Coronary Flow Impacts Aortic Leaflet Mechanics and Aortic Sinus Hemodynamics


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.

This is a preview of subscription content, log in to check access.

Access options

Buy single article

Instant unlimited access to the full article PDF.

US$ 39.95

Price includes VAT for USA

Subscribe to journal

Immediate online access to all issues from 2019. Subscription will auto renew annually.

US$ 199

This is the net price. Taxes to be calculated in checkout.

Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
Figure 10


  1. 1.

    Balachandran, K., P. Sucosky, and A. P. Yoganathan. Hemodynamics and mechanobiology of aortic valve inflammation and calcification. Int. J. Inflamm. 2011. doi:10.4061/2011/263870

  2. 2.

    Beppu, S., S. Suzuki, H. Matsuda, F. Ohmori, S. Nagata, and K. Miyatake. Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves. Am. J. Cardiol. 71:322–327, 1993.

  3. 3.

    Chandra, S., N. M. Rajamannan, and P. Sucosky. Computational assessment of bicuspid aortic valve wall-shear stress: implications for calcific aortic valve disease. Biomech. Model. Mechanobiol. 11:1085–1096, 2012.

  4. 4.

    Davies, P. F., A. G. Passerini, and C. A. Simmons. Aortic valve: turning over a new leaf(let) in endothelial phenotypic heterogeneity. Arterioscler. Thromb. Vasc. Biol. 24:1331–1333, 2004.

  5. 5.

    de Paulis, R., F. Tomai, F. Bertoldo, A. Ghini, R. Scaffa, P. Nardi, L. Chiariello, and R. Depaulis. Coronary flow characteristics after a bentall procedure with or without sinuses of valsalva1. Eur. J. Cardiothorac. Surg. 26:66–72, 2004.

  6. 6.

    Ducci, A., S. Tzamtzis, M. J. Mullen, and G. Burriesci. Hemodynamics in the valsalva sinuses after transcatheter aortic valve implantation (tavi). J. Heart Valve Dis. 22:688–696, 2013.

  7. 7.

    Freeman, R. V., and C. M. Otto. Spectrum of calcific aortic valve disease—pathogenesis, disease progression, and treatment strategies. Circulation 111:3316–3326, 2005.

  8. 8.

    Gharib, M., D. Kremers, M. M. Koochesfahani, and M. Kemp. Leonardo’s vision of flow visualization. Exp. Fluids 33:219–223, 2002.

  9. 9.

    Go, A. S., D. Mozaffarian, V. L. Roger, E. J. Benjamin, J. D. Berry, M. J. Blaha, S. F. Dai, E. S. Ford, C. S. Fox, S. Franco, H. J. Fullerton, C. Gillespie, S. M. Hailpern, J. A. Heit, V. J. Howard, M. D. Huffman, S. E. Judd, B. M. Kissela, S. J. Kittner, D. T. Lackland, J. H. Lichtman, L. D. Lisabeth, R. H. Mackey, D. J. Magid, G. M. Marcus, A. Marelli, D. B. Matchar, D. K. McGuire, E. R. Mohler, C. S. Moy, M. E. Mussolino, R. W. Neumar, G. Nichol, D. K. Pandey, N. P. Paynter, M. J. Reeves, P. D. Sorlie, J. Stein, A. Towfighi, T. N. Turan, S. S. Virani, N. D. Wong, D. Woo, M. B. Turner, American Heart Association Statistics Committee, and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2014 update: a report from the American Heart Association. Circulation 129:E28–E292, 2014.

  10. 10.

    Golzari, M., and J. B. Riebman. The four seasons of ruptured sinus of valsalva aneurysms: case presentations and review. Heart Surg. Forum 7:E577–E583, 2004.

  11. 11.

    Groves, E., A. Falahatpisheh, J. Su, and A. Kheradvar. The effects of positioning of transcatheter aortic valves on fluid dynamics of the aortic root. ASAIO J. 60:545–552, 2014.

  12. 12.

    Johnson, K., P. Sharma, and J. Oshinski. Coronary artery flow measurement using navigator echo gated phase contrast magnetic resonance velocity mapping at 3.0 t. J. Biomech. 41:595–602, 2008.

  13. 13.

    Knight, J., V. Kurtcuoglu, K. Muffly, W. Marshall, Jr., P. Stolzmann, L. Desbiolles, B. Seifert, D. Poulikakos, and H. Alkadhi. Ex vivo and in vivo coronary ostial locations in humans. Surg. Radiol. Anat. 31:597–604, 2009.

