The Relationship Between Intimal Thickening and the Hemodynamic Environment of the Arterial Wall

1988 ◽  
pp. 41-46 ◽  
Author(s):  
M. H. Friedman
Keyword(s):  
Arterial Wall ◽  
Intimal Thickening ◽  
The Relationship

PLATELET DEPOSITION AND PSEUDO-INTIMAL HYPERPLASIA IN PROSTHETIC VASCULAR GRAFTS

1987 ◽  
Author(s):  
R A Harper ◽  
I F Lane ◽  
C M Backhouse ◽  
C N McCollum ◽  
A C Meek
Keyword(s):  
Femoral Artery ◽  
Intimal Hyperplasia ◽  
Vascular Grafts ◽  
Graft Occlusion ◽  
Intimal Thickening ◽  
Arterial Grafts ◽  
Post Operative Period ◽  
Platelet Deposition ◽  
Platelet Accumulation ◽  
The Relationship

Platelet and fibrin accumulation in arterial grafts may cause pseudo-intimal hyperplasia and graft occlusion. The relationship between the rate of post-operative platelet accumulation and subsequent pseudo-intimal hyperplasia has been studied in prosthetic grafts implanted in greyhounds.The femoral artery in 30 greyhounds was replaced by a 6cm length of 6mm PTFE. Autologous 111In-platelet deposition over the graft was measured by probe and ratemeter for 7 days and radioactivity compared to the contralateral thigh. The daily increase in this ratio graft over reference was calculated as the Thrombogenicity Index (TI). Grafts were removed at 8 weeks and sectioned at 5, 30 and 55mm for measurement of pseudo-intimal thickening by grid microscopy.The animals subsequently developing occlusion or pseudo-intimal harrowing of greater than 50% of the lumen had a markedly greater TI of 0.22±0.027 compared to 0.03±0.019 in the 23 grafts maintaining wide patency (p<0.05). TI was highest in the 4 grafts which occluded at 0.3110.09 compared to 0.04±0.02 in the 26 that remained patent (p<0.01). There was a highly significant correlation (r=0.69) between post-operative TI and subsequent pseudo-intimal hyperplasia (p<0.001).Platelet deposition in the early post-operative period appears to promote the development of progressive pseudo-intimal thickening and ultimate occlusion

Collagen, ageing and nutrition

2004 ◽  
Vol 42 (1) ◽  
Author(s):  
Jacques Frey
Keyword(s):  
Arterial Wall ◽  
Heart Ventricle ◽  
Diet Restriction ◽  
Intermediate Target ◽  
Vital Importance ◽  
Collagen Accumulation ◽  
The Relationship

AbstractThe relationship between ageing and nutrition is considered with collagen as the intermediate target. Some data showed that diet restriction resulted in decreased collagen accumulation and collagen ageing. Conversely, being overweight reduced the lifespan and increased collagen ageing.Collagen ageing, which includes low turnover and glycoxidation, involves an increase in both stiffness and weakness. Their consequences concern all tissues including those with vital importance such as cartilage, heart ventricle or arterial wall.

THE RELATIONSHIP BETWEEN ARTERIAL WALL THICKNESS AND SKIN THICKNESS IN THE FOREARM OF ELDERLY HYPERTENSIVES

2000 ◽  
Vol 18 ◽  
pp. S188
Author(s):  
O. Hanon ◽  
S. Nouveau ◽  
G. Franconi ◽  
O. De Lacharrière ◽  
L. A. Bortolotto ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Arterial Wall ◽  
Skin Thickness ◽  
Arterial Wall Thickness ◽  
The Relationship ◽  
Elderly Hypertensives

scholarly journals Association of AGT, ACE, NOS3, TNF, MMP9, CYBA polymorphism with subclinical arterial wall changes

Kardiologiia ◽  
2021 ◽  
Vol 61 (3) ◽  
pp. 57-65
Author(s):  
A. A. Akopyan ◽  
K. I. Kirillova ◽  
I. D. Strazhesko ◽  
L. M. Samokhodskaya ◽  
Ya. A. Orlova
Keyword(s):  
Risk Factors ◽  
Gene Polymorphism ◽  
Arterial Wall ◽  
Intima Media Thickness ◽  
Healthy People ◽  
Fisher Exact Test ◽  
Nos3 Gene ◽  
Wall Stiffness ◽  
The Relationship ◽  
Cyba Gene

