REVIEW 3 major objections 5 minor 52 references
Reliability of characterising coronary artery flow with the flow-split outflow strategy: comparison against the multiscale approach
T0 review · 3 major / 5 minor · reviewed 2026-08-08 · deepseek-v4-flash
Pith's one-line read This paper claims that the simplified flow-split outflow strategy is statistically indistinguishable from reference multiscale simulations for resting coronary flow, but under hyperaemia it significantly overestimates wall shear stress…
desk verdict Useful comparison of flow-split versus multiscale coronary outflow conditions, but the resting 'regardless of severity' claim outruns the n=6 evidence. read the letter →
The pith
A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.
The reading
What carries the argument
The central object is the flow-split outflow condition, a boundary-condition formula that divides the incoming coronary flow among daughter branches in proportion to $D_i^k$, where $D_i$ is the daughter-branch diameter and $k$ is a scaling exponent taken from the literature (2.0, 2.27, 2.33, and 3.0). This formula is used in place of the 0D–3D coupled multiscale model, in which lumped parameter networks at the distal ends of the 3D coronary tree exchange pressure and flow with the full simulation. The comparison here turns on whether this diameter-only proxy for downstream resistance reproduces the multiscale model's pressures and wall-shear metrics under resting and hyperaemic conditions.
What would settle it
Measure invasive fractional flow reserve and distal coronary pressure in the same six patients under hyperaemia and compare the multiscale and flow-split predictions with those direct readings; if the multiscale FFR deviates from the invasive value by as much as or more than the flow-split error of 0.327, the claim that multiscale simulation is the necessary reference for severe stenoses would be called into question.
Extended reading notes
Core claim
The paper's central claim is that the choice of outflow boundary condition, not the choice of scaling exponent, determines whether simplified coronary simulations can be trusted. With a flow-split strategy using any exponent in the range 2.0 to 3.0, resting haemodynamics — time-averaged wall shear stress (TAWSS), relative residence time (RRT), and the instantaneous wave-free ratio (iFR) — match the reference multiscale simulation across both mild and severe stenoses, so the simplified method is appropriate for resting assessment. Under hyperaemic conditions, the same flow-split prescriptions significantly overestimate TAWSS (up to 16.8 Pa, p=0.031) and underestimate fractional flow reserve (FFR) by up to 0.327 (p=0.043), with the largest discrepancies in severe stenoses. Within the flow-split family, the exponent itself makes little statistical difference (p>0.141), although larger exponents consistently move results closer to the multiscale reference.
Load-bearing premise
The entire comparison treats the 0D-3D multiscale simulation as the true haemodynamic reference, based on earlier validation against invasive pressure measurements, but the present study never compares any computed metric against direct clinical measurements in the same six patients; if that multiscale reference is inaccurate, the conclusions about the flow-split method's reliability shift.
Editorial extensions
If this is right
- Resting coronary CFD can be run with the flow-split strategy using any exponent from 2.0 to 3.0 without statistically significant loss of accuracy in TAWSS, RRT, or iFR, even for severe stenoses.
- Under hyperaemia, especially in severe stenosis, flow-split simulations should not be used to quantify TAWSS or FFR, because errors reach 16.8 Pa and 0.327 in this cohort.
- The choice of exponent within 2.0 to 3.0 has little effect on haemodynamic metrics (p>0.141), so the Murray exponent is not the main source of uncertainty.
- Because the flow-split outflow settings require no manual tuning of lumped parameters, whereas the multiscale model takes about six hours of expert work per case, the resting-condition result opens a path to automated, large-scale resting assessments.
Reading between the lines
- Inference: if the resting-condition finding holds for larger cohorts, the flow-split strategy could make resting iFR screening feasible at a volume that multiscale simulation cannot match.
- Inference: the systematic drift toward k=3.0 as the most accurate exponent suggests a testable correction — a severity-dependent exponent or a stenosis-resistance term in the diameter split might extend flow-split accuracy into hyperaemia.
- Inference: the paper reports only spatially averaged metrics, so local wall-shear extremes, which are the ones linked to plaque vulnerability, may be even more sensitive to outflow conditions than the reported means.
- Inference: because the reference itself is a validated model rather than direct pressure measurements in the same six patients, the decisive test of these error magnitudes is an invasive FFR comparison in identical geometries.
