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Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect

Uncorrected atrial septal defect undergoes right ventricle chronic volume overload which may lead to pulmonary hypertension and Eisenmenger Syndrome. The soluble suppression of tumorigenicity-2 is a left ventricle strain biomarker; however, its role in right ventricle strain is unclear. This study a...

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Autores principales: Pratama, Reza S., Hartopo, Anggoro B., Anggrahini, Dyah W., Dewanto, Vera C., Dinarti, Lucia K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252384/
https://www.ncbi.nlm.nih.gov/pubmed/32518620
http://dx.doi.org/10.1177/2045894020915832
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author Pratama, Reza S.
Hartopo, Anggoro B.
Anggrahini, Dyah W.
Dewanto, Vera C.
Dinarti, Lucia K.
author_facet Pratama, Reza S.
Hartopo, Anggoro B.
Anggrahini, Dyah W.
Dewanto, Vera C.
Dinarti, Lucia K.
author_sort Pratama, Reza S.
collection PubMed
description Uncorrected atrial septal defect undergoes right ventricle chronic volume overload which may lead to pulmonary hypertension and Eisenmenger Syndrome. The soluble suppression of tumorigenicity-2 is a left ventricle strain biomarker; however, its role in right ventricle strain is unclear. This study aimed to investigate the implication of serum soluble suppression of tumorigenicity-2 in adult uncorrected atrial septal defect. This was a cross-sectional study. We enrolled 81 adult uncorrected secundum atrial septal defect patients. Clinical and hemodynamic data were collected. Serum samples were withdrawn from the pulmonary artery during right heart catheterization. Serum soluble suppression of tumorigenicity-2 and NT-proBNP levels were measured. Subjects were divided into three groups based on clinical and hemodynamic severity. The correlation of soluble suppression of tumorigenicity-2 with patients' data and comparison among groups were analyzed. A p value <0.05 was considered statistically significant. Results showed that, there were significant correlations between serum soluble suppression of tumorigenicity-2 and mean pulmonary artery pressure (r = 0.203, p = 0.035) and right ventricle end-diastolic diameter (r = 0.203, p <0.05). Median serum soluble suppression of tumorigenicity-2 level was incrementally increased from group I (atrial septal defect and no-pulmonary hypertension), group II (left-to-right atrial septal defect and pulmonary hypertension), to group III (Eisenmenger Syndrome): (17.4 ng/mL, 21.8 ng/mL, and 29.4 ng/mL, respectively). A post-hoc analysis showed that serum soluble suppression of tumorigenicity-2 level was significantly different between groups I and III (p = 0.01). Serum N terminal pro brain natriuretic peptide (NT-proBNP) level was consistently associated with worse clinical and hemodynamic parameters. No correlation was found between serum soluble suppression of tumorigenicity-2 and NT-proBNP level. In conclusion, serum soluble suppression of tumorigenicity-2 level had significant positive correlation with mean pulmonary artery pressure and right ventricle end-diastolic diameter in uncorrected secundum atrial septal defect patients. Higher serum soluble suppression of tumorigenicity-2 level was associated with the presence of pulmonary hypertension and Eisenmenger Syndrome in uncorrected secundum atrial septal defect patients.
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spelling pubmed-72523842020-06-08 Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect Pratama, Reza S. Hartopo, Anggoro B. Anggrahini, Dyah W. Dewanto, Vera C. Dinarti, Lucia K. Pulm Circ Research Article Uncorrected atrial septal defect undergoes right ventricle chronic volume overload which may lead to pulmonary hypertension and Eisenmenger Syndrome. The soluble suppression of tumorigenicity-2 is a left ventricle strain biomarker; however, its role in right ventricle strain is unclear. This study aimed to investigate the implication of serum soluble suppression of tumorigenicity-2 in adult uncorrected atrial septal defect. This was a cross-sectional study. We enrolled 81 adult uncorrected secundum atrial septal defect patients. Clinical and hemodynamic data were collected. Serum samples were withdrawn from the pulmonary artery during right heart catheterization. Serum soluble suppression of tumorigenicity-2 and NT-proBNP levels were measured. Subjects were divided into three groups based on clinical and hemodynamic severity. The correlation of soluble suppression of tumorigenicity-2 with patients' data and comparison among groups were analyzed. A p value <0.05 was considered statistically significant. Results showed that, there were significant correlations between serum soluble suppression of tumorigenicity-2 and mean pulmonary artery pressure (r = 0.203, p = 0.035) and right ventricle end-diastolic diameter (r = 0.203, p <0.05). Median serum soluble suppression of tumorigenicity-2 level was incrementally increased from group I (atrial septal defect and no-pulmonary hypertension), group II (left-to-right atrial septal defect and pulmonary hypertension), to group III (Eisenmenger Syndrome): (17.4 ng/mL, 21.8 ng/mL, and 29.4 ng/mL, respectively). A post-hoc analysis showed that serum soluble suppression of tumorigenicity-2 level was significantly different between groups I and III (p = 0.01). Serum N terminal pro brain natriuretic peptide (NT-proBNP) level was consistently associated with worse clinical and hemodynamic parameters. No correlation was found between serum soluble suppression of tumorigenicity-2 and NT-proBNP level. In conclusion, serum soluble suppression of tumorigenicity-2 level had significant positive correlation with mean pulmonary artery pressure and right ventricle end-diastolic diameter in uncorrected secundum atrial septal defect patients. Higher serum soluble suppression of tumorigenicity-2 level was associated with the presence of pulmonary hypertension and Eisenmenger Syndrome in uncorrected secundum atrial septal defect patients. SAGE Publications 2020-05-26 /pmc/articles/PMC7252384/ /pubmed/32518620 http://dx.doi.org/10.1177/2045894020915832 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Research Article
Pratama, Reza S.
Hartopo, Anggoro B.
Anggrahini, Dyah W.
Dewanto, Vera C.
Dinarti, Lucia K.
Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title_full Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title_fullStr Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title_full_unstemmed Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title_short Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
title_sort serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252384/
https://www.ncbi.nlm.nih.gov/pubmed/32518620
http://dx.doi.org/10.1177/2045894020915832
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