Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone

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Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone. / Andersen, Stine; Axelsen, Julie Birkmose; Ringgaard, Steffen; Nyengaard, Jens Randel; Nielsen, Signe Holm; Genovese, Federica; Karsdal, Morten Asser; Hyldebrandt, Janus Adler; Sørensen, Charlotte Brandt; deMan, Frances; Bogaard, Harm Jan; Nielsen-Kudsk, Jens Erik; Andersen, Asger.

I: Pulmonary Circulation, Bind 9, Nr. 2, 05.2019, s. 1-13.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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Andersen, Stine ; Axelsen, Julie Birkmose ; Ringgaard, Steffen ; Nyengaard, Jens Randel ; Nielsen, Signe Holm ; Genovese, Federica ; Karsdal, Morten Asser ; Hyldebrandt, Janus Adler ; Sørensen, Charlotte Brandt ; deMan, Frances ; Bogaard, Harm Jan ; Nielsen-Kudsk, Jens Erik ; Andersen, Asger. / Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone. I: Pulmonary Circulation. 2019 ; Bind 9, Nr. 2. s. 1-13.

Bibtex

@article{5a46800dc81f4e0aad1673ad8106bf5e,
title = "Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone",
abstract = "Cardiac fibrosis contributes to the development of heart failure in pulmonary hypertension. We aimed to assess the development of fibrosis and the effects of treatment with the anti-fibrotic agent pirfenidone in pressure overload induced right ventricular (RV) failure. Wistar rat weanlings were randomized to pulmonary trunk banding (PTB) or sham surgery. One week after the procedure, PTB rats were randomized into two groups with either six weeks on standard chow or treatment with pirfenidone mixed in chow (700 mg/kg/day). RV hemodynamic effects were evaluated by echocardiography, cardiac magnetic resonance imaging (MRI), and pressure-volume measurements. Sections from the isolated RV, left ventricle, and septum were sampled systematically; stereological point grids and the nucleator were used to estimate volume of fibrosis and cardiac hypertrophy, respectively. PTB caused RV failure in all rats subjected to the procedure. The volume fraction of fibrosis in the RV increased threefold in PTB rats corresponding to a sixfold increase in total volume of RV fibrosis. Volume fraction of fibrosis and total volume of fibrosis also increased in the septum and in the left ventricle. Pirfenidone reduced body weight but did not improve RV hemodynamics or reduce cardiac fibrosis. RV cardiomyocyte profile area was increased twofold in PTB rats without any effect of pirfenidone. RV pressure overload after PTB induced not only RV but also septal and left ventricular fibrosis assessed by stereology. Treatment with pirfenidone reduced body weight but did not reduce the development of cardiac fibrosis or delay the progression of RV failure.",
keywords = "animal models, remodeling, right ventricular function and dysfunction, COLLAGEN, PULMONARY ARTERIAL-HYPERTENSION, BONE MORPHOGENETIC PROTEIN, PREDICTION, BIOMARKERS, INHIBITION, MYOCARDIAL FIBROSIS, CARDIAC FIBROSIS, DYSFUNCTION, CONTRIBUTES",
author = "Stine Andersen and Axelsen, {Julie Birkmose} and Steffen Ringgaard and Nyengaard, {Jens Randel} and Nielsen, {Signe Holm} and Federica Genovese and Karsdal, {Morten Asser} and Hyldebrandt, {Janus Adler} and S{\o}rensen, {Charlotte Brandt} and Frances deMan and Bogaard, {Harm Jan} and Nielsen-Kudsk, {Jens Erik} and Asger Andersen",
year = "2019",
month = may,
doi = "10.1177/2045894019848659",
language = "English",
volume = "9",
pages = "1--13",
journal = "Pulmonary Circulation",
issn = "2045-8932",
publisher = "University of Chicago Press",
number = "2",

