Computational study on phase lag of arterial-wall motion for assessment of plaque vulnerability

2020 ◽  
Vol 234 (5) ◽  
pp. 517-526
Author(s):  
Pengsrorn Chhai ◽  
Kyehan Rhee
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Wall Motion ◽  
Arterial Wall ◽  
Computational Study ◽  
Muscle Cells ◽  
Phase Lag ◽  
Plaque Vulnerability ◽  
Wall Displacement ◽  
Lipid Core

The wall motion of atherosclerotic plaque was analyzed using a computational method, and the effects of tissue viscoelasticity, fibrosis thickness, and lipid-core stiffness on wall displacement waveforms were examined. The viscoelasticity of plaque tissues was modeled using a time Prony series with four Maxwell elements. Computational simulation of tissue indentation tests showed the validity of the proposed viscoelastic constitutive models. Decreasing the relative moduli of the viscoelastic model reduced their viscous characteristics while enhancing the stiffness of the wall, which corresponded with the effects of decreased smooth muscle cells content. A finite-element analysis was conducted for atherosclerotic wall models and wall displacement waveforms were computed. The phase difference between the first harmonics of pressure and displacement waves was selected to represent the time delay of the wall motion. As the relative modulus decreased, the wall displacement and phase lag decreased. A thinner wall and softer lipid core corresponded to a greater wall displacement and smaller phase lag. Because the phase lag of the arterial-wall motion was smaller for the plaque with a thinner cap, lower smooth muscle cells content, and softer lipid core (all features of plaques with high rupture risk), first harmonics of pressure and displacement waves can be used as an index to assess plaque vulnerability.

Matrix Gla Protein Synthesis and Gamma-carboxylation in the Aortic Vessel Wall and Proliferating Vascular Smooth Muscle Cells

1999 ◽  
Vol 82 (12) ◽  
pp. 1764-1767 ◽  
Author(s):  
Dean Cain ◽  
David Sane ◽  
Reidar Wallin
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vitamin K ◽  
Vessel Wall ◽  
Arterial Wall ◽  
Muscle Cells ◽  
Matrix Gla Protein ◽  
Dt Diaphorase

SummaryMatrix GLA protein (MGP) is an inhibitor of calcification in the arterial wall and its activity is dependent upon vitamin K-dependent γ-carboxylation. This modification is carried out by a warfarin sensitive enzyme system that converts specific Glu residues to γ-carboxyglutamic acid (GLA) residues. Recent studies have demonstrated that the γ-carboxylation system in the arterial wall, in contrast to that in the liver, is unable to use vitamin K as an antidote to warfarin.By use of immunohistochemistry we demonstrate that MGP is expressed in the arterial wall and immunocytochemistry localized the MGP precursors to the endoplasmic reticulum in vascular smooth muscle cells. Resting smooth vascular muscle cells in the aortic wall and proliferating cells from explants of the aorta have all the enzymes needed for γ-carboxylation of MGP. However, when compared to the liver system, expression of the enzymes of the γ-carboxylation system in vascular smooth muscle cells is different. Of particular interest is the finding that the specific activity of the warfarin sensitive enzyme vitamin K epoxide reductase is 3-fold higher in vascular smooth muscle cells than in liver. DT-diaphorase, which catalyses the antidotal pathway for vitamin K reduction in liver, is 100-fold less active in resting vascular smooth muscle cells than in liver. Data obtained from an in vitro γ-carboxylation system suggest that the antidotal pathway catalyzed by DT-diaphorase in the vessel wall is unable to provide the carboxylase with enough reduced vitamin K to trigger γ-carboxylation of MGP. This finding provides an explanation to the inability of vitamin K to work as an antidote to warfarin intoxication of the arterial wall. Therefore the vitamin K dependent γ-carboxylation system in the arterial wall share a common feature with the system in bone cells by being unable to utilize vitamin K as an antidote.

Distribution of shear stress over smooth muscle cells in deformable arterial wall

2008 ◽  
Vol 46 (7) ◽  
pp. 649-657 ◽  
Author(s):  
Mahsa Dabagh ◽  
Payman Jalali ◽  
Yrjö T. Konttinen ◽  
Pertti Sarkomaa
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Muscle Cells

Smooth Muscle Cells Influence Monocyte Response to LDL as well as Their Adhesion and Transmigration in a Coculture Model of the Arterial Wall

2001 ◽  
Vol 38 (5) ◽  
pp. 479-491 ◽  
Author(s):  
Fabienne Kinard ◽  
Kathy Jaworski ◽  
Thérèse Sergent-Engelen ◽  
Dan Goldstein ◽  
Paul P. van Veldhoven ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Muscle Cells ◽  
Coculture Model

Calcium sensitivity of vasospastic basilar artery after experimental subarachnoid hemorrhage