Editorial analysis
A structured set of objections, weighed in public.
Referee Report
Summary. This manuscript compares two outflow boundary-condition strategies for patient-specific coronary artery CFD: a simplified flow-split approach using four published scaling exponents (k = 2.0, 2.27, 2.33, 3.0) and a 0D-3D coupled multiscale model taken as the reference standard. Six patient-specific left coronary artery trees from the ASOCA dataset are used, three with severe (>70%) and three with mild (<50%) stenoses. The authors report that, under resting conditions, flow-split and multiscale results do not differ significantly for TAWSS, RRT, or iFR, and conclude that flow-split strategies with exponents between 2.0 and 3.0 are appropriate for resting coronary flow regardless of stenosis severity. Under hyperaemic conditions, the flow-split strategy significantly overestimates TAWSS and underestimates FFR, with larger discrepancies for severely stenosed cases, leading the authors to recommend multiscale simulations for hyperaemic assessment of severe lesions. The paper also reports no statistically significant differences among the four exponents within the flow-split framework.
Significance. The study addresses a practical question in coronary CFD: whether inexpensive diameter-based flow-split outflow conditions can replace expensive multiscale models. Its strengths are a controlled comparison with identical geometry, mesh, and inlet waveform for both methods; use of clinically relevant metrics (iFR, FFR, TAWSS, RRT); and use of publicly available patient data. The mechanistic explanation for hyperaemic discrepancies, namely that diameter-averaged flow splitting underestimates stenosis resistance at high flow, is plausible and consistent with the descriptive results. However, the central resting-condition conclusion is an equivalence claim supported only by non-significant p-values from six patients, with only three severe cases, and no equivalence margin, confidence intervals, or subgroup tests are reported. The lack of direct clinical validation of the multiscale reference in the same patients also limits the strength of the accuracy claims. The paper is useful as a hypothesis-generating comparison, but the current statistical framing overstates the certainty of the resting-condition recommendation.
major comments (3)
- [Section 3.1, Table 2, Conclusions] The conclusion that flow-split strategies are 'appropriate' for resting flow 'regardless of stenosis severity' is an equivalence claim, but it is supported only by non-significant paired comparisons (TAWSS p>0.233, RRT p>0.282, iFR p>0.227) in six patients, with only three severe cases. Table 2 shows a maximum severe-stenosis resting iFR difference of 0.12 and a TAWSS difference of 1.17 Pa relative to the multiscale reference. As the authors themselves note in the Discussion, iFR values in the 0.86-0.93 clinical grey zone are particularly sensitive to flow-split assumptions, and an error of 0.12 can move a lesion across the 0.89 decision threshold. Failure to reject the null hypothesis with n=3 severe cases does not establish agreement within a clinically acceptable tolerance. The authors should either provide a pre-specified equivalence margin with confidence intervals or equivalence tests, or substantially weaken the resting-condition claim to 'no statistically significant difference was detected.'
- [Section 3.4, Abstract, Conclusions] The statement that hyperaemic discrepancies are 'larger' in severe stenoses than in mild ones is only supported descriptively by Table 2 (TAWSS maximum difference 16.80 Pa severe vs. 1.23 Pa mild; FFR 0.33 vs. 0.02). No statistical test for a severity-by-method interaction or a subgroup comparison is reported, and each subgroup contains only three patients. The abstract and conclusions nevertheless present severity-dependent behavior as an established finding ('especially in severely stenosed arteries'). The authors should either report an appropriate interaction or subgroup analysis with confidence intervals, or explicitly present the severity comparison as descriptive and indicative, as they partially do in Section 3.4.
- [Section 2.6 and Section 4 (Limitations)] The multiscale model is called the reference standard based on previous validation of pressure drops in other cohorts, but no haemodynamic quantity from the present six patients is compared against direct clinical measurements. The claim that flow-split simulations 'overestimate' or 'underestimate' iFR/FFR assumes that the multiscale predictions are accurate for these specific cases. The authors acknowledge this limitation, but it is load-bearing for the central conclusion. The manuscript should either provide additional evidence of the multiscale model's accuracy in the present cohort, or reframe the findings as a comparison of agreement between two computational techniques rather than as absolute accuracy against clinical truth.
minor comments (5)
- [Figure 4 caption] The caption twice refers to 'instantaneous wave-Free Ratio (iFR)' for the hyperaemic condition, but the hyperaemic metric is FFR; the text and Figure 4 right panel should be corrected to avoid confusion.
