Hemodynamic Impairment of Blood Pressure and Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Stenosis.

BACKGROUND: Hemodynamic impairment of blood pressure may play a crucial role in determining the mechanisms of stroke in symptomatic intracranial atherosclerotic stenosis). We aimed to elucidate this issue and assess the impacts of modifications to blood pressure on hemodynamic impairment. METHODS: From the Third China National Stroke Registry III, computed fluid dynamics modeling was performed using the Newton-Krylov-Schwarz method in 339 patients with symptomatic intracranial atherosclerotic stenosis during 2015 to 2018. The major exposures were translesional systolic blood pressure (SBP) drop and poststenotic mean arterial pressure (MAP), and the major study outcomes were cortex-involved infarcts and borderzone-involved infarcts, respectively. Multivariate logistic regression models and the bootstrap resampling method were utilized, adjusting for demographics and medical histories. RESULTS: In all, 184 (54.3%) cortex-involved infarcts and 70 (20.6%) borderzone-involved infarcts were identified. In multivariate logistic model, the upper quartile of SBP drop correlated with increased cortex-involved infarcts (odds ratio, 1.92 [95% CI, 1.03-3.57]; bootstrap analysis odds ratio, 2.07 [95% CI, 1.09-3.93]), and the lower quartile of poststenotic MAP may correlate with increased borderzone-involved infarcts (odds ratio, 2.07 [95% CI, 0.95-4.51]; bootstrap analysis odds ratio, 2.38 [95% CI, 1.04-5.45]). Restricted cubic spline analysis revealed a consistent upward trajectory of the relationship between translesional SBP drop and cortex-involved infarcts, while a downward trajectory between poststenotic MAP and borderzone-involved infarcts. SBP drop correlated with poststenotic MAP negatively (rs=-0.765; P<0.001). In generating hemodynamic impairment, simulating blood pressure modifications suggested that ensuring adequate blood pressure to maintain sufficient poststenotic MAP appears preferable to the reverse approach, due to the prolonged plateau period in the association between the translesional SBP drop and cortex-involved infarcts and the relatively short plateau period characterizing the correlation between poststenotic MAP and borderzone-involved infarcts. CONCLUSIONS: This research elucidates the role of hemodynamic impairment of blood pressure in symptomatic intracranial atherosclerotic stenosis-related stroke mechanisms, underscoring the necessity to conduct hemodynamic assessments when managing blood pressure in symptomatic intracranial atherosclerotic stenosis.

Evaluation of cerebrovascular hemodynamics in vascular dementia patients with a new individual computational fluid dynamics algorithm.

BACKGROUND: Cerebral hemodynamic disorders are involved in the occurrence and progression of vascular dementia (VaD), but the methods to detect hemodynamics remainmultifarious and uncertain nowadays. We aim to exploit a computational fluid dynamics (CFD) approach by static and dynamic parameters, which can be used to detect individual cerebrovascular hemodynamics quantitatively. METHODS: A patient-specific CFD model was constructed with geometrical arteries on the magnetic resonance angiography (MRA) and hemodynamic parameters on ultrasound Doppler, by which, the structural and simulated hemodynamic indexes could be obtained, mainly including the cerebral arterial volume (CAV), the number of visible arterial outlets, the total cerebral blood flow (tCBF) index and the total cerebrovascular resistance (tCVR) index. The hemodynamics were detected in subcortical vascular dementia (SVaD) patients (n = 38) and cognitive normal controls (CNCs; n = 40). RESULTS: Compared with CNCs, the SVaD patients had reduced outlets, CAV and tCBF index (all P ≤ 0.001), increased volume of white matter hyperintensity (WMH) and tCVR index (both P ≤ 0.01). The fewer outlets (OR = 0.77), higher Hachinski ischemic score (HIS) (OR = 3.65), increased tCVR index (OR = 1.98) and volume of WMH (OR = 1.12) were independently associated with SVaD. All hemodynamic parameters could differentiate the SVaD patinets and CNCs, especially the composite index calculated by outlets, tCVR index and HIS (AUC = 0.943). Fewer outlets and more WMH increased the odds of SVaD, which were partly mediated by the tCBF index (14.4% and 13.0%, respectively). CONCLUSION: The reduced outlets, higher HIS and tCVR index may be independent risk factors for the SVaD, and a combination of these indexes can differentiate SVaD patients and CNCs reliably. The tCBF index potentially mediates the relationships between hemodynamic indexes and SVaD. Although all simulated indexes only represented the true hemodynamics indirectly, this CFD model can provide patient-specific hemodynamic alterations non-invasively and conveniently.

