Chiastra, Claudio

Gallo, Diego

Iannaccone, Francesco

Migliavacca, Francesco

Morbiducci, Umberto

Tasso, Paola

Wentzel, Jolanda J.

English

GALLO, DIEGO

TASSO, PAOLA

MIGLIAVACCA, FRANCESCO

MORBIDUCCI, UMBERTO

PORTO@iris (Publications Open Repository TOrino - Politecnico di Torino)

04 August 2020POLITECNICO DI TORINORepository ISTITUZIONALEHemodynamic risk in coronary bifurcations: a computational exploration / Gallo, Diego; Chiastra, Claudio; Tasso, Paola;Iannaccone, Francesco; Migliavacca, Francesco; Wentzel, Jolanda J.; Morbiducci, Umberto. - ELETTRONICO. - (2017).((Intervento presentato al convegno 2017 Summer Biomechanics, Bioengineering and Biotransport Conference tenutosia Tucson (AZ, USA) nel June 21-24, 2017.OriginalHemodynamic risk in coronary bifurcations: a computational explorationPublisher:PublishedDOI:Terms of use:openAccessPublisher copyright(Article begins on next page)This article is made available under terms and conditions as specified in the  corresponding bibliographic description inthe repositoryAvailability:This version is available at: 11583/2677971 since: 2017-08-03T10:25:37ZSummer Biomechanics, Bioengineering and Biotransport Conference Organizing Committee  INTRODUCTION  The so-called “hemodynamic hypothesis” suggests that local hemodynamics is a main factor of the onset and progression of lesions at arterial bifurcations [1]. Local hemodynamics is mainly determined by the underlying anatomical features of an arterial bifurcation. For example in carotid arteries, computational fluid dynamics (CFD) studies showed a correlation between geometry and disturbed shear [2]. Furthermore, local geometry of carotid bifurcation has been reported to be significantly correlated with peculiar helical flow structures [3], which in turn have been proven to reduce the likelihood of flow disturbances at the bifurcation [4]. While the interplay between geometry, near-wall and intravascular flow features has been widely studied in carotid bifurcations, less is known about diseased coronary bifurcations. Indeed, several studies focused on the influence on near-wall descriptors attributable to anatomical features, such as the presence of stenosis at varying locations and with different severity/extension, bifurcation angle, curvature [5], and tortuosity [6]. The aim of the present study is to extend the investigation of the influence of peculiar coronary bifurcation anatomical features on both near-wall and intravascular flow features. In particular, the impact of stenosis, bifurcation angle, and curvature on local hemodynamics is analyzed by performing CFD simulations on a population-based, idealized model of coronary bifurcation. Such an idealized model-based approach will enable, by varying one specific geometrical feature at time while keeping the others constant, to clearly identify whether and to which extent specific anatomic features promote atherosensitive hemodynamic phenotypes.   METHODS A parametric model of a coronary bifurcation (Fig.1) representing the left anterior descending (LAD) coronary artery with its diagonal branch was created, as detailed elsewhere [7]. Briefly, the diameter of the proximal main branch (P-MB) is 3.30 mm while the diameters of the distal main branch (D-MB) and the side branch (SB) are 2.77 mm and 2.10 mm, respectively [8]. The distal bifurcation angle was varied within the physiological range. The cardiac curvature was taken into account by bending the model on a sphere of radius ‘R’. A physiological cardiac curvature radius was considered (R=56.3 mm), as well as two extreme values (R=∞, i.e. absence of curvature, and R=16.5 mm). Stenosed (diseased) and unstenosed (healthy) bifurcation models were analyzed. Stenosed models are characterized by 60% diameter stenosis in each branch (Medina classification 1,1,1). The lesion is 12 mm long and eccentric, with plaque located at the inner arc of the vessel (Fig. 1).                     Figure 1 – Parametric model of the healthy left anterior descending / first diagonal coronary bifurcation: (A) top and (B) lateral views. Details of the diseased model are shown in the boxes. SB3C2017 Summer Biomechanics, Bioengineering and Biotransport Conference June 21 – 24, Tucson, AZ, USA HEMODYNAMIC RISK IN CORONARY BIFURCATIONS: A COMPUTATIONAL EXPLORATION D. Gallo (1), C. Chiastra (2,3), P. Tasso (1), F. Iannaccone (4),  F. Migliavacca (2), J.J. Wentzel (3), U. Morbiducci (1) (1) Department of Mechanical and Aerospace Engineering Politecnico di Torino Turin, Italy  (2) Department of Cardiology, Biomedical Engineering Erasmus MC Rotterdam, The Netherlands  (3) Laboratory of Biological Structure Mechanics, Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy (4) FEops NV Ghent, Belgium   In summary, 10 coronary bifurcation models were investigated by combining 3 distal angles (40°, 55°, and 70°) and 3 curvature radii, both for the healthy and the diseased coronary bifurcation models. The governing equations of unsteady fluid motion were solved by using the finite volume method. A typical human LAD flow waveform was imposed at the inlet as a plug velocity profile. A flow-split of 0.65:0.35 for the D-MB and SB, respectively, was applied at outlets. The flow-split was maintained constant in the diseased models in order to focus the analysis only on the impact that geometrical features have on local hemodynamics. Blood was modeled as a non-Newtonian fluid using the Carreau model. The flow was assumed as laminar (max Reynolds number ~ 330 at the P-MB stenosis of diseased models). Intravascular fluid structures were investigated in terms of helical flow topology and content. Helicity intensity h2 and helical rotation balance h4 were calculated, according to [4]: ℎ2 =1𝑇 𝑉∫ ∫ |𝑣∙ ?