- [Table 2] The header 'Maximum Mean Differences' is unclear; the table appears to report maximum absolute differences and standard errors. Consider 'Maximum absolute difference' for clarity and specify over which cases and locations the maximum is taken.
- [Abstract] The abstract states that TAWSS was overestimated 'by up to 16.8 Pa (p=0.031)' and FFR underestimated 'by 0.327 (p=0.043)'; the p-values come from paired tests across all six cases, while the quoted magnitudes are severe-subgroup maxima. Clarify this distinction to avoid implying the p-value refers to the severe subgroup only.
- [Section 2.4] There is a typographical error: 'deteremined' should be 'determined'.
- [Section 3.3] The claim that different exponents 'did not significantly affect' haemodynamics is also an equivalence claim based on non-significant ANOVA p-values from a small sample; report confidence intervals or effect sizes for these comparisons, or temper the wording.
Circularity Check
No significant circularity: the central comparison is an empirical benchmark between two boundary-condition strategies, with the reference standard supported by external clinical validation.
full rationale
This paper does not derive one simulated metric from another; it compares haemodynamic outputs (TAWSS, RRT, iFR/FFR) produced by two different outflow boundary-condition implementations on identical geometries and inflow waveforms. The flow-split exponents (2.0, 2.27, 2.33, 3.0) and the inflow scaling Q=1.43D^2.55 are taken from the external literature [22-25,32], not fitted to the present results. The multiscale reference is justified by prior invasive-pressure validation (Ref. [28], Norgaard et al., not by the present authors), so the reference standard is externally supported rather than supplied by self-citation. The self-citations that do appear (e.g., mesh sensitivity in [27], side-branch handling in [14]) are methodological and not load-bearing for the central claim. The remaining concerns - small n=6, three severe cases, no equivalence margin, acceptance of non-significant p-values as evidence of suitability - are statistical-power and inference issues, not circularity: none of the reported quantities is defined in terms of itself, and no fitted parameter is relabelled as a prediction. The paper's own limitation statement that no direct clinical measurements were matched in the same patients is a validation gap, not a circular step, because the reference model was independently verified in prior external work.
Assumptions & free parameters
free parameters (4)
- Inflow scaling coefficient =
1.43
- Inflow scaling exponent =
2.55
- Hyperaemia flow multiplier =
4
- Flow-split exponent k =
2.0, 2.27, 2.33, 3.0
assumptions (6)
- domain assumption The 0D-3D coupled multiscale model is an accurate reference standard for coronary haemodynamics
- domain assumption Coronary inflow can be scaled by Q=1.43 D^2.55 from the inlet diameter
- domain assumption Hyperaemic flow is four times resting flow
- domain assumption Arterial walls are rigid and blood is incompressible and non-Newtonian (Carreau model)
- domain assumption The velocity profile at the inlet is uniform
- standard math Lumped parameter network equations (Eq. 3) capture distal microcirculation
Cite this review
Pith. "Pith review of Reliability of characterising coronary artery flow with the flow-split outflow strategy: comparison against the multiscale approach." pith.science (2026). https://pith.science/paper/3625AJTC
@misc{pith2026250220406,
author = {Pith},
title = {Pith review of: Reliability of characterising coronary artery flow with the flow-split outflow strategy: comparison against the multiscale approach},
year = {2026},
howpublished = {\url{https://pith.science/paper/3625AJTC}},
note = {Machine review of arXiv:2502.20406}
}
read the original abstract
In computational modelling of coronary haemodynamics, imposing patient-specific flow conditions is paramount, yet often impractical due to resource and time constraints, limiting the ability to perform a large number of simulations particularly for diseased cases. We aimed to compare coronary haemodynamics quantified using a simplified flow-split strategy with varying exponents against the clinically verified but computationally intensive multiscale simulations under both resting and hyperaemic conditions in arteries with varying degrees of stenosis. Six patient-specific left coronary artery trees were segmented and reconstructed, including three with severe (>70%) and three with mild (<50%) focal stenoses. Simulations were performed for the entire coronary tree to account for the flow-limiting effects from epicardial artery stenoses. Both a 0D-3D coupled multiscale model and a flow-split approach with four different exponents (2.0, 2.27, 2.33, and 3.0) were used. The resulting prominent haemodynamic metrics were statistically compared between the two methods. Flow-split and multiscale simulations did not significantly differ under resting conditions regardless of the stenosis severity. However, under hyperaemic conditions, the flow-split method significantly overestimated the time-averaged wall shear stress by up to 16.8 Pa (p=0.031) and underestimate the fractional flow reserve by 0.327 (p=0.043), with larger discrepancies observed in severe stenoses than in mild ones. Varying the exponent from 2.0 to 3.0 within the flow-split methods did not significantly affect the haemodynamic results (p>0.141). Flow-split strategies with exponents between 2.0 and 3.0 are appropriate for modelling stenosed coronaries under resting conditions. Multiscale simulations are recommended for accurate modelling of hyperaemic conditions, especially in severely stenosed arteries.
