Performance Comparison of Ultrasound-Based Methods to Assess Aortic Diameter and Stiffness in Normal and Aneurysmal Mice

Trachet, Bram; Fraga‐Silva, Rodrigo A.; Londoño, Federico Uribe; Swillens, Abigaïl; Stergiopulos, Nikolaos; Segers, Patrick

doi:10.1371/journal.pone.0129007

Cited by 23 publications

(24 citation statements)

References 53 publications

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“…Trachet et al . have shown that in mice, determination of aortic stiffness using pulse wave velocity should be avoided and replaced by local stiffness methods 37 . Arterial distensibility was compared at equivalent blood pressure levels within the cardiac cycle.…”

Section: Discussionmentioning

confidence: 99%

Vimentin knockout results in increased expression of sub-endothelial basement membrane components and carotid stiffness in mice

Langlois

Belozertseva

Parlakian

et al. 2017

Sci Rep

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Intermediate filaments are involved in stress-related cell mechanical properties and in plasticity via the regulation of focal adhesions (FAs) and the actomyosin network. We investigated whether vimentin regulates endothelial cells (ECs) and vascular smooth muscle cells (SMCs) and thereby influences vasomotor tone and arterial stiffness. Vimentin knockout mice (Vim−/−) exhibited increased expression of laminin, fibronectin, perlecan, collagen IV and VE-cadherin as well as von Willebrand factor deposition in the subendothelial basement membrane. Smooth muscle (SM) myosin heavy chain, α-SM actin and smoothelin were decreased in Vim−/− mice. Electron microscopy revealed a denser endothelial basement membrane and increased SM cell-matrix interactions. Integrin αv, talin and vinculin present in FAs were increased in Vim−/− mice. Phosphorylated FA kinase and its targets Src and ERK1/2 were elevated in Vim−/− mice. Knockout of vimentin, but not of synemin, resulted in increased carotid stiffness and contractility and endothelial dysfunction, independently of blood pressure and the collagen/elastin ratio. The increase in arterial stiffness in Vim−/− mice likely involves vasomotor tone and endothelial basement membrane organization changes. At the tissue level, the results show the implication of FAs both in ECs and vascular SMCs in the role of vimentin in arterial stiffening.

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Section: Discussionmentioning

confidence: 99%

Vimentin knockout results in increased expression of sub-endothelial basement membrane components and carotid stiffness in mice

Langlois

Belozertseva

Parlakian

et al. 2017

Sci Rep

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“…LV dimensions were measured, and LV function was evaluated (Gao et al, 2011) using the equations in Table 1. Stiffness of the ascending aorta was assessed by its circumferential strain (Trachet et al, 2015), and cardiac output was estimated as the average of the aortic and pulmonary flow (Tournoux et al, 2011;Slama et al, 2015).…”

Section: Transthoracic Echocardiographymentioning

confidence: 99%

Endothelial Dysfunction and Passive Changes in the Aorta and Coronary Arteries of Diabetic db/db Mice

Beck

Comerma-Steffensen

et al. 2020

Front. Physiol.

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Endothelial cell dysfunction and vessel stiffening are associated with a worsened prognosis in diabetic patients with cardiovascular diseases. The present study hypothesized that sex impacts endothelial dysfunction and structural changes in arteries from diabetic mice. In diabetic (db/db) and normoglycaemic (db/db+) mice, the mechanical properties were investigated in pressurized isolated left anterior descending coronary arteries and aorta segments that were subjected to tensile testing. Functional studies were performed on wire-mounted vascular segments. The male and female db/db mice were hyperglycaemic and had markedly increased body weight. In isolated aorta segments without the contribution of smooth muscle cells, load to rupture, viscoelasticity, and collagen content were decreased suggesting larger distensibility of the arterial wall in both male and female db/db mice. In male db/db aorta segments with smooth muscle cell contribution, lumen diameter was smaller and the passive stretch-tension curve was leftward-shifted, while they were unaltered in female db/db aorta segments versus control db/db+ mice. In contrast to female db/db mice, coronary arteries from male db/db mice had altered stress-strain relationships and increased distensibility. Transthoracic echocardiography revealed a dilated left ventricle with unaltered cardiac output, while aortic flow velocity was decreased in male db/db mice. Impairment of acetylcholine relaxation was aggravated in aorta from female db/db compared to control and male db/db mice, while impairment of sodium nitroprusside relaxations was only observed in aorta from male db/db mice. The remodeling in the coronary arteries and aorta suggests an adaptation of the arterial wall to the reduced flow velocity with sex-specific differences in the passive properties of aorta and coronary arteries. The findings of less distensible arteries and more pronounced endothelial dysfunction in female compared to male diabetic mice may have implications for the observed higher incidence of macrovascular complications in diabetic women.

