Non Invasive Blood Flow Features Estimation in Cerebral Arteries from Uncertain Medical Data.

A methodology for non-invasive estimation of the pressure in internal carotid arteries is proposed. It uses data assimilation and Ensemble Kalman filters in order to identify unknown parameters in a mathematical description of the cerebral network. The approach uses patient specific blood flow rates extracted from Magnetic Resonance Angiography and Magnetic Resonance Imaging. This construction is necessary as the simulation of blood flows in complex arterial networks, such as the circle of Willis, is not straightforward because hemodynamic parameters are unknown as well as the boundary conditions necessary to close this complex system with many outlets. For instance, in clinical cases, the values of Windkessel model parameters or the Young's modulus and the thickness of the arteries are not available on per-patient cases. To make the approach computational efficient, a reduced order zero-dimensional compartment model is used for blood flow dynamics. Using this simplified model, the proof-of-concept study demonstrates how to use the EnKF as an optimization tool to find parameters and how to make the inverse hemodynamic problem tractable. The predicted blood flow rates in the internal carotid arteries and the predicted systolic and diastolic brachial blood pressures are found to be in good agreement with the clinical measurements.

Image-Based Simulations Show Important Flow Fluctuations in a Normal Left Ventricle: What Could be the Implications?

Intra-cardiac flow has been explored for decades but there is still no consensus on whether or not healthy left ventricles (LV) may harbour turbulent-like flow despite its potential physiological and clinical relevance. The purpose of this study is to elucidate if a healthy LV could harbour flow instabilities, using image-based computational fluid dynamics (CFD). 35 cardiac cycles were simulated in a patient-specific left heart model obtained from cardiovascular magnetic resonance (CMR). The model includes the valves, atrium, ventricle, papillary muscles and ascending aorta. We computed phase-averaged flow patterns, fluctuating kinetic energy (FKE) and associated frequency components. The LV harbours disturbed flow during diastole with cycle-to-cycle variations. However, phase-averaged velocity fields much resemble those of CMR measurements and usually reported CFD results. The peak FKE value occurs during the E wave deceleration and reaches 25% of the maximum phase-averaged flow kinetic energy. Highest FKE values are predominantly located in the basal region and their frequency content reach more than 200 Hz. This study suggests that high-frequency flow fluctuations in normal LV may be common, implying deficiencies in the hypothesis usually made when computing cardiac flows and highlighting biases when deriving quantities from velocity fields measured with CMR.

Intracranial aneurysmal pulsatility as a new individual criterion for rupture risk evaluation: biomechanical and numeric approach (IRRAs Project).

BACKGROUND AND PURPOSE: The present study follows an experimental work based on the characterization of the biomechanical behavior of the aneurysmal wall and a numerical study where a significant difference in term of volume variation between ruptured and unruptured aneurysm was observed in a specific case. Our study was designed to highlight by means of numeric simulations the correlation between aneurysm sac pulsatility and the risk of rupture through the mechanical properties of the wall. MATERIALS AND METHODS: In accordance with previous work suggesting a correlation between the risk of rupture and the material properties of cerebral aneurysms, 12 fluid-structure interaction computations were performed on 12 "patient-specific" cases, corresponding to typical shapes and locations of cerebral aneurysms. The variations of the aneurysmal volume during the cardiac cycle (ΔV) are compared by using wall material characteristics of either degraded or nondegraded tissues. RESULTS: Aneurysms were located on 6 different arteries: middle cerebral artery (4), anterior cerebral artery (3), internal carotid artery (1), vertebral artery (1), ophthalmic artery (1), and basilar artery (1). Aneurysms presented different shapes (uniform or multilobulated) and diastolic volumes (from 18 to 392 mm3). The pulsatility (ΔV/V) was significantly larger for a soft aneurysmal material (average of 26%) than for a stiff material (average of 4%). The difference between ΔV, for each condition, was statistically significant: P=.005. CONCLUSIONS: The difference in aneurysmal pulsatility as highlighted in this work might be a relevant patient-specific predictor of aneurysm risk of rupture.

Biomechanical assessment of the individual risk of rupture of cerebral aneurysms: a proof of concept.

This study is a step towards a new biomechanical-based measurement of the patient specific risk of rupture of cerebral aneurysms. Following a previous experimental investigation suggesting a correlation between the risk of rupture and the material properties of cerebral aneurysms, fluid-structure interaction simulations are performed to compare the deformations of a patient-specific aneurysm when using degraded or undegraded materials. Results show that material properties have a major impact on the magnitude of systolic/diastolic aneurysmal volume variations along the cardiac cycle. Changes in terms of aneurysmal volume variations depending on the tissue characteristics are shown to be measurable by medical imaging. A one-at-a-time data uncertainty analysis is also presented and shows the robustness of this result to input data uncertainties. The study thus suggests that aneurysmal volume variations may be used as the basis of a biomechanical index of rupture risk.

