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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Aarhus, Denmark.|Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Peter
authors.initials: P
authors.lastname: Agger
authors.affiliation: Division of Neonatology, Women and Children's Hospital of Buffalo, State University of New York at Buffalo, Buffalo, New York.
authors.forename: Satyan
authors.initials: S
authors.lastname: Lakshminrusimha
authors.affiliation: Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark.|MR Research Centre, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Christoffer
authors.initials: C
authors.lastname: Laustsen
authors.affiliation: Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, New York.
authors.forename: Sylvia
authors.initials: S
authors.lastname: Gugino
authors.affiliation: Center for Functionally Integrative Neuroscience, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Jesper R
authors.initials: JR
authors.lastname: Frandsen
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Morten
authors.initials: M
authors.lastname: Smerup
authors.affiliation: Institute of Genetic Medicine, University of Newcastle, Newcastle-upon-Tyne, UK.
authors.forename: Robert H
authors.initials: RH
authors.lastname: Anderson
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Aarhus, Denmark.|Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Vibeke
authors.initials: V
authors.lastname: Hjortdal
authors.affiliation: Division of Neonatology, UC Davis Children's Hospital, Sacramento, California.
authors.forename: Robin H
authors.initials: RH
authors.lastname: Steinhorn
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D006976:Hypertension, Pulmonary / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D012756:Sheep