}

RIS

TY - JOUR

T1 - Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone

AU - Andersen, Stine

AU - Axelsen, Julie Birkmose

AU - Ringgaard, Steffen

AU - Nyengaard, Jens Randel

AU - Nielsen, Signe Holm

AU - Genovese, Federica

AU - Karsdal, Morten Asser

AU - Hyldebrandt, Janus Adler

AU - Sørensen, Charlotte Brandt

AU - deMan, Frances

AU - Bogaard, Harm Jan

AU - Nielsen-Kudsk, Jens Erik

AU - Andersen, Asger

PY - 2019/5

Y1 - 2019/5

N2 - Cardiac fibrosis contributes to the development of heart failure in pulmonary hypertension. We aimed to assess the development of fibrosis and the effects of treatment with the anti-fibrotic agent pirfenidone in pressure overload induced right ventricular (RV) failure. Wistar rat weanlings were randomized to pulmonary trunk banding (PTB) or sham surgery. One week after the procedure, PTB rats were randomized into two groups with either six weeks on standard chow or treatment with pirfenidone mixed in chow (700 mg/kg/day). RV hemodynamic effects were evaluated by echocardiography, cardiac magnetic resonance imaging (MRI), and pressure-volume measurements. Sections from the isolated RV, left ventricle, and septum were sampled systematically; stereological point grids and the nucleator were used to estimate volume of fibrosis and cardiac hypertrophy, respectively. PTB caused RV failure in all rats subjected to the procedure. The volume fraction of fibrosis in the RV increased threefold in PTB rats corresponding to a sixfold increase in total volume of RV fibrosis. Volume fraction of fibrosis and total volume of fibrosis also increased in the septum and in the left ventricle. Pirfenidone reduced body weight but did not improve RV hemodynamics or reduce cardiac fibrosis. RV cardiomyocyte profile area was increased twofold in PTB rats without any effect of pirfenidone. RV pressure overload after PTB induced not only RV but also septal and left ventricular fibrosis assessed by stereology. Treatment with pirfenidone reduced body weight but did not reduce the development of cardiac fibrosis or delay the progression of RV failure.

AB - Cardiac fibrosis contributes to the development of heart failure in pulmonary hypertension. We aimed to assess the development of fibrosis and the effects of treatment with the anti-fibrotic agent pirfenidone in pressure overload induced right ventricular (RV) failure. Wistar rat weanlings were randomized to pulmonary trunk banding (PTB) or sham surgery. One week after the procedure, PTB rats were randomized into two groups with either six weeks on standard chow or treatment with pirfenidone mixed in chow (700 mg/kg/day). RV hemodynamic effects were evaluated by echocardiography, cardiac magnetic resonance imaging (MRI), and pressure-volume measurements. Sections from the isolated RV, left ventricle, and septum were sampled systematically; stereological point grids and the nucleator were used to estimate volume of fibrosis and cardiac hypertrophy, respectively. PTB caused RV failure in all rats subjected to the procedure. The volume fraction of fibrosis in the RV increased threefold in PTB rats corresponding to a sixfold increase in total volume of RV fibrosis. Volume fraction of fibrosis and total volume of fibrosis also increased in the septum and in the left ventricle. Pirfenidone reduced body weight but did not improve RV hemodynamics or reduce cardiac fibrosis. RV cardiomyocyte profile area was increased twofold in PTB rats without any effect of pirfenidone. RV pressure overload after PTB induced not only RV but also septal and left ventricular fibrosis assessed by stereology. Treatment with pirfenidone reduced body weight but did not reduce the development of cardiac fibrosis or delay the progression of RV failure.

KW - animal models

KW - remodeling

KW - right ventricular function and dysfunction

KW - COLLAGEN

KW - PULMONARY ARTERIAL-HYPERTENSION

KW - BONE MORPHOGENETIC PROTEIN

KW - PREDICTION

KW - BIOMARKERS

KW - INHIBITION

KW - MYOCARDIAL FIBROSIS

KW - CARDIAC FIBROSIS

KW - DYSFUNCTION

KW - CONTRIBUTES

UR - http://www.scopus.com/inward/record.url?scp=85067642348&partnerID=8YFLogxK

U2 - 10.1177/2045894019848659

DO - 10.1177/2045894019848659

M3 - Journal article

C2 - 30997866

VL - 9

SP - 1

EP - 13

JO - Pulmonary Circulation

JF - Pulmonary Circulation

SN - 2045-8932

IS - 2

ER -