Reference graph
Works this paper leans on
-
[1]
J.F. Bentzon, F. Otsuka, R. Virmani, E. Falk, Mechanisms of Plaque Formation and Rupture, Circ Res 114 (2014) 1852–1866. https://doi.org/10.1161/circresaha.114.302721
-
[2]
C.A. Taylor, T.A. Fonte, J.K. Min, Computational Fluid Dynamics Applied to Cardiac Computed Tomography for Noninvasive Quantification of Fractional Flow Reserve, J Am Coll Cardiol 61 (2013) 2233–2241. https://doi.org/10.1016/j.jacc.2012.11.083
-
[3]
A. Candreva, M. Pagnoni, M.L. Rizzini, T. Mizukami, E. Gallinoro, V. Mazzi, D. Gallo, D. Meier, T. Shinke, J. -P. Aben, S. Nagumo, J. Sonck, D. Munhoz, S. Fourni er, E. Barbato, W. Heggermont, S. Cook, C. Chiastra, U. Morbiducci, B. De Bruyne, O. Muller, C. Collet, Risk of myocardial infarction based on endothelial shear stress analysis using coronary ang...
-
[4]
W.F. Fearon, B. Bornschein, P.A.L. Tonino, R.M. Gothe, B.D. Bruyne, N.H.J. Pijls, U. Siebert, Economic evaluation of fractional flow reserve -guided percutaneous coronary intervention in patients with multivessel di sease, Circulation (2010). https://doi.org/10.1161/CIRCULATIONAHA.109.925396
-
[5]
J.M. Lee, G. Choi, B. -K. Koo, D. Hwang, J. Park, J. Zhang, K. -J. Kim, Y. Tong, H.J. Kim, L. Grady, J.-H. Doh, C. -W. Nam, E. -S. Shin, Y. -S. Cho, S. -Y. Choi, E.J. Chun, J. -H. Choi, B.L. Nørgaard, E.H. Christiansen, K. Niemen, H. Otake, M. Penicka, B. De Bruyne, T. Kubo, T. Akasaka, J. Narula, P.S. Douglas, C.A. Taylor, H.-S. Kim, Identification of Hi...
work page 2019
-
[6]
N. Curzen, Z. Nicholas, B. Stuart, S. Wilding, K. Hill, J. Shambrook, Z. Eminton, D. Ball, C. Barrett, L. Johnson, J. Nuttall, K. Fox, D. Connolly, P. O’Kane, A. Hobson, A. Chauhan, N. Uren, G. Mccann, C. Berry, J. Carter, C. Roobottom, M. Mamas, R. Rajani, I. Ford, P. Douglas, M. Hlatky, Fractional flow reserve derived from computed tomography coronar y ...
work page 2021
-
[7]
M. Gulati, P.D. Levy, D. Mukherjee, E. Amsterdam, D.L. Bhatt, K.K. Birtcher, R. Blankstein, J. Boyd, R.P. Bullock-Palmer, T. Conejo, D.B. Diercks, F. Gentile, J.P. Greenwood, E.P. Hess, S.M. Hollenberg, W.A. Jaber, H. Jneid, J.A. Joglar, D.A. Morrow, R.E. O’Connor, M.A. Ross, L.J. Shaw, 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/ SCMR guideline for the evaluation a...
work page 2021
-
[8]
M.T. Corban, P. Eshtehardi, J. Suo, M.C. McDaniel, L.H. Timmins, E. Rassoul -Arzrumly, C. Maynard, G. Mekonnen, S. King, A.A. Quyyumi, D.P. Giddens, H. Samady, Combination of plaque burden, wall shear stress, and plaque phenotype has incremental value for prediction of coronary atherosclerotic plaque progression and vulnerability, Atherosclerosis 232 (201...
