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.
| Original language | English |
|---|---|
| Pages (from-to) | 891-902 |
| Number of pages | 12 |
| Journal | Histology and Histopathology |
| Volume | 29 |
| Issue number | 7 |
| Publication status | Published - 2014 |
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Keywords
- Atrioventricular node
- Atrioventricular ring
- Heart failure
ASJC Scopus subject areas
- Histology
- Pathology and Forensic Medicine
Cite this
Structural and functional alterations in the atrioventricular node and atrioventricular ring tissue in ischaemia-induced heart failure. / Yanni, Joseph; Maczewski, Michal; Mackiewicz, Urszula; Siew, Samuel; Fedorenko, Olga; Atkinson, Andrew; Price, Marcus; Beresewicz, Andrzej; Anderson, Robert H.; Boyett, Mark R.; Dobrzynski, Halina.
In: Histology and Histopathology, Vol. 29, No. 7, 2014, p. 891-902.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Structural and functional alterations in the atrioventricular node and atrioventricular ring tissue in ischaemia-induced heart failure
AU - Yanni, Joseph
AU - Maczewski, Michal
AU - Mackiewicz, Urszula
AU - Siew, Samuel
AU - Fedorenko, Olga
AU - Atkinson, Andrew
AU - Price, Marcus
AU - Beresewicz, Andrzej
AU - Anderson, Robert H.
AU - Boyett, Mark R.
AU - Dobrzynski, Halina
PY - 2014
Y1 - 2014
N2 - 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.
AB - 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.
KW - Atrioventricular node
KW - Atrioventricular ring
KW - Heart failure
UR - http://www.scopus.com/inward/record.url?scp=84902991638&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84902991638&partnerID=8YFLogxK
M3 - Article
C2 - 24368587
AN - SCOPUS:84902991638
VL - 29
SP - 891
EP - 902
JO - Histology and Histopathology
JF - Histology and Histopathology
SN - 0213-3911
IS - 7
ER -