  14. 14.

    Lee, C. S. F., and L. Talbot. A fluid-mechanical study of the closure of heart valves. J. Fluid Mech. 91:41–63, 1978.

  15. 15.

    Melling, A. Tracer particles and seeding for particle image velocimetry. Meas. Sci. Technol. 8:1406–1416, 1997.

  16. 16.

    Moore, B., and L. P. Dasi. Spatiotemporal complexity of the aortic sinus vortex. Exp. Fluids 55:1770, 2014.

  17. 17.

    Nobari, S., R. Mongrain, E. Gaillard, R. Leask, and R. Cartier. Therapeutic vascular compliance change may cause significant variation in coronary perfusion: a numerical study. Comput. Math. Methods Med. 2012. doi:10.1155/2012/791686.

  18. 18.

    Payne, J., W. G. Hundley, R. A. Lange, G. D. Clarke, B. M. Meshack, C. Landau, R. McColl, D. E. Sayad, D. L. Willett, J. E. Willard, L. D. Hillis, and R. M. Peshock. Assessment of coronary arterial flow and flow reserve in humans with magnetic resonance imaging. Circulation 93:1502–1508, 1996.

  19. 19.

    Peacock, J. A. An invitro study of the onset of turbulence in the sinus of valsalva. Circ. Res. 67:448–460, 1990.

  20. 20.

    Roberts, W. C., and J. M. Ko. Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation. Circulation 111:920–925, 2005.

  21. 21.

    Spiller, P., F. K. Schmiel, B. Politz, M. Block, U. Fermor, W. Hackbarth, J. Jehle, R. Korfer, and H. Pannek. Measurement of systolic and diastolic flow-rates in the coronary-artery system by x-ray densitometry. Circulation 68:337–347, 1983.

  22. 22.

    Sucosky, P., K. Balachandran, A. Elhammali, H. Jo, and A. P. Yoganathan. Altered shear stress stimulates upregulation of endothelial vcam-1 and icam-1 in a bmp-4-and tgf-beta 1-dependent pathway. Arterioscler. Thromb. Vasc. Biol. 29:254–260, 2009.

  23. 23.

    Sun, L., S. Chandra, and P. Sucosky. Ex vivo evidence for the contribution of hemodynamic shear stress abnormalities to the early pathogenesis of calcific bicuspid aortic valve disease. Plos One. 7, 2012.

  24. 24.

    Turitto, V. T., and C. L. Hall. Mechanical factors affecting hemostasis and thrombosis. Thromb. Res. 92:S25–S31, 1998.

  25. 25.

    Weinberg, E. J., P. J. Mack, F. J. Schoen, G. Garcia-Cardena, and M. R. K. Mofrad. Hemodynamic environments from opposing sides of human aortic valve leaflets evoke distinct endothelial phenotypes in vitro. Cardiovasc. Eng. 10:5–11, 2010.

  26. 26.

    Wootton, D., and D. Ku. Fluid mechanics of vascular systems, diseases, and thrombosis. Annu. Rev. Biomed. Eng. 1:299–329, 1999.

  27. 27.

    Yap, C. H., N. Saikrishnan, G. Tamilselvan, and A. P. Yoganathan. Experimental technique of measuring dynamic fluid shear stress on the aortic surface of the aortic valve leaflet. J. Biomech. Eng.-Trans. ASME. 133, 2011.

  28. 28.

    Yap, C. H., N. Saikrishnan, G. Tamilselvan, and A. P. Yoganathan. Experimental measurement of dynamic fluid shear stress on the aortic surface of the aortic valve leaflet. Biomech. Model. Mechanobiol. 11:171–182, 2012.

Download references


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.



Author information

Correspondence to Lakshmi Prasad Dasi.

Additional information

Associate Editor Peter E. McHugh oversaw the review of this article.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary material 1 (MP4 31288 kb)

Supplementary material 2 (MP4 33470 kb)

Supplementary material 1 (MP4 31288 kb)

Supplementary material 2 (MP4 33470 kb)

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Moore, B.L., Dasi, L.P. Coronary Flow Impacts Aortic Leaflet Mechanics and Aortic Sinus Hemodynamics. Ann Biomed Eng 43, 2231–2241 (2015).

Download citation


  • Aortic valve
  • Coronary flow
  • Calcification
  • Sinus
  • Vortex