title: Influence of dilated cardiomyopathy and a left ventricular assist device on vortex dynamics in the left ventricle.
abstract: Together with new developments in mechanical cardiac support, the analysis of vortex dynamics in the left ventricle has become an increasingly important topic in literature. The aim of this study was to develop a method to investigate the influence of a left ventricular assist device (LVAD) on vortex dynamics in a failing ventricle. An axisymmetric fluid dynamics model of the left ventricle was developed and coupled to a lumped parameter model of the complete circulation. Simulations were performed for healthy conditions and dilated cardiomyopathy (DCM). Vortex structures in these simulations were analysed by means of automated detection. Results show that the strength of the leading vortex ring is lower in a DCM ventricle than in a healthy ventricle. The LVAD further influences the maximum strength of the vortex and also causes the vortex to disappear earlier in time with increasing LVAD flows. Understanding these phenomena by means of the method proposed in this study will contribute to enhanced diagnostics and monitoring during cardiac support.
authors.affiliation: Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.
authors.forename: S
authors.initials: S
authors.lastname: Loerakker
authors.forename: L G E
authors.initials: LG
authors.lastname: Cox
authors.forename: G J F
authors.initials: GJ
authors.lastname: van Heijst
authors.forename: B A J M
authors.initials: BA
authors.lastname: de Mol
authors.forename: F N
authors.initials: FN
authors.lastname: van de Vosse
mesh_terms: D001783:Blood Flow Velocity; D001794:Blood Pressure; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000503:physiopathology* / Q000601:surgery*; D003198:Computer Simulation; D004867:Equipment Design; D019544:Equipment Failure Analysis; D006353:Heart-Assist Devices; D006801:Humans; D008955:Models, Cardiovascular; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery*