Annals of Biomedical Engineering

, Volume 43, Issue 9, pp 2231–2241 | Cite as

Coronary Flow Impacts Aortic Leaflet Mechanics and Aortic Sinus Hemodynamics

  • Brandon L. Moore
  • Lakshmi Prasad DasiEmail author


Mechanical stresses on aortic valve leaflets are well-known mediators for initiating processes leading to calcific aortic valve disease. Given that non-coronary leaflets calcify first, it may be hypothesized that coronary flow originating from the ostia significantly influences aortic leaflet mechanics and sinus hemodynamics. High resolution time-resolved particle image velocimetry (PIV) measurements were conducted to map the spatiotemporal characteristics of aortic sinus blood flow and leaflet motion with and without physiological coronary flow in a well-controlled in vitro setup. The in vitro setup consists of a porcine aortic valve mounted in a physiological aorta sinus chamber with dynamically controlled coronary resistance to emulate physiological coronary flow. Results were analyzed using qualitative streak plots illustrating the spatiotemporal complexity of blood flow patterns, and quantitative velocity vector and shear stress contour plots to show differences in the mechanical environments between the coronary and non-coronary sinuses. It is shown that the presence of coronary flow pulls the classical sinus vorticity deeper into the sinus and increases flow velocity near the leaflet base. This creates a beneficial increase in shear stress and washout near the leaflet that is not seen in the non-coronary sinus. Further, leaflet opens approximately 10% farther into the sinus with coronary flow case indicating superior valve opening area. The presence of coronary flow significantly improves leaflet mechanics and sinus hemodynamics in a manner that would reduce low wall shear stress conditions while improving washout at the base of the leaflet.


Aortic valve Coronary flow Calcification Sinus Vortex 



The authors gratefully acknowledge funding from National Institutes of Health (NIH) under Award Number R01HL119824, and the American Heart Association under award 11SDG5170011. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.



Supplementary material

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Supplementary material 2 (MP4 33470 kb)


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Copyright information

© Biomedical Engineering Society 2015

Authors and Affiliations

  1. 1.Department of Mechanical EngineeringColorado State UniversityFort CollinsUSA
  2. 2.Department of Mechanical EngineeringColorado State UniversityFort CollinsUSA

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