Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs

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Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs. / Smith, Julie; Goetze, Jens Peter; Søndergaard, Lars; Kjaergaard, Jesper; Iversen, Kasper K; Vejlstrup, Niels G; Hassager, Christian; Andersen, Claus B; Smith, Julie; Goetze, Jens Peter; Søndergaard, Lars; Kjaergaard, Jesper; Iversen, Kasper K; Vejlstrup, Niels G; Hassager, Christian; Andersen, Claus B.

I: International Journal of Cardiology, Bind 159, Nr. 1, 2012, s. 29-33.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Smith, J, Goetze, JP, Søndergaard, L, Kjaergaard, J, Iversen, KK, Vejlstrup, NG, Hassager, C, Andersen, CB, Smith, J, Goetze, JP, Søndergaard, L, Kjaergaard, J, Iversen, KK, Vejlstrup, NG, Hassager, C & Andersen, CB 2012, 'Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs', International Journal of Cardiology, bind 159, nr. 1, s. 29-33. https://doi.org/10.1016/j.ijcard.2011.02.022, https://doi.org/10.1016/j.ijcard.2011.02.022

APA

Smith, J., Goetze, J. P., Søndergaard, L., Kjaergaard, J., Iversen, K. K., Vejlstrup, N. G., ... Andersen, C. B. (2012). Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs. International Journal of Cardiology, 159(1), 29-33. https://doi.org/10.1016/j.ijcard.2011.02.022, https://doi.org/10.1016/j.ijcard.2011.02.022

Vancouver

Smith J, Goetze JP, Søndergaard L, Kjaergaard J, Iversen KK, Vejlstrup NG o.a. Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs. International Journal of Cardiology. 2012;159(1):29-33. https://doi.org/10.1016/j.ijcard.2011.02.022, https://doi.org/10.1016/j.ijcard.2011.02.022

Author

Smith, Julie ; Goetze, Jens Peter ; Søndergaard, Lars ; Kjaergaard, Jesper ; Iversen, Kasper K ; Vejlstrup, Niels G ; Hassager, Christian ; Andersen, Claus B ; Smith, Julie ; Goetze, Jens Peter ; Søndergaard, Lars ; Kjaergaard, Jesper ; Iversen, Kasper K ; Vejlstrup, Niels G ; Hassager, Christian ; Andersen, Claus B. / Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs. I: International Journal of Cardiology. 2012 ; Bind 159, Nr. 1. s. 29-33.

Bibtex

@article{88f598df78fa447e9e2882511285baaa,
title = "Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs",
abstract = "BACKGROUND: Patients may suffer from right ventricular (RV) failure and malignant cardiac arrhythmias after late pulmonary valve replacement correcting pulmonary regurgitation (PR). But the underlying mechanisms of the refractory arrhythmias are not well understood. METHODS: The aim of present study was to characterize the RV myocardium after percutaneous pulmonary valve implantation (PPVI) in a porcine model after severe PR for 3months. RV histology was evaluated with morphometric methods and RV function was assessed with electrophysiology, echocardiography, and biochemical measures: The results were compared with age-matched sham-operated animals. RESULTS: At euthanasia, RV weight was increased compared to sham-animals, median 127g (115-137) vs. 71g (69.5-76.5), p=0.0007. RV myocyte diameters corrected for individual variation with the RV/LV ratio were enlarged, 1.06 (1.02-1.13) vs. 0.84 (0.80-0.91), p=0.0006. There were no excess collagen tissue (RV/LV ratio), p=0.77. Electrophysiological stimulation resulted in RV arrhythmia in 67{\%} of the animals compared to 25{\%} in the sham-operated animals, but this difference was not statistically significant, p=0.28. Echocardiography revealed geometrical dilation in end-systolic RV area, mean±SD, 11.8±4.9cm(2) vs. 6.0±3.5cm(2), p=0.05, and end-diastolic area, 23.3±10.4cm(2) vs. 12.7±2.5cm(2), p=0.08. RV anterior free wall thickness was not increased, 0.7±0.2cm vs. 0.7±0.1cm, p=0.66. Echocardiographic functional parameters and plasma natriuretic peptides were unchanged. CONCLUSIONS: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may be substrate for arrhythmia.",
author = "Julie Smith and Goetze, {Jens Peter} and Lars S{\o}ndergaard and Jesper Kjaergaard and Iversen, {Kasper K} and Vejlstrup, {Niels G} and Christian Hassager and Andersen, {Claus B} and Julie Smith and Goetze, {Jens Peter} and Lars S{\o}ndergaard and Jesper Kjaergaard and Iversen, {Kasper K} and Vejlstrup, {Niels G} and Christian Hassager and Andersen, {Claus B}",
note = "Copyright {\circledC} 2011 Elsevier Ireland Ltd. All rights reserved.",
year = "2012",
doi = "10.1016/j.ijcard.2011.02.022",
language = "English",
volume = "159",
pages = "29--33",
journal = "International Journal of Cardiology",
issn = "0167-5273",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs

