Publication: Structural and functional alterations in the
atrioventricular node and atrioventricular
ring tissue in ischaemia-induced heart failure
Authors
Yanni, Joseph ; Maczewski, MIchal ; Mackiewicz, Urszula ; Siew, Samuel ; Fedorenko, Olga ; Atkinson, Andrew ; Price, Marcus ; Beresewicz, Andrzej ; Anderson, Robert H. ; Boyett, Mark R. ; Dobrzynski, Halina
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
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.
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Citation
Histology and Histopathology, Vol. 29, nº 7 (2014)
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