Numerical analysis of the effect of turbulence transition on the hemodynamic parameters in human coronary arteries

Arun Mahalingam, Udhav Ulhas Gawandalkar, Girish Kini, Abdulrajak Buradi, Tadashi Araki, Nobutaka Ikeda, Andrew Nicolaides, John R. Laird, Luca Saba, Jasjit S. Suri

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Background: Local hemodynamics plays an important role in atherogenesis and the progression of coronary atherosclerosis disease (CAD). The primary biological effect due to blood turbulence is the change in wall shear stress (WSS) on the endothelial cell membrane, while the local oscillatory nature of the blood flow affects the physiological changes in the coronary artery. In coronary arteries, the blood flow Reynolds number ranges from few tens to several hundreds and hence it is generally assumed to be laminar while calculating the WSS calculations. However, the pulsatile blood flow through coronary arteries under stenotic condition could result in transition from laminar to turbulent flow condition. Methods: In the present work, the onset of turbulent transition during pulsatile flow through coronary arteries for varying degree of stenosis (i.e., 0%, 30%, 50% and 70%) is quantitatively analyzed by calculating the turbulent parameters distal to the stenosis. Also, the effect of turbulence transition on hemodynamic parameters such as WSS and oscillatory shear index (OSI) for varying degree of stenosis is quantified. The validated transitional shear stress transport (SST) k-ω model used in the present investigation is the best suited Reynolds averaged Navier-Stokes turbulence model to capture the turbulent transition. The arterial wall is assumed to be rigid and the dynamic curvature effect due to myocardial contraction on the blood flow has been neglected. Results: Our observations shows that for stenosis 50% and above, the WSSavg, WSSmax and OSI calculated using turbulence model deviates from laminar by more than 10% and the flow disturbances seems to significantly increase only after 70% stenosis. Our model shows reliability and completely validated. Conclusions: Blood flow through stenosed coronary arteries seems to be turbulent in nature for area stenosis above 70% and the transition to turbulent flow begins from 50% stenosis.

Original languageEnglish (US)
Pages (from-to)208-220
Number of pages13
JournalCardiovascular Diagnosis and Therapy
Volume6
Issue number3
DOIs
StatePublished - 2016
Externally publishedYes

Fingerprint

Coronary Vessels
Pathologic Constriction
Hemodynamics
Pulsatile Flow
Myocardial Contraction
Coronary Disease
Coronary Artery Disease
Atherosclerosis
Endothelial Cells
Cell Membrane

Keywords

  • Coronary artery
  • Curvature
  • IVUS
  • Oscillatory shear index (OSI)
  • Stenosis
  • Turbulence transition
  • Wall shear stress (WSS)

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Numerical analysis of the effect of turbulence transition on the hemodynamic parameters in human coronary arteries. / Mahalingam, Arun; Gawandalkar, Udhav Ulhas; Kini, Girish; Buradi, Abdulrajak; Araki, Tadashi; Ikeda, Nobutaka; Nicolaides, Andrew; Laird, John R.; Saba, Luca; Suri, Jasjit S.

In: Cardiovascular Diagnosis and Therapy, Vol. 6, No. 3, 2016, p. 208-220.

Research output: Contribution to journalArticle

Mahalingam, A, Gawandalkar, UU, Kini, G, Buradi, A, Araki, T, Ikeda, N, Nicolaides, A, Laird, JR, Saba, L & Suri, JS 2016, 'Numerical analysis of the effect of turbulence transition on the hemodynamic parameters in human coronary arteries', Cardiovascular Diagnosis and Therapy, vol. 6, no. 3, pp. 208-220. https://doi.org/10.21037/cdt.2016.03.08
Mahalingam, Arun ; Gawandalkar, Udhav Ulhas ; Kini, Girish ; Buradi, Abdulrajak ; Araki, Tadashi ; Ikeda, Nobutaka ; Nicolaides, Andrew ; Laird, John R. ; Saba, Luca ; Suri, Jasjit S. / Numerical analysis of the effect of turbulence transition on the hemodynamic parameters in human coronary arteries. In: Cardiovascular Diagnosis and Therapy. 2016 ; Vol. 6, No. 3. pp. 208-220.
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abstract = "Background: Local hemodynamics plays an important role in atherogenesis and the progression of coronary atherosclerosis disease (CAD). The primary biological effect due to blood turbulence is the change in wall shear stress (WSS) on the endothelial cell membrane, while the local oscillatory nature of the blood flow affects the physiological changes in the coronary artery. In coronary arteries, the blood flow Reynolds number ranges from few tens to several hundreds and hence it is generally assumed to be laminar while calculating the WSS calculations. However, the pulsatile blood flow through coronary arteries under stenotic condition could result in transition from laminar to turbulent flow condition. Methods: In the present work, the onset of turbulent transition during pulsatile flow through coronary arteries for varying degree of stenosis (i.e., 0{\%}, 30{\%}, 50{\%} and 70{\%}) is quantitatively analyzed by calculating the turbulent parameters distal to the stenosis. Also, the effect of turbulence transition on hemodynamic parameters such as WSS and oscillatory shear index (OSI) for varying degree of stenosis is quantified. The validated transitional shear stress transport (SST) k-ω model used in the present investigation is the best suited Reynolds averaged Navier-Stokes turbulence model to capture the turbulent transition. The arterial wall is assumed to be rigid and the dynamic curvature effect due to myocardial contraction on the blood flow has been neglected. Results: Our observations shows that for stenosis 50{\%} and above, the WSSavg, WSSmax and OSI calculated using turbulence model deviates from laminar by more than 10{\%} and the flow disturbances seems to significantly increase only after 70{\%} stenosis. Our model shows reliability and completely validated. Conclusions: Blood flow through stenosed coronary arteries seems to be turbulent in nature for area stenosis above 70{\%} and the transition to turbulent flow begins from 50{\%} stenosis.",
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AU - Mahalingam, Arun