2006 ◽  
Vol 290 (6) ◽  
pp. H2329-H2336 ◽  
Author(s):  
R. Loch Macdonald ◽  
Zhen-Du Zhang ◽  
Masataka Takahashi ◽  
Elena Nikitina ◽  
J. Young ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Arterial Compliance ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Calcium Sensitivity ◽  
Basilar Arteries

Arteries that develop vasospasm after subarachnoid hemorrhage (SAH) may have altered contractility and compliance. Whether these changes are due to alterations in the smooth muscle cells or the arterial wall extracellular matrix is unknown. This study elucidated the location of such changes and determined the calcium sensitivity of vasospastic arteries. Dogs were placed under general anesthesia and underwent creation of SAH using the double-hemorrhage model. Vasospasm was assessed by angiography performed before and 4, 7, or 21 days after SAH. Basilar arteries were excised from SAH or control dogs ( n = 8–52 arterial rings from 2–9 dogs per measurement) and studied under isometric tension in vitro before and after permeabilization of smooth muscle with α-toxin. Endothelium was removed from all arteries. Vasospastic arteries demonstrated significantly reduced contractility to KCl with a shift in the EC50 toward reduced sensitivity to KCl 4 and 7 days after SAH ( P < 0.05, ANOVA). There was reduced compliance that persisted after permeabilization ( P < 0.05, ANOVA). Calcium sensitivity was decreased during vasospasm 4 and 7 days after SAH, as assessed in permeabilized arteries and in those contracted with BAY K 8644 in the presence of different concentrations of extracellular calcium ( P < 0.05, ANOVA). Depolymerization of actin with cytochalasin D abolished contractions to KCl but failed to alter arterial compliance. In conclusion, it is shown for the first time that calcium sensitivity is decreased during vasospasm after SAH in dogs, suggesting that other mechanisms are involved in maintaining the contraction. Reduced compliance seems to be due to an alteration in the arterial wall extracellullar matrix rather than the smooth muscle cells themselves because it cannot be alleviated by depolymerization of smooth muscle actin.

scholarly journals MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells

2005 ◽  
Vol 202 (5) ◽  
pp. 663-671 ◽  
Author(s):  
Sergey Filippov ◽  
Gerald C. Koenig ◽  
Tae-Hwa Chun ◽  
Kevin B. Hotary ◽  
Ichiro Ota ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Matrix Metalloproteinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Arterial Wall ◽  
Neointimal Hyperplasia ◽  
Muscle Cells

During pathologic vessel remodeling, vascular smooth muscle cells (VSMCs) embedded within the collagen-rich matrix of the artery wall mobilize uncharacterized proteolytic systems to infiltrate the subendothelial space and generate neointimal lesions. Although the VSMC-derived serine proteinases, plasminogen activator and plasminogen, the cysteine proteinases, cathepsins L, S, and K, and the matrix metalloproteinases MMP-2 and MMP-9 have each been linked to pathologic matrix-remodeling states in vitro and in vivo, the role that these or other proteinases play in allowing VSMCs to negotiate the three-dimensional (3-D) cross-linked extracellular matrix of the arterial wall remains undefined. Herein, we demonstrate that VSMCs proteolytically remodel and invade collagenous barriers independently of plasmin, cathepsins L, S, or K, MMP-2, or MMP-9. Instead, we identify the membrane-anchored matrix metalloproteinase, MT1-MMP, as the key pericellular collagenolysin that controls the ability of VSMCs to degrade and infiltrate 3-D barriers of interstitial collagen, including the arterial wall. Furthermore, genetic deletion of the proteinase affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo. These studies suggest that therapeutic interventions designed to target MT1-MMP could prove beneficial in a range of human vascular disease states associated with the destructive remodeling of the vessel wall extracellular matrix.

scholarly journals Factors Controlling Growth of Arterial Cells following Injury*

1990 ◽  
Vol 18 (4a) ◽  
pp. 547-553 ◽  
Author(s):  
Michael A. Reidy ◽  
Christopher L. Jackson
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Arterial Wall ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Experimental Models ◽  
Smooth Muscle Cell Proliferation

The proliferation of vascular smooth muscle cells is a key event in the development of arterial lesions. In experimental models, loss of arterial endothelium followed by platelet adherence does not necessarily stimulate smooth muscle cell proliferation. Furthermore, using animals deficient in platelets, smooth muscle cell proliferation was induced to an equal extent as in control animals following injury with a balloon catheter. Modulation of the smooth muscle response, however, was achieved by totally denuding arteries with a technique which did not traumatize medial cells. These data suggested that injury and cell death might induce proliferation of cells by release of endogenous mitogen. Basic FGF is present in the arterial wall and addition of this mitogen to denuded arteries was found to cause a highly significant increase in smooth muscle cell proliferation. These studies suggest that smooth muscle cell proliferation could be induced by factors present in the arterial wall and does not require exogenous factors. Smooth muscle cell proliferation following balloon catheter injury is significantly reduced by administration of calcium antagonists. Repeated administration of nifedipine caused a significant reduction in intimal lesion size induced by injury. The anti-proliferative. effect was not observed in other tissues. Influx of Ca++ ions into medial smooth muscle cells may therefore be an obligatory step for replication.

