Circumferential Variation of Mechanical Properties of Ascending Aorta (AA): A Comparative Study of Healthy and Dilated AA

2007 ◽  
Author(s):  
Dominique Tremblay ◽  
Raymond Cartier ◽  
Louis Leduc ◽  
Rosaire Mongrain ◽  
Richard Leask
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Aortic Valve ◽  
Aortic Wall ◽  
Vascular Tissue ◽  
Vascular System ◽  
Cardiovascular Complications ◽  
Ascending Aorta ◽  
Local Properties

The biomechanics within the ascending aorta (AA) characterizes the pressure and flow for the entire vascular system. In the aortic wall, it is the structured medial layer that is responsible for the mechanical properties of the AA. The mechanical properties are determined to a large extent by the composition of elastin, collagen and smooth muscle cells (SMCs). Changes in AA biomechanics that arise with age and/or disease can lead to cardiovascular complications and death. Most studies that have investigated the biomechanics of these diseases have assumed homogeneous and isotropic aortic wall properties. Very little work has been done in vitro to determine the local mechanical properties of human vascular tissue. In order to better understand the biomechanics of the human AA, the local properties of pathologic AA tissue from both tricuspid and bicuspid aortic valve patients have been studied and compared with the properties of healthy aortas.

scholarly journals WALL STRESS IN ASCENDING AORTA ANEURYSMS AS A PREDICTIVE FACTOR OF BREAKAGE

2021 ◽  
Vol 108 (Supplement_3) ◽  
Author(s):  
R J Burgos Lázaro ◽  
N Burgos Frías ◽  
S Serrano-Fiz García ◽  
V Ospina Mosquera ◽  
F Rojo Pérez ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Wall Stress ◽  
Middle Layer ◽  
Ascending Aorta ◽  
Aortic Aneurysms ◽  
Maximum Diameter ◽  
Resistance Factors ◽  
Risk Of Rupture ◽  
Traction Test

Abstract INTRODUCTION The surgical indication for ascending aortic aneurysms (AAA) is established when the maximum diameter > 50 mm; It responds to Laplace's Law (T wall = P × r / 2e). The aim of the study is to define wall stress in AAA. MATERIAL AND METHODS 218 ascending aortic walls have been studied: 96 from organ donors, and 122 from AAA: Marfán 58 (47.5%), bicuspid aortic valve 26 (21.4%), and atherosclerosis 38 (31.1%). The samples were studied "in vitro", according to the model Young's (relationship between stress and deformed area), by means of the mechanical traction test (Tension = Force / Area). The analysis was performed with the stress-elongation curve (d Tension / d Elongation). RESULTS The stress of the aortic wall, classified from highest to lowest according to pathology and age was: cystic necrosis of the middle layer, arteriosclerosis, age > 60 years, between 35 and 59, and < 34 years. The stress of “control aortas” wall increased directly in relation to the age of the donors. CONCLUSIONS The maximum diameter of the ascending aorta, the patient's type of pathology and age are factors that affect the maximum tension of the aortic wall and resistance, factors that allow differentiation and prediction of the risk of rupture of the AAA. The validation of the results obtained through numerical simulation was significant and the uniaxial analysis has modeled the response of the vessels to their internal pressure.

scholarly journals Bicuspid aortic valve morphology and aortic valvular outflow jets: an experimental analysis using an MRI-compatible pulsatile flow circulation system

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kaoru Hattori ◽  
Natsuki Nakama ◽  
Jumpei Takada ◽  
Gohki Nishimura ◽  
Ryo Moriwaki ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Bicuspid Aortic Valve ◽  
Pulsatile Flow ◽  
Aortic Wall ◽  
Ascending Aorta ◽  
Circulation System ◽  
Resonance Imaging ◽  
Left Posterior ◽  
Flow Circulation ◽  
The Right

