Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/71978

Title: Structural and functional alterations in the atrioventricular node and atrioventricular ring tissue in ischaemia-induced heart failure
Issue Date: 2014
Publisher: F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
Citation: Histology and Histopathology, Vol. 29, nº 7 (2014)
ISSN: 1699-5848
0213-3911
Related subjects: CDU::6 - Ciencias aplicadas::61 - Medicina
Keywords: Heart failure
Atrioventricular node
Atrioventricular ring
Abstract: Heart failure (HF) causes dysfunction of the atrioventricular node (AVN) – first or second-degree heart block is a risk factor for sudden cardiac death in HF patients. The aim of the study was to determine if HF causes remodelling of the AVN and right atrioventricular ring (RAVR). HF was induced in rats (n=4) by ligation of the proximal left coronary artery, which resulted in a large infarct of the left ventricle. Sham-operated rats (n=4) were used as controls. Eight weeks after surgery, functional experiments were performed and the hearts were frozen. The body weight of HF rats was similar to control rats, but the mean heart weight of HF rats was significantly enlarged. In HF rats compared to controls, the left ventricle was dilated, left ventricular enddiastolic pressure elevated (21.0±0.6 and 5.4±0.2 mm Hg), left ventricular ejection fraction reduced (0.2±0.02 and 0.5±0.02) and left ventricular end-systolic pressure reduced (102±4.2 and 127±3.1 mm Hg). In HF rats, the in vivo and in vitro PR intervals were increased (41% and 20%), as was the Wenckebach cycle length, indicative of AVN dysfunction. The collagen content was significantly increased in the AVN and RAVR indicating fibrosis. Immunolabelling of caveolin3 (cell membrane marker) showed that there was hypertrophy in HF (cell diameter was increased by 63%, 39% in AVN, RAVR). The TUNEL assay showed that the myocytes of the AVN and RAVR in HF undergo apoptotic cell death. Immunolabelling showed that expression of HCN4 was significantly decreased in the AVN and RAVR (43% and 47%) in HF. We conclude that in HF there is remodelling of the AVN and RAVR and this remodelling may explain the AVN dysfunction.
Primary author: Yanni, Joseph
Maczewski, MIchal
Mackiewicz, Urszula
Siew, Samuel
Fedorenko, Olga
Atkinson, Andrew
Price, Marcus
Beresewicz, Andrzej
Anderson, Robert H.
Boyett, Mark R.
Dobrzynski, Halina
URI: http://hdl.handle.net/10201/71978
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 12
Rights: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 International
Appears in Collections:Vol.29, nº 7 (2014)

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