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“…Because 1D and 2D ultrasound strongly depend on the field of view chosen by the user, 16 these findings indicate that for follow-up studies on aneurysm formation, 3D images should be acquired when possible. Both aortic regurgitation and ascending aortic volume were significantly increased after 10 days of angiotensin II infusion ( Figure 1G-1H).…”

Section: Trachet Et Al Ascending Aortic Aneurysm In Ang Ii-infused MImentioning

confidence: 99%

Ascending Aortic Aneurysm in Angiotensin II–Infused Mice

Trachet

Piersigilli

Fraga‐Silva

et al. 2016

ATVB

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A ortic aneurysm is clinically defined as a local increase in aortic diameter of at least 50% compared with the normal diameter.1 Abdominal aortic aneurysms (AAA) are associated with cardiovascular risk factors, such as smoking, age, male sex, hyperlipidemia, hypertension, and chronic obstructive pulmonary disease.2 Although these factors also underlie the majority of thoracic aortic aneurysms, the latter subgroup incidence is more often related to family history than to the above mentioned factors.3 Because most aneurysms remain asymptomatic until-often fatal-complications such as rupture occur, our understanding of the pathogenesis, especially in early stages, is limited. Angiotensin II infusion into hypercholesterolemic ApoE −/− mice is a well-known experimental model of both AAAs 4 and thoracic aortic aneurysms. 5 We have recently explored a novel imaging technique, phase contrast X-ray tomographic microscopy (PCXTM), to visualize the abdominal lesions of angiotensin II-infused mice. 6 Because the axial resolution of our PCXTM scans (6.5 μm) was close to the thickness of histological coupes for routine morphological evaluation (4 μm), we introduced PCXTM-guided histology to select sections of the aorta in a highly precise manner for pathology analysis. 6 This approach allowed us to demonstrate that the abdominal lesions in these mice stem from medial ruptures in the suprarenal side branches, leading to media-adventitia dissection with intramural bleeding and thrombus formation. 6 Much like in humans, data on thoracic aortic aneurysms are scarcer than data on AAAs in mouse models. Daugherty et al reported dilatation of the ascending aorta as semiquantified on histological sections after 28 days of continuous angiotensin II infusion in ApoE −/− mice. 5 They observed expansion of interlaminar spaces, collagen deposition, and macrophage © 2016 American Heart Association, Inc. Objective-To understand the anatomy and physiology of ascending aortic aneurysms in angiotensin II-infused ApoE −/− mice. Approach and Results-We combined an extensive in vivo imaging protocol (high-frequency ultrasound and contrastenhanced microcomputed tomography at baseline and after 3, 10, 18, and 28 days of angiotensin II infusion) with synchrotron-based ultrahigh resolution ex vivo imaging (phase contrast X-ray tomographic microscopy) in n=47 angiotensin II-infused mice and 6 controls. Aortic regurgitation increased significantly over time, as did the luminal volume of the ascending aorta. In the samples that were scanned ex vivo, we observed one or several focal dissections, with the largest located in the outer convex aspect of the ascending aorta. The volume of the dissections moderately correlated to the volume of the aneurysm as measured in vivo (r 2 =0.46). After 3 days of angiotensin II infusion, we found an interlaminar hematoma in 7/12 animals, which could be linked to an intimal tear. There was also a significant increase in single laminar ruptures, which may have facilitated a progressive enlargement of the focal dis...

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Performance Comparison of Ultrasound-Based Methods to Assess Aortic Diameter and Stiffness in Normal and Aneurysmal Mice

Cited by 23 publications

References 53 publications

Vimentin knockout results in increased expression of sub-endothelial basement membrane components and carotid stiffness in mice

Vimentin knockout results in increased expression of sub-endothelial basement membrane components and carotid stiffness in mice

Endothelial Dysfunction and Passive Changes in the Aorta and Coronary Arteries of Diabetic db/db Mice

Ascending Aortic Aneurysm in Angiotensin II–Infused Mice

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