AbstractThe characteristics of aortic valvular outflow jet affect aortopathy in the bicuspid aortic valve (BAV). This study aimed to elucidate the effects of BAV morphology on the aortic valvular outflow jets. Morphotype-specific valve-devising apparatuses were developed to create aortic valve models. A magnetic resonance imaging-compatible pulsatile flow circulation system was developed to quantify the outflow jet. The eccentricity and circulation values of the peak systolic jet were compared among tricuspid aortic valve (TAV), three asymmetric BAVs, and two symmetric BAVs. The results showed mean aortic flow and leakage did not differ among the five BAVs (six samples, each). Asymmetric BAVs demonstrated the eccentric outflow jets directed to the aortic wall facing the smaller leaflets. In the asymmetric BAV with the smaller leaflet facing the right-anterior, left-posterior, and left-anterior quadrants of the aorta, the outflow jets exclusively impinged on the outer curvature of the ascending aorta, proximal arch, and the supra-valvular aortic wall, respectively. Symmetric BAVs demonstrated mildly eccentric outflow jets that did not impinge on the aortic wall. The circulation values at peak systole increased in asymmetric BAVs. The bicuspid symmetry and the position of smaller leaflet were determinant factors of the characteristics of aortic valvular outflow jet.

Mechanical properties of human bronchial smooth muscle in vitro

1992 ◽  
Vol 73 (4) ◽  
pp. 1481-1485 ◽  
Author(s):  
K. Ishida ◽  
P. D. Pare ◽  
J. Hards ◽  
R. R. Schellenberg
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Tracheal Smooth Muscle ◽  
Cross Sectional ◽  
Velocity Of Shortening ◽  
Muscle Shortening ◽  
Tension Generation ◽  
Very High

The in vitro mechanical properties of smooth muscle strips from 10 human main stem bronchi obtained immediately after pneumonectomy were evaluated. Maximal active isometric and isotonic responses were obtained at varying lengths by use of electrical field stimulation (EFS). At the length (Lmax) producing maximal force (Pmax), resting tension was very high (60.0 +/- 8.8% Pmax). Maximal fractional muscle shortening was 25.0 +/- 9.0% at a length of 75% Lmax, whereas less shortening occurred at Lmax (12.2 +/- 2.7%). The addition of increasing elastic loads produced an exponential decrease in the shortening and velocity of shortening but increased tension generation of muscle strips stimulated by EFS. Morphometric analysis revealed that muscle accounted for 8.7 +/- 1.5% of the total cross-sectional tissue area. Evaluation of two human tracheal smooth muscle preparations revealed mechanics similar to the bronchial preparations. Passive tension at Lmax was 10-fold greater and maximal active shortening was threefold less than that previously demonstrated for porcine trachealis by us of the same apparatus. We attribute the limited shortening of human bronchial and tracheal smooth muscle to the larger load presumably provided by a connective tissue parallel elastic component within the evaluated tissues, which must be overcome for shortening to occur. We suggest that a decrease in airway wall elastance could increase smooth muscle shortening, leading to excessive responses to contractile agonists, as seen in airway hyperresponsiveness.

scholarly journals Genetic and Epigenetic Mechanisms Underlying Vascular Smooth Muscle Cell Phenotypic Modulation in Abdominal Aortic Aneurysm

2020 ◽  
Vol 21 (17) ◽  
pp. 6334
Author(s):  
Rijan Gurung ◽  
Andrew Mark Choong ◽  
Chin Cheng Woo ◽  
Roger Foo ◽  
Vitaly Sorokin
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Aortic Wall ◽  
Epigenetic Mechanisms ◽  
Phenotypic Modulation ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) refers to the localized dilatation of the infra-renal aorta, in which the diameter exceeds 3.0 cm. Loss of vascular smooth muscle cells, degradation of the extracellular matrix (ECM), vascular inflammation, and oxidative stress are hallmarks of AAA pathogenesis and contribute to the progressive thinning of the media and adventitia of the aortic wall. With increasing AAA diameter, and left untreated, aortic rupture ensues with high mortality. Collective evidence of recent genetic and epigenetic studies has shown that phenotypic modulation of smooth muscle cells (SMCs) towards dedifferentiation and proliferative state, which associate with the ECM remodeling of the vascular wall and accompanied with increased cell senescence and inflammation, is seen in in vitro and in vivo models of the disease. This review critically analyses existing publications on the genetic and epigenetic mechanisms implicated in the complex role of SMCs within the aortic wall in AAA formation and reflects the importance of SMCs plasticity in AAA formation. Although evidence from the wide variety of mouse models is convincing, how this knowledge is applied to human biology needs to be addressed urgently leveraging modern in vitro and in vivo experimental technology.

