title: Models of ventricular structure and function reviewed for clinical cardiologists.
abstract: The architectural arrangement of cardiomyocytes aggregated together within the ventricular walls remains controversial. Two models currently attract clinical attention, with neither model standing rigorous anatomical scrutiny. The first is based on the notion that ventricular mass can be unraveled consistently to produce a unique myocardial band. The second model was initially based on the notion that cardiomyocytes were bundled together in uniform fashion, with fibrous shelves interposed in transmural fashion. This concept was subsequently modified to accept the fact that the fibrous matrix supporting the cardiomyocytes within the ventricular walls does not form transmural sheets. Current observations demonstrate that not all cardiomyocytes are aggregated together in tangential fashion. A significant netting component is aligned in obliquely intruding and transversal fashion. The interaction between the tangential and transversal chains of cardiomyocytes with the fibrous matrix produces antagonistic forces, with both unloading and auxotonic forces necessary to explain normal and abnormal cardiodynamics. This article is part of a JCTR special issue on Cardiac Anatomy.
authors.affiliation: Department of Experimental Thoraco-Vascular Surgery, Universitätsklinik, Münster, Domagkstraße 11, 48149 Münster, Germany. P.P.Lunkenheimer@web.de
authors.forename: Paul P
authors.initials: PP
authors.lastname: Lunkenheimer
authors.forename: Peter
authors.initials: P
authors.lastname: Niederer
authors.forename: Damian
authors.initials: D
authors.lastname: Sanchez-Quintana
authors.forename: Margarita
authors.initials: M
authors.lastname: Murillo
authors.forename: Morten
authors.initials: M
authors.lastname: Smerup
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D005109:Extracellular Matrix / Q000502:physiology; D006352:Heart Ventricles / Q000033:anatomy & histology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008953:Models, Anatomic; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000473:pathology / Q000503:physiopathology; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right