⃗⃗?|𝑑𝑉𝑑𝑡𝑉𝑇    (1)             ℎ4 =|∫ ∫ ?⃗⃗?∙?⃗⃗⃗⃗? 𝑑𝑉𝑑𝑡𝑉𝑇 |∫ ∫ |?⃗⃗?∙?⃗⃗⃗⃗?|𝑑𝑉𝑑𝑡𝑉𝑇      (2) where 𝑣, ?⃗⃗? are the velocity and vorticity vectors, respectively, V is the volumetric fluid domain of interest, T is the cardiac cycle. Helicity intensity h2 is an indicator of the total amount of helical flow, while h4 measures the strength of relative rotations of helical flow structures. Near-wall hemodynamics was evaluated in terms of time-averaged WSS (TAWSS), oscillatory shear index (OSI), and relative residence time (RRT). In particular, the fraction of the luminal surface area exposed to TAWSS < 0.4 Pa, OSI > 0.2, and RRT > 4.17 Pa-1 (in consequence of values set for TAWSS and OSI) was calculated.   RESULTS AND DISCUSSION  The analysis was carried out on the entire bifurcation and single branches. Findings related to the hemodynamic descriptors over the entire bifurcation are summarized in Tables 1 and 2. Generation and transport of helical flow structures is influenced by the curvature radius. Smaller curvature radius is associated with higher helicity intensity in both unstenosed and stenosed cases. In healthy cases, helical flow topology is driven mainly by the curvature of the vessel. In diseased cases, the impact of curvature on helical flow structures piles up with the helicity generated because of the lumen reduction (Fig. 2A). Consequently, helicity intensity h2 of diseased models is one order of magnitude higher than healthy cases. Globally, helical flow structures are symmetrical, as demonstrated by the nearly 0 values of the helical rotation balance h4. The surface areas exposed to atherosensitive RRT values can be observed in diseased cases at the distal MB and at the SB, close to the reattachment point of the recirculation regions (Fig. 2B). The curvature radius moderately affects the near-wall hemodynamics of the diseased cases. In particular, smaller curvature radius leads to larger lumen area exposed to low TAWSS and smaller lumen area exposed to high OSI and RRT. The bifurcation angle has a minor effect on the calculated hemodynamic variables. Helicity intensity is not dependent from the bifurcation angle in both healthy and diseased cases. Furthermore, in the healthy cases, the fraction of the lumen surface area exposed to low TAWSS slightly decreases with increasing bifurcation angle, while the exposure to high OSI and RRT is negligible. In the diseased cases, the surface area exposed to low TAWSS increases to ~3.3%. Surface areas exposed to high OSI and RRT show a poor dependence on the bifurcation angle.  In conclusion, the approach proposed in this study provides a controlled benchmark to investigate the effect of various geometrical features on local hemodynamics, highlighting the complex interplay between anatomy and intricate fluid structures in coronary bifurcations.       Figure 2 – Hemodynamics results of the diseased cases with different curvature radii: A) Isosurfaces of local normalized helicity (LNH); positive and negative values of LNH indicate counter-rotating flow structures. B) Contour maps of relative residence time (RRT, Pa-1).  ACKNOWLEDGEMENTS  C. Chiastra and J.J. Wentzel are supported by the ERC starting grant (No. 310457, BioCCora).  REFERENCES  [1] Morbiducci, U et al., Thromb Haemost, 115(3):484-92, 2016. [2] Lee, SW et al., Stroke, 39:2341–2347, 2008. [3] Gallo, D et al., Ann Biomed Eng, 43:68–81, 2015. [4] Gallo, D et al., J Biomech, 45:2398–2404, 2012. [5] Peng, C et al., PLoS One, 11, e0157490, 2016. [6] Vorobtsova, N et al., Ann Biomed Eng, 44(7):2228-39, 2016. [7] Chiastra, C et al., Biomed Eng Online, 15(1):91, 2016. [8] Finet, G et al., EuroIntervention, 3:490–8, 2008. Table 1 – Near-wall hemodynamic descriptors for cases with different curvature radius ‘R’. Stenosis R [mm] Relative surface area [%] h2 [m/s2] h4 TAWSS<0.4Pa OSI>0.2 RRT>4.17Pa-1 No ∞ 0.00 0.00 0.00 0.20 0.00 56.3 0.07 0.00 0.00 0.43 0.02 16.5 0.07 0.00 0.00 1.12 0.00 Yes ∞ 2.74 2.08 2.12 4.56 0.01 56.3 3.21 2.04 2.01 5.13 0.06 16.5 3.81 1.11 1.56 6.60 0.08  Table 2 – Near-wall hemodynamic descriptors  for cases with different bifurcation angles ‘α’. Stenosis α Relative surface area [%] h2 [m/s2] h4 TAWSS<0.4Pa OSI>0.2 RRT>4.17Pa-1 No 40° 0.42 0.00 0.00 0.43 0.00 55° 0.07 0.00 0.00 0.43 0.02 70° 0.00 0.00 0.00 0.44 0.02 Yes 40° 3.35 1.58 2.04 4.58 0.07 55° 3.31 2.04 2.01 5.13 0.06 70° 3.24 2.07 2.06 4.85 0.01  

Hemodynamic risk in coronary bifurcations: a computational exploration

https://iris.polito.it/retrieve/handle/11583/2677971/158355/SB3C2017_Abstract_IdealizedCoronary.pdf

Hemodynamic risk in coronary bifurcations: a computational exploration

Abstract

Similar works

Full text

Available Versions

PORTO@iris (Publications Open Repository TOrino - Politecnico di Torino)