Non-invasive assessment of intracranial wall shear stress using high-resolution magnetic resonance imaging in combination with computational fluid dynamics technique.

In vivo studies on association between wall shear stress (WSS) and intracranial plaque are deficient. Based on the three-dimensional T1-weighted high-resolution magnetic resonance imaging (3DT1 HR-MRI) data of patients with low-grade stenotic (<50%) atherosclerotic middle cerebral artery (MCA) and subjects with normal MCA, we built a three-dimensional reconstructed WSS model by computational fluid dynamics (CFD) technique. Three-dimensional registration of the CFD model to the HR-MRI was performed with projections based on the resolution and thickness of the images. The relationships between the WSS at each side of the vessel wall and plaque location were analyzed. A total of 94 MCA plaques from 43 patients and 50 normal MCAs were analyzed. In the normal MCAs, WSS was lower at the ventral-inferior wall than at the dorsal-superior wall (proximal segment, p < 0.001; middle segment, p < 0.001) and lower at the inner wall than at the outer wall of the MCA curve (p < 0.001). In atherosclerotic MCAs, similar low WSS regions were observed where plaques developed. The WSS ratio of the ventral-inferior wall to the dorsal-superior wall in atherosclerotic MCAs was lower than that in normal MCAs (p = 0.002). The WSSinner-outer ratio in atherosclerotic MCAs was lower than that in normal MCAs (p = 0.002). Low WSS was associated with MCA atherosclerosis formation and occurred mainly at the ventral-inferior wall, which was anatomically opposite the orifices of penetrating arteries, and at the inner wall of the MCA curve. Overall, the results were well consistent with the low WSS theory in atherosclerosis formation. The reconstructed WSS model is a promising novel method for assessing an individualized vascular profile once validated by further studies.

Personalized 0D-1D multiscale hemodynamic modeling and wave dynamics analysis of cerebral circulation for an elderly patient with dementia.

Senile dementia is associated with pronounced alterations in cerebral circulation. A fundamental understanding of intracranial hemodynamics and wave dynamics is essential for assessing dementia risk. Recent findings suggest that higher carotid artery wave intensity (WI) can predict future cognitive impairments in the elderly. However, wave power (WP) is more advantageous for assessing the risk of cognitive impairment and dementia because of its conservative form, which allows quantification of detailed WP distribution among the entire cerebrovascular network. Unfortunately, intracranial hemodynamics and wave dynamics in elderly patients with dementia remain poorly understood due to ethical issues and technical challenges. In this paper, we proposed a novel and easily achievable personalized methodology for the 0D-1D model of cerebral circulation using widely available clinical data on transcranial Doppler ultrasonography velocity, cerebral artery anatomy from magnetic resonance imaging, and brachial artery pressure. Using the proposed model, we simulated the cerebral blood flows and compared the wave dynamics between a healthy elderly subject and one living with dementia. Moreover, we performed a variance-based global sensitivity analysis to quantify the model-predicted WI and WP sensitivity to the uncertainties of model inputs. This provided more precise information for model personalization and further insights into the wave dynamics of cerebral circulation. In conclusion, the proposed personalized model framework provides a practical approach for patient-specific modeling and WI/WP analysis of cerebral circulation through noninvasive clinical data. The wave dynamics features of higher WI and lower WP in cerebral arteries may be an invaluable biomarker for assessing dementia risk.

Expanding the coronary tree reconstruction to smaller arteries improves the accuracy of FFRCT.