The Effects of Arterial Tissue Reorganization on the Geometrical Outputs of Pressure- and Flow-Induced Remodeling: A Theoretical Study

2012 ◽  
Author(s):  
Tarek Shazly ◽  
Alexander Rachev
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Vascular Tissue ◽  
Arterial Remodeling ◽  
Structural Components ◽  
Constrained Mixture ◽  
Mass Redistribution ◽  
Mass Fractions ◽  
Tissue Reorganization ◽  
Induced Changes

Arterial remodeling in response to sustained alterations in blood pressure and/or flow induces changes in vessel geometry, structure, and composition. In conditions of hypertension and elevated blood flow, remodeling results in increased vessel mass that is distributed in a manner to maintain the local mechanical environment of the vascular cells at a baseline state. A majority of theoretical studies on remodeling have assumed that new mass is formed via a proportional production of load-bearing constituents, namely elastin, collagen, and smooth muscle. Therefore, when the vascular tissue is considered as a constrained mixture of these structural components, their mass fractions do not change as a result of remodeling. However, increased arterial mass is primarily attributed to smooth muscle cell hypertrophy and upregulated collagen production, implying a change in the mass fractions of all constituents and therefore the tissue mechanical properties [1]. Moreover, few papers account for remodeling-induced changes in the configuration and/or orientation of collagen fibers, both of which may also alter tissue mechanical properties. The objective of this study is to build a mathematical model that enables evaluation of the effects of mass redistribution among structural components and changes in collagen fiber configuration on the geometrical outputs of arterial remodeling.

scholarly journals Intravascular Glucocorticoid Metabolism during Inflammation and Injury in Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 166-172 ◽  
Author(s):  
Anna R. Dover ◽  
Patrick W. F. Hadoke ◽  
Linsay J. Macdonald ◽  
Eileen Miller ◽  
David E. Newby ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Tissue ◽  
Reductase Activity ◽  
Vascular Inflammation ◽  
Feedback Regulation ◽  
Muscle Cells ◽  
Femoral Arteries

11β-Hydroxysteroid dehydrogenases (11βHSDs) catalyze interconversion of 11-hydroxy-glucocorticoids with inactive 11-keto metabolites. In blood vessel walls, loss of 11βHSD1 is thought to reduce local glucocorticoid concentrations, reducing the progression of atheroma and enhancing angiogenesis. Conversely, on the basis that 11βHSD1 is up-regulated approximately 5-fold by inflammatory cytokines in cultured human vascular smooth muscle cells, it has been proposed that increased 11βHSD1 during vascular inflammation provides negative feedback suppression of inflammation. We aimed to determine whether inflammation and injury selectively up-regulate 11βHSD1 reductase activity in vitro and in vivo in intact vascular tissue in mice. In isolated mouse aortae and femoral arteries, reductase activity (converting 11-dehydrocorticosterone to corticosterone) was approximately 10-fold higher than dehydrogenase activity and was entirely accounted for by 11βHSD1 because it was abolished in vessels from 11βHSD1−/− mice. Although 11βHSD1 activity was up-regulated by proinflammatory cytokines in cultured murine aortic smooth muscle cells, no such effect was evident in intact aortic rings in vitro. Moreover, after systemic inflammation induced by ip lipopolysaccharide injection, there was only a modest (18%) increase in 11β-reductase activity in the aorta and no increase in the perfused hindlimb. Furthermore, in femoral arteries in which neointimal proliferation was induced by intraluminal injury, there was no change in basal 11βHSD1 activity or the sensitivity of 11βHSD1 to cytokine up-regulation. We conclude that increased generation of glucocorticoids by 11βHSD1 in the murine vessel wall is unlikely to contribute to feedback regulation of inflammation.

scholarly journals Ascending aorta dilation in association with bicuspid aortic valve: A maturation defect of the aortic wall

2014 ◽  
Vol 148 (4) ◽  
pp. 1583-1590 ◽  
Author(s):  
Nimrat Grewal ◽  
Adriana C. Gittenberger-de Groot ◽  
Robert E. Poelmann ◽  
Robert J.M. Klautz ◽  
Johannes H.N. Lindeman ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Bicuspid Aortic Valve ◽  
Aortic Wall ◽  
Ascending Aorta ◽  
Maturation Defect

