ms) between atrial and His electrograms than sham controls across a range of pacing cycle lengths. This difference was accompanied by increased effective refractory period and Wenckebach cycle length, suggesting significantly altered AVN electrophysiology post-MI. The AVN origin of abnormality was further highlighted by optical mapping of the isolated AVN. Immunohistochemistry of AVN preparations revealed increased fibrosis and gap junction proteins (connexin43 and 40) remodelling in the AVN of LVD animals compared to sham. A significant increase in myocyte-non-myocyte connexin co-localization was also observed after LVD. These changes may increase the electrotonic load experienced by AVN muscle cells and contribute to slowed conduction velocity within the AVN.

Item Type: Article
Subjects : subj_Biosciences
Divisions : Faculty of Health and Medical Sciences > School of Biosciences and Medicine
Authors :
AuthorsEmailORCID
Nisbet, AMUNSPECIFIEDUNSPECIFIED
Camelliti, PUNSPECIFIEDUNSPECIFIED
Walker, NLUNSPECIFIEDUNSPECIFIED
Burton, FLUNSPECIFIEDUNSPECIFIED
Cobbe, SMUNSPECIFIEDUNSPECIFIED
Kohl, PUNSPECIFIEDUNSPECIFIED
Smith, GLUNSPECIFIEDUNSPECIFIED
Date : 1 May 2016
Funders : British Heart Foundation
Identification Number : 10.1016/j.yjmcc.2016.03.011
Copyright Disclaimer : © 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license
Uncontrolled Keywords : Myocardial infarction; Heart failure; Left ventricular dysfunction; Conduction; Optical mapping; Connexins
Related URLs :
Depositing User : Symplectic Elements
Date Deposited : 12 Jul 2016 13:37
Last Modified : 12 Jul 2016 13:37
URI: http://epubs.surrey.ac.uk/id/eprint/810689

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