Ex vivo vessel wall thickness measurements of the human circle of Willis using 7T MRI

The intracranial arteries play a major role in cerebrovascular disease, but arterial remodeling due to hypertension has not been well described in humans. We aimed to quantify this remodeling for: the basilar artery, the vertebral, internal carotid, middle/anterior (inferior)/posterior cerebral, posterior communicating, and superior cerebellar arteries of the circle of Willis. Ex vivo circle of Willis specimens, selected from individuals with (n=24) and without (n=25) a history of hypertension, were imaged at 7T magnetic resonance imaging using a 3-dimensional gradient-echo sequence. Subsequently, histological analysis was performed. We validated the vessel wall thickness and area measurements from magnetic resonance imaging against histology. Next, we investigated potential differences in vessel wall thickness and area between both groups using both techniques. Finally, using histological analysis, we investigated potential differences in arterial wall stiffness and atherosclerotic plaque severity and load. All analyses were unadjusted. Magnetic resonance imaging and histology showed comparable vessel wall thickness (mean difference: 0.04 mm (limits of agreement:−0.12 to 0.19 mm) and area (0.43 mm 2 [−0.97 to 1.8 mm 2 ]) measurements. We observed no statistically significant differences in vessel wall thickness and area between both groups using either technique. Histological analysis showed early and advanced atherosclerotic plaques in almost all arteries for both groups. The arterial wall stiffness was significantly higher for the internal carotid artery in the hypertensive group. Concluding, we did not observe vessel wall thickening in the circle of Willis arteries in individuals with a history of hypertension using either technique. Using histological analysis, we observed a difference in vessel wall composition for the internal carotid artery.

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A neutralizing IL-11 antibody reduces vessel hyperplasia in a mouse carotid artery wire injury model

Scientific Reports ◽

10.1038/s41598-021-99880-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

David Schumacher ◽

Elisa A. Liehn ◽

Pakhwan Nilcham ◽

David Castaño Mayan ◽

Chutima Rattanasopa ◽

...

Keyword(s):

Smooth Muscle ◽

Wall Thickness ◽

Vessel Wall ◽

Neointimal Hyperplasia ◽

Endothelial Injury ◽

Collagen Content ◽

Arterial Stenosis ◽

Matrix Metalloproteinase 2 ◽

Vessel Wall Thickness ◽

Artery Disease

AbstractVascular restenosis remains a major problem in patients with coronary artery disease (CAD) and peripheral artery disease (PAD). Neointimal hyperplasia, defined by post-procedure proliferation and migration of vascular smooth muscle cells (VSMCs) is a key underlying pathology. Here we investigated the role of Interleukin 11 (IL-11) in a mouse model of injury-related plaque development. Apoe−/− mice were fed a hyperlipidaemic diet and subjected to carotid wire injury of the right carotid. Mice were injected with an anti-IL11 antibody (X203), IgG control antibody or buffer. We performed ultrasound analysis to assess vessel wall thickness and blood velocity. Using histology and immunofluorescence approaches, we determined the effects of IL-11 inhibition on VSMC and macrophages phenotypes and fibrosis. Treatment of mice with carotid wire injury using X203 significantly reduced post-endothelial injury vessel wall thickness, and injury-related plaque, when compared to control. Immunofluorescence staining of the injury-related plaque showed that X203 treatment did not reduce macrophage numbers, but reduced the number of VSMCs and lowered matrix metalloproteinase 2 (MMP2) levels and collagen content in comparison to control. X203 treatment was associated with a significant increase in smooth muscle protein 22α (SM22α) positive cells in injury-related plaque compared to control, suggesting preservation of the contractile VSMC phenotype. Interestingly, X203 also reduced the collagen content of uninjured carotid arteries as compared to IgG, showing an additional effect on hyperlipidemia-induced arterial remodeling in the absence of mechanical injury. Therapeutic inhibition of IL-11 reduced vessel wall thickness, attenuated neointimal hyperplasia, and has favorable effects on vascular remodeling following wire-induced endothelial injury. This suggests IL-11 inhibition as a potential novel therapeutic approach to reduce arterial stenosis following revascularization in CAD and PAD patients.

