Flow-Induced Damage to Blood Cells in Aortic Valve Stenosis
- 870 Downloads
Valvular hemolysis and thrombosis are common complications associated with stenotic heart valves. This study aims to determine the extent to which hemodynamics induce such traumatic events. The viscous shear stress downstream of a severely calcified bioprosthetic valve was evaluated via in vitro 2D particle image velocimetry measurements. The blood cell membrane response to the measured stresses was then quantified using 3D immersed-boundary computational simulations. The shear stress level at the boundary layer of the jet flow formed downstream of the valve orifice was observed to reach a maximum of 1000–1700 dyn/cm2, which was beyond the threshold values reported for platelet activation (100–1000 dyn/cm2) and within the range of thresholds reported for red blood cell (RBC) damage (1000–2000 dyn/cm2). Computational simulations demonstrated that the resultant tensions at the RBC membrane surface were unlikely to cause instant rupture, but likely to lead to membrane plastic failure. The resultant tensions at the platelet surface were also calculated and the potential damage was discussed. It was concluded that although shear-induced thrombotic trauma is very likely in stenotic heart valves, instant hemolysis is unlikely and the shear-induced damage to RBCs is mostly subhemolytic.
KeywordsValvular hemolysis and thrombosis Flow-induced blood cell damage Particle image velocimetry 3D Immersed-boundary method
This work was supported by the American Heart Association and University of Denver Postdoctoral Fellowship Award. We thank Bruce Van Daman from Edwards Lifesciences for providing us with the degenerated PERIMOUNT bioprosthesis. Computational support from SOE HPC at Rutgers University, School of Engineering is acknowledged.
Conflict of interest
The authors have no conflict of interest to declare.
- 5.Browne, P., A. Ramuzat, R. Saxena, and A. P. Yoganathan. Experimental investigation of the steady flow downstream of the St. Jude bileaflet heart valve: a comparison between laser Doppler velocimetry and particle image velocimetry techniques. Ann. Biomed. Eng. 28:39–47, 2000.CrossRefPubMedGoogle Scholar
- 18.Gitz, E., C. D. Koopman, A. Giannas, C. A. Koekman, D. J. van den Heuvel, H. Deckmyn, J. W. Akkerman, H. C. Gerritsen, and R. T. Urbanus. Platelet interaction with von Willebrand factor is enhanced by shear-induced clustering of glycoprotein Ibalpha. Haematologica 98:1810–1818, 2013.CrossRefPubMedPubMedCentralGoogle Scholar
- 19.Helfrich, W. Elastic properties of lipid bilayers—theory and possible experiments. Zeitschrift Fur Naturforschung C-J. Biosci. C 28:693–703, 1973.Google Scholar
- 24.Kheradvar, A., E. M. Groves, A. Falahatpisheh, M. K. Mofrad, S. H. Alavi, R. Tranquillo, L. P. Dasi, C. A. Simmons, K. J. Grande-Allen, C. J. Goergen, F. Baaijens, S. H. Little, S. Canic, and B. Griffith. Emerging trends in heart valve engineering: Part IV. Computational modeling and experimental studies. Ann. Biomed. Eng. 43:2314–2333, 2015.CrossRefPubMedGoogle Scholar
- 25.Leung SL L. Y., Bluestein D, Slepian MJ. Dielectrophoresis-mediated electrodeformation as a means of determining individual platelet stiffness. Ann. Biomed. Eng. 2015.Google Scholar
- 34.Pothapragada S., P. Zhang, J. Sheriff, M. Livelli, M. J. Slepian, Y. F. Deng and D. Bluestein. A phenomenological particle-based platelet model for simulating filopodia formation during early activation. International J. Numer. Methods Biomed. Eng. 31: 2015.Google Scholar