An in vitro investigation of the influence of stenosis severity on the flow in the ascending aorta

• Published in: Medical engineering & physics Vol. 36; no. 9; pp. 1147 - 1155
• Main Authors: Gülan, Utku, Lüthi, Beat, Holzner, Markus, Liberzon, Alex, Tsinober, Arkady, Kinzelbach, Wolfgang
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.09.2014
• Subjects: 3D-PTV; Aorta - physiopathology; Aortic flow; Aortic Valve Stenosis - physiopathology; Biomechanical Phenomena; Blood Flow Velocity; Diastole - physiology; Hemodynamics; Humans; Kinetics; Lagrangian acceleration; Models, Cardiovascular; Pulsatile Flow; Radiology; Shear stress; Stenosis; Systole - physiology; Turbulence; Aortic flow; Stenosis; Shear stress; Turbulence; Lagrangian acceleration; 3D-PTV
• ISSN: 1350-4533; 1873-4030
• DOI: 10.1016/j.medengphy.2014.06.018

Abstract Cardiovascular diseases can lead to abnormal blood flows, some of which are linked to hemolysis and thrombus formation. Abnormal turbulent flows of blood in the vessels with stenosis create strong shear stresses on blood elements and may cause blood cell destruction or platelet activation. We implemented a Lagrangian (following the fluid elements) measurement technique of three dimensional particle tracking velocimetry that provides insight on the evolution of viscous and turbulent stresses along blood element trajectories. We apply this method to study a pulsatile flow in a compliant phantom of an aorta and compare the results in three cases: the reference case (called “healthy” case), and two cases of abnormal flows due to mild and severe stenosis, respectively. The chosen conditions can mimic a clinical application of an abnormal flow due to a calcific valve. We estimate the effect of aortic stenosis on the kinetic energy of the mean flow and the turbulent kinetic energy, which increases about two orders of magnitude as compared with the healthy flow case. Measuring the total flow stress acting on a moving fluid element that incorporates viscous stresses and the apparent turbulent-induced stresses (the so-called Reynolds stresses) we find out similar increase of the stresses with the increased severity of the stenosis. Furthermore, these unique Lagrangian measurements provide full acceleration and, consequently, the forces acting on the blood elements that are estimated to reach the level that can considerably deform red blood cells. These forces are strong and abrupt due to the contribution of the turbulent fluctuations which is much stronger than the typically measured phase-averaged values.