OBJECTIVES: We attempted to improve the accuracy of coronary CT angiography (CCTA)-derived fractional flow reserve (FFR) (FFRCT) by expanding the coronary tree in the computational fluid dynamics (CFD) domain. An observational study was performed to evaluate the effects of extending the coronary tree analysis for FFRCT from a minimal diameter of 1.2 to 0.8 mm. METHODS: Patients who underwent CCTA and interventional FFR were enrolled retrospectively. Seventy-six patients qualified based on the inclusion criteria. The three-dimensional (3D) coronary artery tree was reconstructed to generate a finite element mesh for each subject with different lower limits of luminal diameter (1.2 mm and 0.8 mm). Outlet boundary conditions were defined according to Murray's law. The Newton-Krylov-Schwarz (NKS) method was applied to solve the governing equations of CFD to derive FFRCT. RESULTS: At the individual patient level, extending the minimal diameter of the coronary tree from 1.2 to 0.8 mm improved the sensitivity of FFRCT by 16.7% (p = 0.022). This led to the conversion of four false-negative cases into true-positive cases. The AUC value of the ROC curve increased from 0.74 to 0.83. Moreover, the NKS method can solve the computational problem of extending the coronary tree to an 0.8-mm luminal diameter in 10.5 min with 2160 processor cores. CONCLUSIONS: Extending the reconstructed coronary tree to a smaller luminal diameter can considerably improve the sensitivity of FFRCT. The NKS method can achieve favorable computational times for future clinical applications. KEY POINTS: • Extending the reconstructed coronary tree to a smaller luminal diameter can considerably improve the sensitivity of FFRCT. • The NKS method applied in our study can effectively reduce the computational time of this process for future clinical applications.

A parallel non-nested two-level domain decomposition method for simulating blood flows in cerebral artery of stroke patient.

Numerical simulation of blood flows in patient-specific arteries can be useful for the understanding of vascular diseases, as well as for surgery planning. In this paper, we simulate blood flows in the full cerebral artery of stroke patients. To accurately resolve the flow in this rather complex geometry with stenosis is challenging and it is also important to obtain the results in a short amount of computing time so that the simulation can be used in pre- and/or post-surgery planning. For this purpose, we introduce a highly scalable, parallel non-nested two-level domain decomposition method for the three-dimensional unsteady incompressible Navier-Stokes equations with an impedance outlet boundary condition. The problem is discretized with a stabilized finite element method on unstructured meshes in space and a fully implicit method in time, and the large nonlinear systems are solved by a preconditioned parallel Newton-Krylov method with a two-level Schwarz method. The key component of the method is a non-nested coarse problem solved using a subset of processor cores and its solution is interpolated to the fine space using radial basis functions. To validate and verify the proposed algorithm and its highly parallel implementation, we consider a case with available clinical data and show that the computed result matches with the measured data. Further numerical experiments indicate that the proposed method works well for realistic geometry and parameters of a full size cerebral artery of an adult stroke patient on a supercomputers with thousands of processor cores.

Characteristics of Wall Shear Stress and Pressure of Intracranial Atherosclerosis Analyzed by a Computational Fluid Dynamics Model: A Pilot Study.

Background: Although wall shear stress (WSS) and pressure play important roles in plaque vulnerability, characteristics of the two indices in intracranial atherosclerosis (ICAS) have not been fully investigated yet. This study aimed to elucidate this issue by means of establishing a non-invasive computational fluid dynamics method with time-of-flight magnetic resonance angiography (TOF-MRA) of the whole cerebral artery. Materials and Methods: Subjects with symptomatic ICAS in the middle cerebral artery domain were enrolled, excluding those with concomitant internal carotid artery stenosis. Based on patient-specific TOF-MRA images for three-dimensional (3D) meshes and arterial blood pressure with patient-specific carotid artery ultrasonography for inlet boundary conditions, patients' three-dimensional hemodynamics were modeled by a finite element method governed by Navier-Stokes equations. Results: Among the 55 atherosclerotic lesions analyzed by this TOF-MRA based computational fluid dynamics model, the maximum WSS (WSSmax) was most frequently detected at the apex points and the upper half of the upstream sections of the lesions, whereas the maximum pressure was most often located at the lower half of the upstream sections. As the percent stenosis increases, the relative value of WSSmax and pressure drop increased with significantly increasing steep beyond 50% stenosis. Moreover, WSSmax was found to linearly correlate with pressure drop in ICAS. Conclusions: This study on ICAS revealed certain trends of longitudinal distribution of WSS and pressure and the influences of percent stenosis on cerebral hemodynamics, as well as the correlations between WSS and pressure drop. It represents a step forward in applying computational flow simulation techniques in studying ICAS and stroke, in a patient-specific manner.