title: Hydraulic forces contribute to left ventricular diastolic filling.
abstract: Myocardial active relaxation and restoring forces are known determinants of left ventricular (LV) diastolic function. We hypothesize the existence of an additional mechanism involved in LV filling, namely, a hydraulic force contributing to the longitudinal motion of the atrioventricular (AV) plane. A prerequisite for the presence of a net hydraulic force during diastole is that the atrial short-axis area (ASA) is smaller than the ventricular short-axis area (VSA). We aimed (a) to illustrate this mechanism in an analogous physical model, (b) to measure the ASA and VSA throughout the cardiac cycle in healthy volunteers using cardiovascular magnetic resonance imaging, and (c) to calculate the magnitude of the hydraulic force. The physical model illustrated that the anatomical difference between ASA and VSA provides the basis for generating a hydraulic force during diastole. In volunteers, VSA was greater than ASA during 75-100% of diastole. The hydraulic force was estimated to be 10-60% of the peak driving force of LV filling (1-3 N vs 5-10 N). Hydraulic forces are a consequence of left heart anatomy and aid LV diastolic filling. These findings suggest that the relationship between ASA and VSA, and the associated hydraulic force, should be considered when characterizing diastolic function and dysfunction.
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet, and Karolinska University Hospital, Stockholm, Sweden.|Department of Medical Engineering, School of Technology and Health, KTH Royal Institute of Technology, Stockholm, Sweden.
authors.forename: Elira
authors.initials: E
authors.lastname: Maksuti
authors.affiliation: Lund University, Skane University Hospital, Department of Clinical Sciences Lund, Clinical Physiology, Lund, Sweden.
authors.forename: Marcus
authors.initials: M
authors.lastname: Carlsson
authors.affiliation: Lund University, Skane University Hospital, Department of Clinical Sciences Lund, Clinical Physiology, Lund, Sweden.
authors.forename: Håkan
authors.initials: H
authors.lastname: Arheden
authors.affiliation: Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri, USA.
authors.forename: Sándor J
authors.initials: SJ
authors.lastname: Kovács
authors.affiliation: Department of Medical Engineering, School of Technology and Health, KTH Royal Institute of Technology, Stockholm, Sweden.|Anaesthesiology and Intensive Care, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.|ECMO Department, Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Michael
authors.initials: M
authors.lastname: Broomé
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet, and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Martin
authors.initials: M
authors.lastname: Ugander
mesh_terms: D001696:Biomechanical Phenomena; D003971:Diastole / Q000502:physiology*; D006321:Heart / Q000000981:diagnostic imaging / Q000502:physiology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D016277:Ventricular Function, Left