Heart valve disease (aortic valve disease): anatomy and pathology of the aortic valve

2016 ◽  
Author(s):  
Cristina Basso ◽  
Gaetano Thiene ◽  
Siew Yen Ho
Keyword(s):  
Aortic Valve ◽  
Aortic Wall ◽  
Ascending Aorta ◽  
Valve Disease ◽  
Heart Valve Disease ◽  
Distinctive Features ◽  
Aorta Aneurysm ◽  
Rheumatic Valve Disease ◽  
Relationship Of ◽  
The Relationship

The gross features of the aortic valve apparatus, consisting of three semilunar leaflets, three interleaflet triangles, three commissures, and the aortic wall, are discussed both in terms of normal and pathological anatomy. The concept of aortic annulus and the relationship of the aortic valve with the coronary arteries, the membranous septum, and conduction system and the mitral valve are addressed. When dealing with pathology, the chapter focuses on the main distinctive features of aortic valve stenosis and aortic valve incompetence. Regarding the former, the abnormalities reside in the cusps, either two or three in number, with cusp thickening, and calcification with or without commissural fusion (thus distinguishing senile and chronic rheumatic valve disease); in the latter, the gross changes can affect either the cusps (infective endocarditis with tissue perforation/laceration and rheumatic valve disease with tissue retraction) or the aortic wall (ascending aorta aneurysm either inflammatory or degenerative). The distinctive gross abnormalities in the various conditions are illustrated.

Abstract 19655: Elevated Oxidative Stress Induces Smooth Muscle Cell Death via Superoxide Anion in Bicuspid Aortic Valve-associated Aortopathy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Julie A Phillippi ◽  
Marie Billaud ◽  
Jennifer C Hill ◽  
Julianna E Buchwald ◽  
Mary P Kotlarczyk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cell Death ◽  
Smooth Muscle ◽  
Aortic Valve ◽  
Bicuspid Aortic Valve ◽  
Superoxide Anion ◽  
Ascending Aorta ◽  
Oxidative Stress Defense ◽  
Stress Defense

Introduction: Bicuspid aortic valve (BAV) is associated with an aortopathy that manifests as a dilatation of the proximal ascending aorta. The mechanisms of aneurysm formation in BAV patients are not completely understood. Our group established that medial smooth muscle cells (SMC) from aneurysmal BAV patients exhibit a weakened oxidative stress defense. Hypothesis: The weakened oxidative stress defense of medial SMCs in BAV patients leads to elevated oxidative stress in the proximal ascending aorta and decreases SMC viability. Methods: Aortic specimens were harvested from patients undergoing aortic valve and/or ascending aortic replacement due to aneurysm, or heart transplant, with IRB approval and informed patient consent. Levels of the superoxide anion-specific oxidation product 2-OH-E + was detected via HPLC in hydroethidine-exposed fresh human aortic specimens. Lipid peroxidation was quantified by ELISA-based detection of 8-iso-prostaglandin F2α. Superoxide anion (O 2 •- ) production and cell viability in primary SMC were detected using the cytochrome c reduction assay, and the MTT assay respectively. Results: Levels of O 2 •- and lipid peroxidation were elevated in BAV specimens when compared with tricuspid aortic valve (TAV) specimens (8.7 ± 0.90 vs 6.1 ± 0.90 pmol/mg, and 610±32 vs 458±45 pg/mg, Fig A and B respectively). Elevated O 2 •- production was detected in primary SMC in vitro when compared with SMC from TAV patients (13.2 ± 2.9 vs 6.7 ± 1.7 pmol/min/mg, Fig C). Addition of peroxide to primary SMC resulted in intracellular O 2 •- -mediated cell death (Fig D). Conclusions: Our results indicate that accumulation of O 2 •- in SMC is associated with increased oxidative stress and with increased cell death in the setting of BAV. Ongoing studies are focused on defining mechanisms of O 2 •- generation and the impact on aortic wall biomechanics. Importantly, this could help to develop novel interventions for BAV patients who are at risk for aortic catastrophe.

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