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    Numerical analysis of the effect of turbulence transition on the hemodynamic parameters in human coronary arteries
    (AME Publishing Company info@amepc.org, 2016) Mahalingam, A.; Gawandalkar, U.U.; Kini, G.; Buradi, A.; Araki, T.; Ikeda, N.; Nicolaïdes, A.; Laird, J.R.; Saba, L.; Suri, J.S.
    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-? 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. © Cardiovascular Diagnosis and Therapy. All rights reserved.
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    Impact of coronary tortuosity on the artery hemodynamics
    (Elsevier Sp. z o.o., 2020) Buradi, A.; Mahalingam, A.
    The presence of tortuosity in coronary artery (CA) affects the local wall shear stress (WSS) which is an influencing hemodynamic descriptor (HD) for the development of atherosclerotic sites. To conduct a morphological parametric study in coronary arteries (CAs), several idealized tortuous artery models were obtained by varying three morphological indices namely, curvature radius (CR), distance between two bends (DBB) and the angle of bend (AoB). Computational fluid dynamics methodology with multiphase mixture theory is used to explore the effect of coronary tortuosity on various WSS based hemodynamic descriptors (HDs) namely, time-averaged WSS, oscillatory shear index, time-averaged WSS gradient, endothelial cell activation potential and the relative residence time that are used to determine the vulnerable locations for the onset of thrombosis and atherosclerosis. Our findings suggest that all the tortuosity morphological indices, CR, DBB and AoB have significant influence on the distributions of various HDs and hemodynamics. It is also observed that atherosclerosis prone sites were witnessed at the inner artery wall at downstream regions of the bend section 1 and bend section 2 in all the tortuous artery models studied and found to increase as the CR and DBB were reduced however, found to increase as the AoB is increased. Hence, severe coronary tortuosity in CAs with small CR, small DBB and higher AoB may have lower WSS zones at inner bend sections which promote atherosclerosis plaque progression. The analysis obtained from this multiphase blood flow study can be employed potentially in the clinical assessment on the severity of atherosclerosis lesions as well as in understanding the underlying mechanisms of localization and formation of atherosclerotic plaques. © 2019 Nalecz Institute of Biocybernetics and Biomedical Engineering of the Polish Academy of Sciences