Abstract 879: The Chemokine CXCL10 Is Involved In The Development Of Atherosclerotic Plaque Vulnerability

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dolf Segers ◽  
Rini de Crom ◽  
Pieter Leenen ◽  
Gerard Pasterkamp ◽  
Rob Krams
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mhc Class Ii ◽  
Immune Activation ◽  
Vulnerable Plaque ◽  
Muscle Cells ◽  
Class Ii ◽  
Collagen Content ◽  
Pivotal Role ◽  
Plaque Vulnerability

Introduction: Atherosclerosis is an inflammatory disease in which monocyte/macrophages and Th1 cells are crucial cell types. The CXC-chemokine CXCL10 might play a pivotal role in its pathogenesis as it mediates chemoattraction of these cells. We previously found that high CXCL10 levels in human carotid plaques are associated with a vulnerable phenotype. Moreover, we identified CXCL10 as a possible biomarker for vulnerability in a mouse model for vulnerable plaque. The aim of the current study was to evaluate if CXCL10 has a critical role in the development of plaque vulnerability. Methods: Atherosclerosis-susceptible female ApoE -/-mice on high fat, high cholesterol diet were instrumented with a perivascular shear stress-altering plastic cylinder to induce vulnerable plaque. In the first three weeks following surgery, mice were injected 3 times/week with a bioactivity-neutralizing CXCL10 antibody. After 9 weeks, plaques were harvested and sections were evaluated for macrophages (CD68), immune activation (MHC class II), smooth muscle cells (a-actin), lipids (Oil Red O) and collagen (picrosirius red). Results: Lesion sizes were equal in both the intervention group and the control group. Also lipid accumulation was comparable in both groups. Despite unaffected macrophage content (30.1 vs 28.7% p = 0.73), we did find a 2-fold reduction of MHC class-II expression (4.9 vs 14.5% p = 0.011) in the antibody-treated group. This decline in activation of the immune system coincided with an increase in the presence of smooth muscle cells (12.6 vs 4.2% p = 0.034) and an increase in collagen content (9.7 vs 21.8% p = 0.014). Conclusion: This study confirms a pivotal role of CXCL10 in the development of vulnerable plaque. Inhibiting CXCL10 resulted in an increase of plaque stability by decreasing immune activation and increasing smooth muscle cell and collagen content. Accordingly, CXCL10 is a potential marker for both diagnostic and therapeutic intervention.

Atheromatosis of arterial intima

2016 ◽  
Vol 94 (8) ◽  
pp. 582-590
Author(s):  
Vladimir N. Titov ◽  
T. A. Rozhkova ◽  
V. A. Amelyushkina
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Proteolytic Enzymes ◽  
Muscle Cells ◽  
Acid Hydrolases ◽  
The Matrix ◽  
Arterial Intima ◽  
Hydrolysis Of

Phylogenetically late arterial intima of the elastic type contains no proteins for the transfer of ligandless oxidized low density lipoproteins (LDLP) for sedentary macrophages adsorbed on the matrix. Phylogenetically early cells realize the extracellular digestive reaction by releasing proteolytic enzymes (metalloproteinases) into intimal matrix that hydrolize matrix proteoglycans, adsorbed ligandless LDLP, detritus, and complete lysosomal hydrolysis of the most hydrophobic polyenic cholesterol esters (poly-ECS). Smooth muscle cells migrate from the middle muscular layer of the arterial wall, change their contractile phenotype to secretory one, and synthesize in situ de novomatrix proteoglycans. The arterial wall has three layers (monolayer endothelium, intimal media (smooth muscle cells), and adventitia) only in elastic type arteries. It is desirable to elucidate functional differences between phylogenetically early sedentarymacrophages and monocytes-macrophages of later origin and understand whether theydepends on specific features of activity of scavenger eceptors, CD36 translocases, expression of acid hydrolases synthesis for poly-ECS or realization of the extracellular digestion reaction. We believe that formation of atheromatous masses takes place in the matrix of arterial intima rather than in lysosomes taking into account limited possibilities for monocytes-macrophages to realize endocytosis of ligandless LDLP from the matrix. Given that atheromatosis is a syndrome of deficit of essential polyenic fatty acids (PFA) in the cells, intimal atheromatosisshould be regarded only as partial utilization of excess PFA in the matrix of elastic type arteries. At later stages of phylogenesis, intima was formed from media smooth muscle cells.

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