Show all 52 references
-
[9]
Y. Dai, Y. Qian, M. Zhang, Y. Li, P. Lv, X. Tang, A. Javadzadegan, J. Lin, Associations between local haemodynamics and carotid intraplaque haemorrhage with different stenosis severities: A preliminary study based on MRI and CFD, J Clin Neurosci 66 (2019) 220 –225. https://doi...
2019 doi
-
[10]
Morbiducci, A.M
U. Morbiducci, A.M. Kok , B.R. Kwak, P.H. Stone, D.A. Steinman, J.J. Wentzel, Atherosclerosis at arterial bifurcations: evidence for the role of haemodynamics and geometry, Thromb Haemost 115 (2016) 484–492. https://doi.org/10.1160/th15-07-0597. pg. 14/18
2016 doi
-
[11]
Hoi, Y.-Q
Y. Hoi, Y.-Q. Zhou, X. Zhang, R.M. Henkelman, D.A. Steinman, Correlation Between Local Hemodynamics and Lesion Distribution in a Novel Aortic Regurgitation Murine Model of Atherosclerosis, Ann Biomed Eng 39 (2011) 1414 –1422. https://doi.org/10.1007/s10439-011- 0255-z
2011 doi
-
[12]
Stone, S
P.H. Stone, S. Saito, S. Takahashi, Y. Makita, S. Nakamura, T. Kawasaki, A. Takahashi, T. Katsuki, S. Nakamura, A. Namiki, A. Hirohata, T. Matsumura, S. Yamazaki, H. Yokoi, S. Tanaka, S. Otsuji, F. Yoshimachi, J. Honye, D. Harwood, M. Reitman, A.U. Coskun, M.I. Papafaklis, C.L...
2012
-
[13]
Mazzi, G
V. Mazzi, G. De Nisco, A. Hoogendoorn, K. Calò, C. Chiastra, D. Gallo, D.A. Steinman, J.J. Wentzel, U. Morbiducci, Early Atherosclerotic Changes in Coronary Arteries are Associated with Endothelium Shear Stress Contraction/Expansion Variability, Ann Biomed Eng 49 (2021) 2606–2...
2021 doi
-
[14]
Zhang, R
M. Zhang, R. Gharleghi, C. Shen, S. Beier, A new understanding of coronary curvature and haemodynamic impact on the course of plaque ons et and progression, R Soc Open Sci 11 (2024) 241267. https://doi.org/10.1098/rsos.241267
2024 doi
-
[15]
Gijsen, Y
F. Gijsen, Y. Katagiri, P. Barlis, C. Bourantas, C. Collet, U. Coskun, J. Daemen, J. Dijkstra, E. Edelman, P. Evans, K. Van Der Heiden, R. Hose, B. -K. Koo, R. Kr ams, A. Marsden, F. Migliavacca, Y. Onuma, A. Ooi, E. Poon, H. Samady, P. Stone, K. Takahashi, D. Tang, V. Thondap...
2019
-
[16]
J. Liu, X. Wang, B. Li, S. Huang, H. Sun, L. Zhang, Y. Sun, Z. Liu, J. Liu, L. Wang, X. Zhao, W. Wang, M. Zhang, Y. Liu, Non -Invasive Quantification of Fraction Flow Reserve Based on Steady-State Geometric Multiscale Models, Front Physiol 13 (2022) 881826. https://doi.org/10....