AU - Gawandalkar, Udhav Ulhas

AU - Kini, Girish

AU - Buradi, Abdulrajak

AU - Araki, Tadashi

AU - Ikeda, Nobutaka

AU - Nicolaides, Andrew

AU - Laird, John R.

AU - Saba, Luca

AU - Suri, Jasjit S.

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N2 - Background: Local hemodynamics plays an important role in atherogenesis and the progression of coronary atherosclerosis disease (CAD). The primary biological effect due to blood turbulence is the change in wall shear stress (WSS) on the endothelial cell membrane, while the local oscillatory nature of the blood flow affects the physiological changes in the coronary artery. In coronary arteries, the blood flow Reynolds number ranges from few tens to several hundreds and hence it is generally assumed to be laminar while calculating the WSS calculations. However, the pulsatile blood flow through coronary arteries under stenotic condition could result in transition from laminar to turbulent flow condition. Methods: In the present work, the onset of turbulent transition during pulsatile flow through coronary arteries for varying degree of stenosis (i.e., 0%, 30%, 50% and 70%) is quantitatively analyzed by calculating the turbulent parameters distal to the stenosis. Also, the effect of turbulence transition on hemodynamic parameters such as WSS and oscillatory shear index (OSI) for varying degree of stenosis is quantified. The validated transitional shear stress transport (SST) k-ω model used in the present investigation is the best suited Reynolds averaged Navier-Stokes turbulence model to capture the turbulent transition. The arterial wall is assumed to be rigid and the dynamic curvature effect due to myocardial contraction on the blood flow has been neglected. Results: Our observations shows that for stenosis 50% and above, the WSSavg, WSSmax and OSI calculated using turbulence model deviates from laminar by more than 10% and the flow disturbances seems to significantly increase only after 70% stenosis. Our model shows reliability and completely validated. Conclusions: Blood flow through stenosed coronary arteries seems to be turbulent in nature for area stenosis above 70% and the transition to turbulent flow begins from 50% stenosis.

AB - Background: Local hemodynamics plays an important role in atherogenesis and the progression of coronary atherosclerosis disease (CAD). The primary biological effect due to blood turbulence is the change in wall shear stress (WSS) on the endothelial cell membrane, while the local oscillatory nature of the blood flow affects the physiological changes in the coronary artery. In coronary arteries, the blood flow Reynolds number ranges from few tens to several hundreds and hence it is generally assumed to be laminar while calculating the WSS calculations. However, the pulsatile blood flow through coronary arteries under stenotic condition could result in transition from laminar to turbulent flow condition. Methods: In the present work, the onset of turbulent transition during pulsatile flow through coronary arteries for varying degree of stenosis (i.e., 0%, 30%, 50% and 70%) is quantitatively analyzed by calculating the turbulent parameters distal to the stenosis. Also, the effect of turbulence transition on hemodynamic parameters such as WSS and oscillatory shear index (OSI) for varying degree of stenosis is quantified. The validated transitional shear stress transport (SST) k-ω model used in the present investigation is the best suited Reynolds averaged Navier-Stokes turbulence model to capture the turbulent transition. The arterial wall is assumed to be rigid and the dynamic curvature effect due to myocardial contraction on the blood flow has been neglected. Results: Our observations shows that for stenosis 50% and above, the WSSavg, WSSmax and OSI calculated using turbulence model deviates from laminar by more than 10% and the flow disturbances seems to significantly increase only after 70% stenosis. Our model shows reliability and completely validated. Conclusions: Blood flow through stenosed coronary arteries seems to be turbulent in nature for area stenosis above 70% and the transition to turbulent flow begins from 50% stenosis.

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KW - Curvature

KW - IVUS

KW - Oscillatory shear index (OSI)

KW - Stenosis

KW - Turbulence transition

KW - Wall shear stress (WSS)

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