Aim    Activation of the renin-angiotensin-aldosterone system, decreased nitric oxide production, chronic inflammation, and oxidative stress result in subclinical changes in the arterial wall, which favor the development of cardiovascular diseases (CVD). The effect of allelic gene variants that encode the proteins participating in pathogenetic pathways of age-associated diseases with subclinical changes in the arterial wall [increased pulse wave velocity (PWV), increased intima-media thickness, endothelial dysfunction (ED), presence of atherosclerotic plaques (ASP)] are understudied. This study analyzed the relationship between AGT, ACE, NOS3 TNF, MMP9, and CYBA gene polymorphism and the presence of subclinical changes in the arterial wall, including the dependence on risk factors for CVD, in arbitrarily healthy people of various age.Material and methods    The relationship of polymorphisms с.521С>Т of AGT gene, Ins>Del of AСE gene, с.894G>T of NOS3 gene, – 238G>A of TNF gene, – 1562С>T of MMP9 gene, and c.214Т>С of CYBA gene with indexes of changes in the arterial wall and risk factors for CVD was studied in 160 arbitrarily healthy people by building models of multiple logistic regression and also by analyzing frequencies of co-emergence of two signs with the Pearson chi-squared test (χ2) and Fisher exact test.Results    The DD-genotype of Ins>Del ACE gene polymorphism was correlated with increased PWV (p=0.006; odds ratio (OR) =3.41, 95 % confidence interval (CI): 1.48–8.67) and ED (p=0.014; OR=2.60, 95 % CI: 1.22–5.68). The GG genotype of с.894G>T NOS3 gene polymorphism was correlated with ED (p=0.0087; OR=2.65, 95 % CI: 1.26–5.72); the ТТ-genotype of с.894G>T NOS3 gene polymorphism was correlated with ASP (p=0.033; OR=0.034, 95 % CI: 0.001–0.549).Conclusion    Polymorphic variants of AСE and NOS3 genes correlated with ED, increased arterial wall stiffness, and the presence of subclinical changes in the arterial wall.

Effect of Sulfinpyrazone on Experimental Atherosclerosis in Rats

1979 ◽  
Author(s):  
A.K. Horsch ◽  
P. Klaiber ◽  
K. Dennig ◽  
W. Hofmann
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Immune Complexes ◽  
Arterial Wall ◽  
Experimental Atherosclerosis ◽  
Control Group ◽  
Intimal Thickening ◽  
Cholesterol Feeding ◽  
Lesion Formation ◽  
Atherosclerotic Lesions

Early atherosclerotic lesions in rat aortas were produced by synergy of cholesterol feeding (4 g cholesterol and 2 g cholate in Ioo g pellets) and immunological injury (5 repeated immunizations with 1 mg of horse-radishperoxidase). Cholesterol feeding and immunization was started the same day and resulted after 6 weeks in endothelial injury, intimal thickening and edema, in proliferation of intimal smooth muscle cells and in deposition of lipids and immune complexes in the arterial wall.100 rats were studied and no lesions were detected in the control group, minimal changes were seen in the animals receiving cholesterol or immunization alone, but lesions were constantly present in the group receiving both regimens. One group of cholesterol fed and immunized rats was given sulfinpyrazone from the beginning of the experiment (160 mg/kg/d) over the 6 weeks and a significant reduction in lesion formation was observed compared to the non treated animals. These results suggest a protection of the arterial wall by sulfinpyrazone in experimental atherosclerosis.

Myopericytoma and arterial intimal thickening: the relationship between myopericytes and myointimal cells

2011 ◽  
Vol 38 (11) ◽  
pp. 857-864 ◽  
Author(s):  
Lucio Díaz-Flores ◽  
Ricardo Gutiérrez ◽  
Maria P. García ◽  
Hugo Álvarez-Argüelles ◽  
Lucio Díaz-Flores ◽  
...  
Keyword(s):  
Intimal Thickening ◽  
The Relationship

Experimental Investigation of Mechanical and Structural Inhomogeneity in Bovine Carotid Arteries

2008 ◽  
Author(s):  
Lucas H. Timmins ◽  
Christopher A. Evagora ◽  
James E. Moore ◽  
Stephen E. Greenwald
Keyword(s):  
Arterial Wall ◽  
Constitutive Models ◽  
Wall Structure ◽  
Histological Structure ◽  
Energy Functions ◽  
Arterial Structure ◽  
Wall Deformation ◽  
And Function ◽  
Strain Energy Functions ◽  
The Relationship

Many constitutive models have been proposed to assess arterial mechanical behavior. Most, however, are largely phenomenological and lack a detailed consideration of arterial wall constituents and the manner in which mechanical loads are distributed amongst them. Recently, strain energy functions (SEF) that consider histological evidence about arterial wall structure have been developed [1,2]. These SEFs incorporate fiber bundle orientation and consider the relative proportions of the major wall constituents to offer a better description of arterial wall deformation. Including histological structure and its affects on arterial elasticity could provide a better understanding of the relationship between arterial structure and function. Further shortcomings in arterial modeling include the assumption that the arterial wall is a homogeneous structure, when in fact it is well known to be a non homogenous, although there are notable exceptions [3,4].

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