2022
-
[17]
Taylor, K
C.A. Taylor, K. Petersen, N. Xiao, M . Sinclair, Y. Bai, S.R. Lynch, A. UpdePac, M. Schaap, Patient-specific modeling of blood flow in the coronary arteries, Computer Methods in Applied Mechanics and Engineering 417 (2023) 116414. https://doi.org/10.1016/j.cma.2023.116414
2023
-
[18]
Kim, I.E
H.J. Kim, I.E. Vignon-Clementel, J.S. Coogan, C.A. Figueroa, K.E. Jansen, C.A. Taylor, Patient-Specific Modeling of Blood Flow and Pressure in Human Coronary Arteries, Ann Biomed Eng 38 (2010) 3195–3209. https://doi.org/10.1007/s10439-010-0083-6
2010 doi
-
[19]
J. Liu, B. Li, Y. Zhang, L. Zhang, S. Huang, H. Sun, J. Liu, X. Zhao, M. Zhang, W. Wang, Y. Liu, A high -fidelity geometric multiscale hemodynamic model for predicting myocardial ischemia, Comput Methods Programs Biomed 233 (2023) 107476. https://doi.org/10.1016/j.cmpb.2023.107476
2023
-
[20]
Kassab, Scaling laws of vascular trees: of form and function, American Journal of Physiology-Heart and Circulatory Physiology 290 (2006) H894 –H903
G.S. Kassab, Scaling laws of vascular trees: of form and function, American Journal of Physiology-Heart and Circulatory Physiology 290 (2006) H894 –H903. https://doi.org/10.1152/ajpheart.00579.2005
2006
-
[21]
Murray, The physiological principle of minimum work: I
C.D. Murray, The physiological principle of minimum work: I. The vascular system and the cost of blood volume, Proc Natl Acad Sci 12 (1926) 207 –214. https://doi.org/10.1073/pnas.12.3.207
1926 doi
-
[22]
Huo, G.S
Y. Huo, G.S. Kassab, Intraspecific scaling laws of vascular trees, Journal of the Royal Society, Interface 9 (2012) 190–200. https://doi.org/10.1098/rsif.2011.0270. pg. 15/18
2012
-
[23]
Doriot, P.-A
P.-A. Doriot, P.-A. Dorsaz, L. Dorsaz, E. De Benedetti, P. Chatelain, P. Delafontaine, In-vivo measurements of wall shear stress in human coronary arteries:, Coron Artery Dis 11 (2000) 495–502. https://doi.org/10.1097/00019501-200009000-00008
2000 doi
-
[24]
Van Der Giessen, H.C
A.G. Van Der Giessen, H.C. Groen, P.-A. Doriot, P.J. De Feyter, A.F.W. Van Der Steen, F.N. Van De Vosse, J.J. Wentzel, F.J.H. Gijsen, The influence of boundary conditions on wall shear stress dist ribution in patients specific coronary trees, J Biomech 44 (2011) 1089 –1095. ht...
2011 doi
-
[25]
Zhou, G.S
Y. Zhou, G.S. Kassab, S. Molloi, On the design of the coronary arterial tree: a generalization of murray’s law, Phys Med Biol 44 (1999) 2929 –2945. https://doi.org/10.1088/0031 - 9155/44/12/306
1999 doi
-
[26]
Lodi Rizzini, A
M. Lodi Rizzini, A. Candreva, C. Chiastra, E. Gallinoro, K. Calò, F. D’Ascenzo, B. De Bruyne, T. Mizukami, C. Collet, D. Gallo, U. Morbiducci, Modelling coronary flows: impact of differently measured inflow boundary conditions on vessel -specific computational hemodynamic prof...
2022
-
[27]
Zhang, C
M. Zhang, C. Shen, S. Beier, Comparison of two common outflo w strategies for resolving coronary haemodynamics under resting and hyperaemic flow conditions., in: Proceedings of the 23rd Australasin Fluid Mechanics Conference - 23AFMC, Australasian Fluid Mechanics Society (2022...
2022
-
[28]
Nørgaard, J
B.L. Nørgaard, J. Leipsic, S. Gaur, S. Seneviratne, B.S. Ko, H. Ito, J.M. Jensen, L. Mauri, B. De Bruyne, H. Bezerra, K. Osawa, M. Marwan, C. Naber, A. Erglis, S.-J. Park, E.H. Christiansen, A. Kaltoft, J.F. Lassen, H.E. Bøtker, S. Achenbach, Di agnostic Performance of Noninva...