Biomechanical wall properties of human intracranial aneurysms resected following surgical clipping (IRRAs Project).

BACKGROUND AND PURPOSE: Individual rupture risk assessment of intracranial aneurysms is a major issue in the clinical management of asymptomatic aneurysms. Aneurysm rupture occurs when wall tension exceeds the strength limit of the wall tissue. At present, aneurysmal wall mechanics are poorly understood and thus, risk assessment involving mechanical properties is inexistent. Aneurysm computational hemodynamics studies make the assumption of rigid walls, an arguable simplification. We therefore aim to assess mechanical properties of ruptured and unruptured intracranial aneurysms in order to provide the foundation for future patient-specific aneurysmal risk assessment. This work also challenges some of the currently held hypotheses in computational flow hemodynamics research. METHODS: A specific conservation protocol was applied to aneurysmal tissues following clipping and resection in order to preserve their mechanical properties. Sixteen intracranial aneurysms (11 female, 5 male) underwent mechanical uniaxial stress tests under physiological conditions, temperature, and saline isotonic solution. These represented 11 unruptured and 5 ruptured aneurysms. Stress/strain curves were then obtained for each sample, and a fitting algorithm was applied following a 3-parameter (C(10), C(01), C(11)) Mooney-Rivlin hyperelastic model. Each aneurysm was classified according to its biomechanical properties and (un)rupture status. RESULTS: Tissue testing demonstrated three main tissue classes: Soft, Rigid, and Intermediate. All unruptured aneurysms presented a more Rigid tissue than ruptured or pre-ruptured aneurysms within each gender subgroup. Wall thickness was not correlated to aneurysmal status (ruptured/unruptured). An Intermediate subgroup of unruptured aneurysms with softer tissue characteristic was identified and correlated with multiple documented risk factors of rupture. CONCLUSION: There is a significant modification in biomechanical properties between ruptured aneurysm, presenting a soft tissue and unruptured aneurysms, presenting a rigid material. This finding strongly supports the idea that a biomechanical risk factor based assessment should be utilized in the to improve the therapeutic decision making.

A numerical assessment of wall shear stress changes after endovascular stenting.

This theoretical/numerical study aims at assessing the haemodynamic changes induced by endovascular stenting. By using the classical one-dimensional linear pressure waves theory in elastic vessels, we first show that the modulus of the reflection coefficient induced by an endovascular prosthesis is most likely small since it is proportional to the stent-to-wavelength ratio. As a direct consequence, the wall motion of the elastic (stented) artery can be prescribed a priori and the coupled fluid-structure problem does not have to be solved for assessing the haemodynamic changes due to stenting. Several 2D axisymetric calculations are performed to solve the unsteady incompressible Navier-Stokes equations on moving meshes for different types of (stented) arteries. The numerical results suggest that endovascular stenting increases the systo-diastolic variations of the wall shear stress (by 35% at the middle of the stent, by almost 50% in the proximal transition region). Additional calculations show that over-dilated stents produce less haemodynamic perturbations. Indeed, the increase of the amplitude of the wall shear stress variations over the cardiac cycle is only 10% when the stent radius is equal to the radius of the elastic artery at systole (instead of being equal to the mean artery radius).

Increased cardiac angiotensin II levels induce right and left ventricular hypertrophy in normotensive mice.

Angiotensin II is a potent arterial vasoconstrictor and induces hypertension. Angiotensin II also exerts a trophic effect on cardiomyocytes in vitro. The goals of the present study were to document an in vivo increase in cardiac angiotensins in the absence of elevated plasma levels or hypertension and to investigate prevention or regression of ventricular hypertrophy by renin-angiotensin system blockade. We demonstrate that high cardiac angiotensin II is directly responsible for right and left ventricular hypertrophy. We used transgenic mice overexpressing angiotensinogen in cardiomyocytes characterized by cardiac hypertrophy without fibrosis and normal blood pressure. Angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade prevent or normalize ventricular hypertrophy. Surprisingly, in control mice, receptor blockade decreases tissue angiotensin II despite increased plasma levels. This suggests that angiotensin II may be protected from metabolization by binding to its receptor. Blocking of the angiotensin II type 1 receptor rather than enhanced stimulation of the angiotensin II type 2 receptor may prevent remodeling and account for the beneficial effects of angiotensin antagonists.