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Atherosclerosis: Carotid vessel wall thickness and aortic stiffness compared to stenosis class in peripheral arterial disease

European Journal of Internal Medicine ◽

10.1016/j.ejim.2013.08.093 ◽

2013 ◽

Vol 24 ◽

pp. e38-e39

Author(s):

Harrie CM van den Bosch ◽

Jos JM Westenberg ◽

Wikke Setz-Pels ◽

Alette Daniels-Gooszen ◽

Lucien EM Duijm ◽

...

Keyword(s):

Peripheral Arterial Disease ◽

Wall Thickness ◽

Vessel Wall ◽

Aortic Stiffness ◽

Arterial Disease ◽

Vessel Wall Thickness ◽

Carotid Vessel Wall ◽

Peripheral Arterial ◽

Carotid Vessel

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Towards Non-Invasive Pressure Assessment

ASME 2010 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2010-19214 ◽

2010 ◽

Author(s):

Nathalie Bijnens ◽

Bart Beulen ◽

Peter Brands ◽

Marcel Rutten ◽

Frans van de Vosse

Keyword(s):

Wall Thickness ◽

Vessel Wall ◽

Biomechanical Properties ◽

Vessel Diameter ◽

Local Pressure ◽

Vessel Wall Thickness ◽

Non Invasive ◽

Vascular Impedance ◽

Vessel Wall Properties ◽

Invasive Techniques

In clinical practice, ultrasound is frequently applied to non-invasively assess blood velocity, blood volume flow and blood vessel wall properties such as vessel wall thickness and vessel diameter waveforms. To convert these properties into relevant biomechanical properties that are related to cardiovascular disease (CVD), such as elastic modulus and compliance of the vessel wall, local pressure has to be assessed simultaneously with vessel wall thickness and vessel diameter waveforms. Additionally, accurate estimates of vascular impedance (transfer function between pressure and blood flow) can be a valuable tool for the estimation of the condition of the vessel, e.g., to diagnose stenosis. Studies of arterial impedance in humans, however, are hampered by the lack of reliable non-invasive techniques to simultaneously record pressure and flow locally as a function of time. Local pressure assessment together with flow has great potential for improving the ability to diagnose and monitor CVD.

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Human Carotid Atherosclerotic Plaque Growth Function and Progression Simulation Using Meshless GFD and Statistical Methods Based on Multi-Year In Vivo MRI

Volume 2: Biomedical and Biotechnology Engineering ◽

10.1115/imece2008-66759 ◽

2008 ◽

Author(s):

Chun Yang ◽

Joseph D. Petruccelli ◽

Zhongzhao Teng ◽

Chun Yuan ◽

Gador Canton ◽

...

Keyword(s):

Atherosclerotic Plaque ◽

Wall Thickness ◽

Vessel Wall ◽

Plaque Rupture ◽

Patient Specific ◽

Tracking Data ◽

Plaque Progression ◽

Vessel Wall Thickness ◽

Plaque Growth

Atherosclerotic plaque rupture and progression have been the focus of intensive investigations in recent years. The mechanisms governing plaque progression and rupture process are not well understood. Using computational models based on patient-specific multi-year in vivo MRI data, our recent results indicated that 18 out of 21 patients studied showed significant negative correlation between plaque progression measured by vessel wall thickness increase (WTI) and plaque wall (structural) stress (PWS) [1]. In this paper, a computational procedure based on meshless generalized finite difference (MGFD) method and serial magnetic resonance imaging (MRI) data was introduced to simulate plaque progression. Participating patients were scanned three times (T1, T2, and T3, at intervals of approximately 18 months) to obtain plaque progression data. Vessel wall thickness (WT) changes were used as the measure for plaque progression. Starting from T2 plaque geometry, plaque progression was simulated by solving the solid model and adjusting wall thickness using plaque growth functions iteratively until time T3 is reached. Numerically simulated plaque progression showed very good agreement with actual plaque geometry at T3 given by MRI data. We believe this is the first time plaque progression simulation results based on multi-year patient-tracking data are reported. Multi-year tracking data and MRI-based progression simulation add time dimension to plaque vulnerability assessment and will improve prediction accuracy.

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