AU - Smith, Julie

AU - Goetze, Jens Peter

AU - Søndergaard, Lars

AU - Kjaergaard, Jesper

AU - Iversen, Kasper K

AU - Vejlstrup, Niels G

AU - Hassager, Christian

AU - Andersen, Claus B

AU - Smith, Julie

AU - Goetze, Jens Peter

AU - Søndergaard, Lars

AU - Kjaergaard, Jesper

AU - Iversen, Kasper K

AU - Vejlstrup, Niels G

AU - Hassager, Christian

AU - Andersen, Claus B

N1 - Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

PY - 2012

Y1 - 2012

N2 - BACKGROUND: Patients may suffer from right ventricular (RV) failure and malignant cardiac arrhythmias after late pulmonary valve replacement correcting pulmonary regurgitation (PR). But the underlying mechanisms of the refractory arrhythmias are not well understood. METHODS: The aim of present study was to characterize the RV myocardium after percutaneous pulmonary valve implantation (PPVI) in a porcine model after severe PR for 3months. RV histology was evaluated with morphometric methods and RV function was assessed with electrophysiology, echocardiography, and biochemical measures: The results were compared with age-matched sham-operated animals. RESULTS: At euthanasia, RV weight was increased compared to sham-animals, median 127g (115-137) vs. 71g (69.5-76.5), p=0.0007. RV myocyte diameters corrected for individual variation with the RV/LV ratio were enlarged, 1.06 (1.02-1.13) vs. 0.84 (0.80-0.91), p=0.0006. There were no excess collagen tissue (RV/LV ratio), p=0.77. Electrophysiological stimulation resulted in RV arrhythmia in 67% of the animals compared to 25% in the sham-operated animals, but this difference was not statistically significant, p=0.28. Echocardiography revealed geometrical dilation in end-systolic RV area, mean±SD, 11.8±4.9cm(2) vs. 6.0±3.5cm(2), p=0.05, and end-diastolic area, 23.3±10.4cm(2) vs. 12.7±2.5cm(2), p=0.08. RV anterior free wall thickness was not increased, 0.7±0.2cm vs. 0.7±0.1cm, p=0.66. Echocardiographic functional parameters and plasma natriuretic peptides were unchanged. CONCLUSIONS: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may be substrate for arrhythmia.

AB - BACKGROUND: Patients may suffer from right ventricular (RV) failure and malignant cardiac arrhythmias after late pulmonary valve replacement correcting pulmonary regurgitation (PR). But the underlying mechanisms of the refractory arrhythmias are not well understood. METHODS: The aim of present study was to characterize the RV myocardium after percutaneous pulmonary valve implantation (PPVI) in a porcine model after severe PR for 3months. RV histology was evaluated with morphometric methods and RV function was assessed with electrophysiology, echocardiography, and biochemical measures: The results were compared with age-matched sham-operated animals. RESULTS: At euthanasia, RV weight was increased compared to sham-animals, median 127g (115-137) vs. 71g (69.5-76.5), p=0.0007. RV myocyte diameters corrected for individual variation with the RV/LV ratio were enlarged, 1.06 (1.02-1.13) vs. 0.84 (0.80-0.91), p=0.0006. There were no excess collagen tissue (RV/LV ratio), p=0.77. Electrophysiological stimulation resulted in RV arrhythmia in 67% of the animals compared to 25% in the sham-operated animals, but this difference was not statistically significant, p=0.28. Echocardiography revealed geometrical dilation in end-systolic RV area, mean±SD, 11.8±4.9cm(2) vs. 6.0±3.5cm(2), p=0.05, and end-diastolic area, 23.3±10.4cm(2) vs. 12.7±2.5cm(2), p=0.08. RV anterior free wall thickness was not increased, 0.7±0.2cm vs. 0.7±0.1cm, p=0.66. Echocardiographic functional parameters and plasma natriuretic peptides were unchanged. CONCLUSIONS: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may be substrate for arrhythmia.

U2 - 10.1016/j.ijcard.2011.02.022

DO - 10.1016/j.ijcard.2011.02.022

M3 - Journal article

C2 - 21411159

VL - 159

SP - 29

EP - 33

JO - International Journal of Cardiology

JF - International Journal of Cardiology

SN - 0167-5273

IS - 1

ER -

ID: 40115623