2014 doi
-
[29]
Gharleghi, D
R. Gharleghi, D. Adikari, K. Ellenberger, S. -Y. Ooi, C. Ellis, C. -M. Chen, R. Gao, Y. He, R. Hussain, C.-Y. Lee, J. Li, J. Ma, Z. Nie, B. Oliveira, Y. Qi, Y. Skandarani, J.L. Vilaça, X. Wang, S. Yang, A. Sowmya, S. Beier, Automated segmentation of normal and diseased coro na...
2022
-
[30]
Gharleghi, D
R. Gharleghi, D. Adikari, K. Ellenberger, M. Webster, C. Ellis, A. Sowmya, S. Ooi, S. Beier, Annotated computed tomograp hy coronary angiogram images and associated data of normal and diseased arteries, Sci Data 10 (2023) 128. https://doi.org/10.1038/s41597 -023- 02016-2
2023 doi
-
[31]
Antiga, D.A
L. Antiga, D.A. Steinman, VMTK: vascular modeling toolkit, 2012
2012
-
[32]
Vlachopoulos, M
C. Vlachopoulos, M. O’Rourke, W.W. Nichols, McDonald’s blood flow in arteries: theoretical, experimental and clinical principles, CRC press, 2011
2011
-
[33]
Kishi, A.A
S. Kishi, A.A. Giannopoulos, A. Tang, N. Kato, Y.S. Chatzizisis, C. Dennie, Y. Horiuchi, K. Tanabe, J.A.C. Lima, F.J. Rybicki, D. Mitso uras, Fractional Flow Reserve Estimated at Coronary CT Angiography in Intermediate Lesions: Comparison of Diagnostic Accuracy of Different Me...
2018 doi
-
[34]
Coogan, J.D
J.S. Coogan, J.D. Humphrey, C.A. Figueroa, Computational simulations of hemodynamic changes within thoracic, coronary, and cerebral arteries following early wall remodeling in response to distal aortic coarctation, Biomech Model Mechanobiol 12 (201 3) 79 –93. https://doi.org/1...
-
[35]
Keramati, A
H. Keramati, A. de Vecchi, R. Rajani, S.A. Niederer, Using Gaussian process for velocity reconstruction after coronary stenosis applicable in positron emission particle tracking: An in-silico study, Plos One 18 (2023) e0295789. pg. 16/18
2023
-
[36]
Jonášová, J
A. Jonášová, J. Vimmr, On the relevance of boundary conditions and viscosity models in blood flow simulations in patient -specific aorto -coronary bypass models, International Journal for Numerical Methods in Biomedical Engineering 37 (2021) e3439
2021
-
[37]
Eslami, J
P. Eslami, J. Tran, Z. Jin, J. Karady, R. Sotoodeh, M.T. Lu, U. Hoffmann, A. Marsden, Effect of Wall Elasticity on Hemodynamics and Wall Shear Stress in Patient-Specific Simulations in the Coronary Arteries, J Biomech Eng 142 (2020) 0245031 –02450310. https://doi.org/10.1115/1.4043722
2020 doi
-
[38]
Razavi, E
A. Razavi, E. Shirani, M.R. Sadeghi, Numerical simulation of blood pulsatile flow in a stenosed carotid artery using different rheological models, J Biomech 44 (2011) 2021 –2030. https://doi.org/10.1016/j.jbiomech.2011.04.023
2011 doi
-
[39]
Kung, A.M
E. Kung, A.M. Kahn, J.C. Burns, A. Marsden, In Vitro Validation of Patient -Specific Hemodynamic Simulations in Coronary Aneurysms Caused by Kawasaki Disease, Cardiovasc. Eng. Technol. 5 (2014) 189–201. https://doi.org/10.1007/s13239-014-0184-8
2014 doi
-
[40]
Costopoulos, L.H
C. Costopoulos, L.H. Timmins, Y. Huang, O.Y. Hung, D.S. Molony, A.J. Brown, E.L. Davis, Z. Teng, J.H. Gillard, H. Samady, M.R. Bennett, Impact of combined plaque structural stress and wall shear stress on coronary plaque progression, regression, and changes in composition, Eur...
2019 doi
-
[41]
S. Sen, J. Escaned, I.S. Malik, G.W. Mikhail, R.A. Foale, R. Mila, J. Tarkin, R. Petraco, C. Broyd, R. Jabbour, A. Sethi, C.S. Baker, M. Bellamy, M. Al-Bustami, D. Hackett, M. Khan, D. Lefroy, K.H. Parker, A.D. Hughes, D.P. Francis, C. Di Mario, J. Mayet, J.E. Davies, Developm...
