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Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study

Pulmonary arterial hypertension (PAH) is a common complication of a congenital heart defect (CHD). Recent studies suggest metformin may be a potential drug to improve cardiac function in PAH. A pilot study was conducted to investigate the efficacy of short-term treatment with a combination regimen c...

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Autores principales: Liao, Shutan, Li, Dongsheng, Hui, Zheng, McLachlan, Craig S., Zhang, Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: European Respiratory Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104295/
https://www.ncbi.nlm.nih.gov/pubmed/30151369
http://dx.doi.org/10.1183/23120541.00060-2018
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author Liao, Shutan
Li, Dongsheng
Hui, Zheng
McLachlan, Craig S.
Zhang, Yang
author_facet Liao, Shutan
Li, Dongsheng
Hui, Zheng
McLachlan, Craig S.
Zhang, Yang
author_sort Liao, Shutan
collection PubMed
description Pulmonary arterial hypertension (PAH) is a common complication of a congenital heart defect (CHD). Recent studies suggest metformin may be a potential drug to improve cardiac function in PAH. A pilot study was conducted to investigate the efficacy of short-term treatment with a combination regimen consisting of bosentan and metformin in PAH-CHD patients as compared with bosentan monotherapy in a prospective, randomised study. Patients with PAH-CHD were randomised to receive bosentan (initially at 62.5 mg twice daily for 4 weeks and then 125 mg twice daily) for 3 months with or without the combination treatment of metformin (500 mg twice daily). 93 patients were enrolled to bosentan monotherapy (n=48) or bosentan/metformin combination treatment (n=45). After 3 months, both treatments significantly improved World Health Organization functional class, 6-min walking distance (6MWD), N-terminal pro-brain natriuretic peptide and right heart haemodynamic parameters. The improvements in 6MWD and pulmonary vascular resistance index were significantly greater in patients treated with combination therapy than in those who received monotherapy (mean±sd 95±136 versus 48±119 m (p=0.017) and −1.8±1.2 versus −1.2±1.3 Wood units per m(2) (p<0.001), respectively). Pulmonary endothelin (EDN)1 was significantly decreased after combination therapy (p=0.006). However, plasma EDN1 levels were not affected. Combination therapy with bosentan and metformin in PAH-CHD patients provides improvements in important outcomes such as exercise capacity and pulmonary haemodynamics, compared with bosentan alone.
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spelling pubmed-61042952018-08-27 Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study Liao, Shutan Li, Dongsheng Hui, Zheng McLachlan, Craig S. Zhang, Yang ERJ Open Res Original Articles Pulmonary arterial hypertension (PAH) is a common complication of a congenital heart defect (CHD). Recent studies suggest metformin may be a potential drug to improve cardiac function in PAH. A pilot study was conducted to investigate the efficacy of short-term treatment with a combination regimen consisting of bosentan and metformin in PAH-CHD patients as compared with bosentan monotherapy in a prospective, randomised study. Patients with PAH-CHD were randomised to receive bosentan (initially at 62.5 mg twice daily for 4 weeks and then 125 mg twice daily) for 3 months with or without the combination treatment of metformin (500 mg twice daily). 93 patients were enrolled to bosentan monotherapy (n=48) or bosentan/metformin combination treatment (n=45). After 3 months, both treatments significantly improved World Health Organization functional class, 6-min walking distance (6MWD), N-terminal pro-brain natriuretic peptide and right heart haemodynamic parameters. The improvements in 6MWD and pulmonary vascular resistance index were significantly greater in patients treated with combination therapy than in those who received monotherapy (mean±sd 95±136 versus 48±119 m (p=0.017) and −1.8±1.2 versus −1.2±1.3 Wood units per m(2) (p<0.001), respectively). Pulmonary endothelin (EDN)1 was significantly decreased after combination therapy (p=0.006). However, plasma EDN1 levels were not affected. Combination therapy with bosentan and metformin in PAH-CHD patients provides improvements in important outcomes such as exercise capacity and pulmonary haemodynamics, compared with bosentan alone. European Respiratory Society 2018-08-22 /pmc/articles/PMC6104295/ /pubmed/30151369 http://dx.doi.org/10.1183/23120541.00060-2018 Text en Copyright ©ERS 2018 http://creativecommons.org/licenses/by-nc/4.0/ This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.
spellingShingle Original Articles
Liao, Shutan
Li, Dongsheng
Hui, Zheng
McLachlan, Craig S.
Zhang, Yang
Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title_full Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title_fullStr Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title_full_unstemmed Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title_short Metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
title_sort metformin added to bosentan therapy in patients with pulmonary arterial hypertension associated with congenital heart defects: a pilot study
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104295/
https://www.ncbi.nlm.nih.gov/pubmed/30151369
http://dx.doi.org/10.1183/23120541.00060-2018
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