ArticleJournal of molecular and cellular cardiology2016
Prolongation of atrio-ventricular node conduction in a rabbit model of ischaemic cardiomyopathy: Role of fibrosis and connexin remodelling.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
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- A novel method to extend viability and functionality of living heart slices.Frontiers in cardiovascular medicine · 2023Article
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- Dynamic but discordant alterations in zDHHC5 expression and palmitoylation of its substrates in cardiac pathologies.Frontiers in physiology · 2022Article
- Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model.The Journal of international medical research · 2020Article
- Skin sympathetic nerve activity and ventricular rate control during atrial fibrillation.Heart rhythm · 2020Article
- Implantation of engineered conduction tissue in the rat heart.Molecular medicine reports · 2019Article
- Role of Non-Myocyte Gap Junctions and Connexin Hemichannels in Cardiovascular Health and Disease: Novel Therapeutic Targets?International journal of molecular sciences · 2018Review
- Cardiac fibroblasts : Active players in (atrial) electrophysiology?Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- Age-dependent electrocardiographic changes in Pgc-1β deficient murine hearts.Clinical and experimental pharmacology & physiology · 2018Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
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 the 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 protein (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.
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