The Myocardial Architecture changes in Persistent Pulmonary Hypertension of the Newborn in an Ovine Animal Model

Peter Agger, Satyan Lakshminrusimha, Christoffer Laustsen, Sylvia Gugino, Jesper Frandsen, Morten Holdgaard Smerup, Robert H Anderson, Vibeke Hjortdal, Robin H Steinhorn

24 Citationer (Scopus)


BACKGROUND: Persistent pulmonary hypertension in the newborn, remains a syndrome with high mortality. Knowledge of changes 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 6 ovine fetuses. The hearts were compared ex-vivo with 5 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.Pediatric Research (2015); doi:10.1038/pr.2015.263.

TidsskriftPediatric Research
StatusUdgivet - 17 dec. 2015
Udgivet eksterntJa


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