title: Normal right ventricular three-dimensional architecture, as assessed with diffusion tensor magnetic resonance imaging, is preserved during experimentally induced right ventricular hypertrophy.
abstract: The three-dimensional architecture of the right ventricular myocardium is a major determinant of function, but as yet no investigator-independent methods have been used to characterize either the normal or hypertrophied state. We aimed to assess and compare, using diffusion tensor magnetic resonance imaging, the normal architecture with the arrangement induced by chronic hypertrophy. We randomized 20 female 5 kg piglets into pulmonary trunk banding (N = 16) and sham operation (N = 4). Right ventricular hypertrophy was assessed after 8 weeks. The excised and fixed hearts were subject to diffusion tensor imaging to determine myocyte helical angles, and the presence of any reproducible tracks formed by the aggregated myocytes. All banding animals developed significant right ventricular hypertrophy, albeit that no difference was observed in terms of helical angles or myocardial pathways between the banded animals and sham group animals. Helical angles varied from approximately 70 degrees endocardially to -50 degrees epicardially. Very few tracks were circular, with helical angles approximating zero. Reproducible patterns of chains of aggregated myocytes were observed in all hearts, regardless of group. The architecture of the myocytes aggregated in the walls of the right ventricle is comparable to that found in the left ventricle in terms of endocardial and epicardial helical angles, however the right ventricle both in the normal and the hypertrophied state lacks the extensive zone of circular myocytes seen in the mid-portion of the left ventricular walls. Without such beneficial architectural remodelling, the porcine right ventricle seems unsuited structurally to sustain a permanent increase in afterload.
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.
authors.forename: Eva
authors.initials: E
authors.lastname: Nielsen
authors.forename: Morten
authors.initials: M
authors.lastname: Smerup
authors.forename: Peter
authors.initials: P
authors.lastname: Agger
authors.forename: Jesper
authors.initials: J
authors.lastname: Frandsen
authors.forename: Steffen
authors.initials: S
authors.lastname: Ringgard
authors.forename: Michael
authors.initials: M
authors.lastname: Pedersen
authors.forename: Peter
authors.initials: P
authors.lastname: Vestergaard
authors.forename: Jens R
authors.initials: JR
authors.lastname: Nyengaard
authors.forename: Johnnie B
authors.initials: JB
authors.lastname: Andersen
authors.forename: Paul P
authors.initials: PP
authors.lastname: Lunkenheimer
authors.forename: Robert H
authors.initials: RH
authors.lastname: Anderson
authors.forename: Vibeke
authors.initials: V
authors.lastname: Hjortdal
mesh_terms: D000465:Algorithms; D000818:Animals; D049109:Cell Proliferation; D038524:Diffusion Magnetic Resonance Imaging; D004195:Disease Models, Animal; D004699:Endocardium / Q000473:pathology / Q000502:physiology; D005260:Female; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000473:pathology* / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D021621:Imaging, Three-Dimensional; D008953:Models, Anatomic; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology; D011652:Pulmonary Circulation / Q000502:physiology; D012984:Software; D034421:Sus scrofa