2012 doi
-
[42]
Rodriguez-Leor, J.M
O. Rodriguez-Leor, J.M. De La Torre Hernández, T. García-Camarero, B. García Del Blanco, R. López-Palop, E. Fernández-Nofrerías, C. Cuellas Ramón, M. Jiménez-Kockar, J. Jiménez- Mazuecos, F. Fernández Salinas, J. Gómez -Lara, S. Brugaletta, F. Alfonso, R. Palma, A.E. Gómez-Men...
2022
-
[43]
Kumar, P.K
S. Kumar, P.K. Mehta, P. Eshtehardi, O.Y. Hung, J.-S. Koh, A. Kumar, A. Al-Badri, R. Rabah, M. D’Souza, S. Gupta, others, Functional coronary angiography in symptomatic patients with no obstructive coronary artery disease, Catheterization and Cardiovascular Interventions 98 (2...
2021
-
[44]
Y. Geng, H. Liu, X. Wang, J. Zhang, Y. Gong, D. Zheng, J. Jiang, L. Xia, Effect of microcirculatory dysfunction on coronary hemodynamics: A pilot study based on computational fluid dynamics simulation, Comput Biol Med 146 (2022) 105583
2022
-
[45]
Ihdayhid, J
A.R. Ihdayhid, J. Sapontis, The fractional flow reserve grey zone: a blueprint for the future of coronary revascularisation, Heart 106 (2020) 714 –715. https://doi.org/10.1136/heartjnl - 2019-316435
2020 doi
-
[46]
Haley, M
H.A. Haley, M. Ghobrial, P.D. Morris, R. Gosling, G. Willi ams, M.T. Mills, T. Newman, V. Rammohan, G. Pederzani, P.V. Lawford, others, Virtual (computed) fractional flow reserve: future role in acute coronary syndromes, Frontiers in Cardiovascular Medicine 8 (2021) 735008. pg. 17/18
2021
-
[47]
Schwarz, L
E.L. Schwarz, L. Pegolotti, M.R. Pf aller, A.L. Marsden, Beyond CFD: Emerging methodologies for predictive simulation in cardiovascular health and disease, Biophysics Reviews 4 (2023)
2023
-
[48]
Lee, J.-H
J.M. Lee, J.-H. Jung, D. Hwang, J. Park, Y. Fan, S.-H. Na, J.-H. Doh, C.-W. Nam, E.-S. Shin, B.- K. Koo, Coronary flow reserve and microcirculatory resistance in patients with intermediate coronary stenosis, J Am Coll Cardiol 67 (2016) 1158–1169
2016
-
[49]
S. Yang, D. Hwang, J.M. Lee, S.H. Lee, C.K. Boerhout, J. Woudstra, C.E. Vink, G.A. de Waard, J.H. Jung, H.M. Renteria, others, Prognostic implications of individual and combinations of resting and hyperemic coronary pressure and flow parameters, JACC: Asia 3 (2023) 865–877
2023
-
[50]
Balasso, J.S
A. Balasso, J.S. Bauer, T. Liebig, F. Dorn, C. Zimmer, D. Liepsch, S. Prothmann, Ev aluation of intra -aneurysmal hemodynamics after flow diverter placement in a patient -specific aneurysm model, Biorheology 51 (2015) 341–354. https://doi.org/10.3233/bir-14019
2015 doi
-
[51]
Kannojiya, A.K
V. Kannojiya, A.K. Das, P.K. Das, Simulation of Blood as Fluid: A Review From Rheological Aspects, IEEE Rev Biomed Eng 14 (2021) 327–341. https://doi.org/10.1109/rbme.2020.3011182
2021
-
[52]
B.-K. Koo, A. Erglis, J.-H. Doh, D.V. Daniels, S. Jegere, H.-S. Kim, A. Dunning, T. DeFrance, A. Lansky, J. Leipsic, J.K. Min, Diagnosis of Ische mia-Causing Coronary Stenoses by Noninvasive Fractional Flow Reserve Computed From Coronary Computed Tomographic Angiograms, J Am C...
2011 doi
Reviewed August 8, 2026 · model on record in the stance chip above.
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