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

Lookup NU author(s): Professor Bob Anderson

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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 degrees 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.

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Author(s): Agger P, Lakshminrusimha S, Laustsen C, Gugino S, Frandsen JR, Smerup M, Anderson RH, Hjortdal V, Steinhorn RH

Publication type: Article

Publication status: Published

Journal: Pediatric Research

Year: 2016

Volume: 79

Issue: 4

Pages: 565-574

Print publication date: 01/04/2016

Online publication date: 17/12/2015

Acceptance date: 28/09/2015

ISSN (print): 0031-3998

ISSN (electronic): 1530-0447

Publisher: Nature Publishing Group

URL: http://dx.doi.org/10.1038/pr.2015.263

DOI: 10.1038/pr.2015.263

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