Author Correction: Comparison of 1D and 3D Models for the Estimation of Fractional Flow Reserve.

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Comparison of 1D and 3D Models for the Estimation of Fractional Flow Reserve.

In this work we propose to validate the predictive capabilities of one-dimensional (1D) blood flow models with full three-dimensional (3D) models in the context of patient-specific coronary hemodynamics in hyperemic conditions. Such conditions mimic the state of coronary circulation during the acquisition of the Fractional Flow Reserve (FFR) index. Demonstrating that 1D models accurately reproduce FFR estimates obtained with 3D models has implications in the approach to computationally estimate FFR. To this end, a sample of 20 patients was employed from which 29 3D geometries of arterial trees were constructed, 9 obtained from coronary computed tomography angiography (CCTA) and 20 from intra-vascular ultrasound (IVUS). For each 3D arterial model, a 1D counterpart was generated. The same outflow and inlet pressure boundary conditions were applied to both (3D and 1D) models. In the 1D setting, pressure losses at stenoses and bifurcations were accounted for through specific lumped models. Comparisons between 1D models (FFR1D) and 3D models (FFR3D) were performed in terms of predicted FFR value. Compared to FFR3D, FFR1D resulted with a difference of 0.00 ± 0.03 and overall predictive capability AUC, Acc, Spe, Sen, PPV and NPV of 0.97, 0.98, 0.90, 0.99, 0.82, and 0.99, with an FFR threshold of 0.8. We conclude that inexpensive FFR1D simulations can be reliably used as a surrogate of demanding FFR3D computations.

Computational modeling of blood flow steal phenomena caused by subclavian stenoses.

The study of steal mechanisms caused by vessel obstructions is of the utmost importance to gain understanding about their pathophysiology, as well as to improve diagnosis and management procedures. The goal of this work is to perform a computational study to gain insight into the hemodynamic forces that drive blood flow steal mechanisms caused by subclavian artery stenosis. Such condition triggers a flow disorder known as subclavian steal. When this occurs in patients with internal thoracic artery anastomosed to the coronary vessels, the phenomenon includes a coronary-subclavian steal. True steal can exist in cases of increased arm blood flow, potentially resulting in neurological complications and, in the case of coronary-subclavian steal, graft function failure. In this context, the anatomically detailed arterial network (ADAN) model is employed to simulate subclavian steal and coronary-subclavian steal phenomena. Model results are verified by comparison with published data. It is concluded that this kind of model allows us to effectively address complex hemomdynamic phenomena occurring in clinical practice. More specifically, in the studied conditions it is observed that a regional brain steal occurs, primarily affecting the posterior circulation, not fully compensated by the anterior circulation. In the case of patients with coronary revascularization, it is concluded that there is a large variability in graft hemodynamic environments, which physically explain both the success of the procedure in cases of severe occlusive disease, and the reason for graft dysfunction in mildly stenosed left anterior descending coronary artery, due to alternating graft flow waveform signatures.

Impact of CCSVI on cerebral haemodynamics: a mathematical study using MRI angiographic and flow data.

BACKGROUND: The presence of abnormal anatomy and flow in neck veins has been recently linked to neurological diseases. The precise impact of extra-cranial abnormalities such as stenoses remains unexplored. METHODS: Pressure and velocity fields in the full cardiovascular system are computed by means of a global mathematical model that accounts for the relationship between pulsating cerebral blood flow and intracranial pressure. RESULTS: Our model predicts that extra-cranial strictures cause increased pressure in the cerebral venous system. Specifically, there is a predicted pressure increase of about 10% in patients with a 90% stenoses. Pressure increases are related to significant flow redistribution with flow reduction of up to 70% in stenosed vessels and consequent flow increase in collateral pathways. CONCLUSIONS: Extra-cranial venous strictures can lead to pressure increases in intra-cranial veins of up to 1.3 mmHg, despite the shielding role of the Starling resistor. The long-term clinical implications of the predicted pressure changes are unclear.

Simulation of one-dimensional blood flow in networks of human vessels using a novel TVD scheme.

An extension of a total variation diminishing (TVD) scheme to solve one-dimensional (1D) blood flow for human circulation is proposed. This method is simple as it involves only a few modifications to existing shock-capturing TVD schemes. We have applied the method to a wide range of test cases including a complete simulation of the human vascular network. Excellent solutions have been demonstrated for problems involving varying and discontinuous mechanical properties of blood vessels. For 1D network simulations, the method has been shown to agree well with the reported computational results. Finally, the method has been demonstrated to compare favorably with in vivo experiments set up to study the impact of circle of Willis anomalies on flow patterns in the cerebral arterial system.