The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

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Standard

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model. / Agger, Peter; Lakshminrusimha, Satyan; Laustsen, Christoffer; Gugino, Sylvia; Frandsen, Jesper R; Smerup, Morten; Anderson, Robert H; Hjortdal, Vibeke; Steinhorn, Robin H.

I: Pediatric Research, Bind 79, Nr. 4, 04.2016, s. 565-74.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Agger, P, Lakshminrusimha, S, Laustsen, C, Gugino, S, Frandsen, JR, Smerup, M, Anderson, RH, Hjortdal, V & Steinhorn, RH 2016, 'The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model', Pediatric Research, bind 79, nr. 4, s. 565-74. https://doi.org/10.1038/pr.2015.263

APA

Agger, P., Lakshminrusimha, S., Laustsen, C., Gugino, S., Frandsen, J. R., Smerup, M., Anderson, R. H., Hjortdal, V., & Steinhorn, R. H. (2016). The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model. Pediatric Research, 79(4), 565-74. https://doi.org/10.1038/pr.2015.263

Vancouver

Agger P, Lakshminrusimha S, Laustsen C, Gugino S, Frandsen JR, Smerup M o.a. The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model. Pediatric Research. 2016 apr.;79(4):565-74. https://doi.org/10.1038/pr.2015.263

Author

Agger, Peter ; Lakshminrusimha, Satyan ; Laustsen, Christoffer ; Gugino, Sylvia ; Frandsen, Jesper R ; Smerup, Morten ; Anderson, Robert H ; Hjortdal, Vibeke ; Steinhorn, Robin H. / The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model. I: Pediatric Research. 2016 ; Bind 79, Nr. 4. s. 565-74.

Bibtex

@article{280aab806ad246d0a417f20697708fff,
title = "The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model",
abstract = "BACKGROUND: Persistent pulmonary hypertension in the newborn remains a syndrome with high mortality. Knowledge of changes in myocardial architecture in the setting of heart failure in persistent pulmonary hypertension is lacking, and could aid in the explanation of the prevailing high mortality.METHODS: Persistent pulmonary hypertension was induced by antenatal ligation of the arterial duct in six ovine fetuses. The hearts were compared ex vivo with five matched control hearts, using diffusion tensor imaging to provide the overall anatomical arrangement, and assessment of the angulations and course of the cardiomyocytes. Fibrosis was assessed with histology.RESULTS: We found an overall increase in heart size in pulmonary hypertension, with myocardial thickening confined to the interventricular septum. An increase of 3.5° in angulation of myocyte aggregations was found in hypertensive hearts. In addition, we observed a 2.2% increase in collagen content in the right ventricular free wall. Finally, we found a previously undescribed subepicardial layer of strictly longitudinally oriented cardiomyocytes confined to the right ventricle in all hearts.CONCLUSION: Myocardial fibrosis and possibly changes in angulations of myocytes seem to play a part in the etiology of persistent pulmonary hypertension. Moreover, a new anatomical arrangement of right ventricular mural architecture is described.",
keywords = "Animals, Animals, Newborn, Disease Models, Animal, Hypertension, Pulmonary/pathology, Myocardium/pathology, Sheep",
author = "Peter Agger and Satyan Lakshminrusimha and Christoffer Laustsen and Sylvia Gugino and Frandsen, {Jesper R} and Morten Smerup and Anderson, {Robert H} and Vibeke Hjortdal and Steinhorn, {Robin H}",
year = "2016",
month = apr,
doi = "10.1038/pr.2015.263",
language = "English",
volume = "79",
pages = "565--74",
journal = "Pediatric Research",
issn = "0031-3998",
publisher = "nature publishing group",
number = "4",

}

RIS

TY - JOUR

T1 - The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

AU - Agger, Peter

AU - Lakshminrusimha, Satyan

AU - Laustsen, Christoffer

AU - Gugino, Sylvia

AU - Frandsen, Jesper R

AU - Smerup, Morten

AU - Anderson, Robert H

AU - Hjortdal, Vibeke

AU - Steinhorn, Robin H

PY - 2016/4

Y1 - 2016/4

N2 - BACKGROUND: Persistent pulmonary hypertension in the newborn remains a syndrome with high mortality. Knowledge of changes in myocardial architecture in the setting of heart failure in persistent pulmonary hypertension is lacking, and could aid in the explanation of the prevailing high mortality.METHODS: Persistent pulmonary hypertension was induced by antenatal ligation of the arterial duct in six ovine fetuses. The hearts were compared ex vivo with five matched control hearts, using diffusion tensor imaging to provide the overall anatomical arrangement, and assessment of the angulations and course of the cardiomyocytes. Fibrosis was assessed with histology.RESULTS: We found an overall increase in heart size in pulmonary hypertension, with myocardial thickening confined to the interventricular septum. An increase of 3.5° in angulation of myocyte aggregations was found in hypertensive hearts. In addition, we observed a 2.2% increase in collagen content in the right ventricular free wall. Finally, we found a previously undescribed subepicardial layer of strictly longitudinally oriented cardiomyocytes confined to the right ventricle in all hearts.CONCLUSION: Myocardial fibrosis and possibly changes in angulations of myocytes seem to play a part in the etiology of persistent pulmonary hypertension. Moreover, a new anatomical arrangement of right ventricular mural architecture is described.

AB - BACKGROUND: Persistent pulmonary hypertension in the newborn remains a syndrome with high mortality. Knowledge of changes in myocardial architecture in the setting of heart failure in persistent pulmonary hypertension is lacking, and could aid in the explanation of the prevailing high mortality.METHODS: Persistent pulmonary hypertension was induced by antenatal ligation of the arterial duct in six ovine fetuses. The hearts were compared ex vivo with five matched control hearts, using diffusion tensor imaging to provide the overall anatomical arrangement, and assessment of the angulations and course of the cardiomyocytes. Fibrosis was assessed with histology.RESULTS: We found an overall increase in heart size in pulmonary hypertension, with myocardial thickening confined to the interventricular septum. An increase of 3.5° in angulation of myocyte aggregations was found in hypertensive hearts. In addition, we observed a 2.2% increase in collagen content in the right ventricular free wall. Finally, we found a previously undescribed subepicardial layer of strictly longitudinally oriented cardiomyocytes confined to the right ventricle in all hearts.CONCLUSION: Myocardial fibrosis and possibly changes in angulations of myocytes seem to play a part in the etiology of persistent pulmonary hypertension. Moreover, a new anatomical arrangement of right ventricular mural architecture is described.

KW - Animals

KW - Animals, Newborn

KW - Disease Models, Animal

KW - Hypertension, Pulmonary/pathology

KW - Myocardium/pathology

KW - Sheep

U2 - 10.1038/pr.2015.263

DO - 10.1038/pr.2015.263

M3 - Journal article

C2 - 26679151

VL - 79

SP - 565

EP - 574

JO - Pediatric Research

JF - Pediatric Research

SN - 0031-3998

IS - 4

ER -

ID: 246355949