Relevant bibliographies by topics / Intima Hyperplasia

Academic literature on the topic 'Intima Hyperplasia'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Intima Hyperplasia"

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Yan, Huifang, Xiwei Peng, Hao Xu, Jiahuan Zhu, and Changqing Deng. "Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus–Angelica Combination." Evidence-Based Complementary and Alternative Medicine 2018 (August 13, 2018): 1–15. http://dx.doi.org/10.1155/2018/1508637.

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VSMC proliferation and ECM deposition always resulted in intimal hyperplasia. Astragalus–Angelica combination has a protective effect on the cardiovascular system. The inhibition effect of different Astragalus–Angelica combination on the hyperplastic intima after vascular balloon injury in rats was investigated in this study. Astragalus–Angelica combination can inhibit the intima hyperplasia after balloon injury, in which a 1:1 ratio shows excellent results. Astragalus–Angelica combination can enhance the expression of smooth muscleα-actin (SMа-actin) and inhibit the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin E, collagen I (Col-I), fibronectin (FN), and matrix metallopeptidase-9 (MMP-9) in hyperplastic intima, suggesting that Astragalus–Angelica combination can inhibit the intimal hyperplasia of blood vessels in rats. The mechanism is related to the inhibition of PI3K/Akt signaling pathway activation and thereby inhibits the phenotypic transformation and cell proliferation of VSMCs and thus inhibits the extracellular matrix (ECM) deposition of vascular wall during intimal hyperplasia.
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Mesfin, G. M., M. J. Higgins, W. P. Brown, and D. Rosnick. "Cardiovascular Complications of Chronic Catheterization of the Jugular Vein in the Dog." Veterinary Pathology 25, no. 6 (November 1988): 492–502. http://dx.doi.org/10.1177/030098588802500613.

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Cardiovascular changes associated with indwelling catheters were evaluated in 51 adult beagle dogs catheterized for 4 to 9 weeks. Pathologic changes consistent with traumatic injury were in the vena cava and endocardium of the right atrium of 88% of cannulated dogs. Lesions were characterized by surface denudation and diffuse intimal thickening due to myointimal hyperplasia and deposition of extracellular matrix. Affected intima was lined by hyperplastic, poorly differentiated endothelial cells and contained round to oval cells with characteristics of smooth muscle cells. After 9 weeks, thickened intima was vascularized and composed of spindle-shaped cells and fibrillar stroma. Intimal sclerosis and localized proliferative papillary projections in the vena cava cranial to areas of myointimal hyperplasia occurred infrequently. Traumatic lesions, regardless of location or severity, did not extend below the internal elastic membrane. Inflammatory cellular responses, when present, were minimal. The location, distribution, and morphogenesis of catheter-related cardiovascular lesions distinguishes them from those induced by chemical toxicity or pharmacotoxicity.
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Jalaeefar, Amirmohsen, Arash Mohammadi Tofigh, Atoosa Gharib, Mohsen Khandaghy, and Mohammad Reza Rahimi. "Effects of N-acetylcysteine on arterial neo-intimal hyperplasia in rat model of arteriovenous fistula." Journal of Vascular Access 20, no. 2 (August 24, 2018): 190–94. http://dx.doi.org/10.1177/1129729818793368.

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Introduction: Arteriovenous fistula is the best choice for vascular access in hemodialysis patients. However, arteriovenous fistula dysfunction is a major clinical issue. The most common cause of arteriovenous fistula failure is intimal hyperplasia. In this study, we have investigated the effect of N-acetylcysteine on neo-intimal hyperplasia after arteriovenous fistula creation in rats. Methods: This study was conducted in 24 rats which were randomly divided into two groups: control and N-acetylcysteine groups. An end-to-side anastomosis was made between the femoral artery and vein. The control group received distilled water intraperitoneally while the animals in N-acetylcysteine group received 300 mg/kg/day of N-acetylcysteine via the same route. After 28 days, the thickness of intima and media was measured using hematoxylin and eosin. Results: There was no significant difference between the two groups regarding age ( p = 0.6) and weight ( p = 0.1). The mean intima thickness in N-acetylcysteine group was significantly less than control group (17 ± 20 and 119 ± 46 µm, respectively; p < 0.001). The mean intima/media thickness in the N-acetylcysteine group was significantly less than control group (0.5 ± 0.63 vs 2.05 ± 1.17 µm; p < 0.001). Conclusion: N-acetylcysteine is effective in inhibiting neo-intimal hyperplasia in a rat model of arteriovenous fistula.
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Van Phung, Doan, Takeshi Kinoshita, Tohru Asai, and Tomoaki Suzuki. "Histological and Morphometric Properties of Skeletonized Gastroepiploic Artery and Risk Factors for Intimal Hyperplasia." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 7, no. 3 (May 2012): 191–94. http://dx.doi.org/10.1097/imi.0b013e318264f4cb.

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Objective The aim of the present study was to examine the histological and morphometric properties of skeletonized gastroepiploic artery (GEA) and the risk factors for intimal hyperplasia. Methods We obtained the redundant distal segments of skeletonized GEAs from 33 patients undergoing coronary bypass surgery and microscopically examined the transverse sections just distal to the most distal anastomoses. Intimal hyperplasia was evaluated on the basis of intima-to-media ratio and percentage of luminal narrowing. Risk factors were examined using multivariate linear regression analysis. Results The median (range) of lumen diameter at the most distal anastomosis was 3.8 (2.4–6.4) mm; width of intima, 82 (8–418) μm; width of media, 167 (88–351) μm; wall thickness, 250 (118–554) μm; intima-to-media ratio, 0.59 (0.04–3.88), and percentage of luminal narrowing, 12.3 (1.5–28.9). The number of elastic lamina in the media was 4.2 ± 1.8. Atherosclerosis was found in six patients, and medial calcification, in three patients. The median (range) of graft flow and pulsatile index measured by intraoperative transit-time flow meter was 65 (11–141) mL/min and 3.1 (1.4–5.9), respectively. All GEA grafts were patent at the coronary computed tomography angiography before discharge. Estimated glomerular filtration rate was independently associated with intima-to-media ratio (β coefficient = −0.016, P < 0.01) and percentage of luminal narrowing (β coefficient = −0.012, P < 0.01). Conclusions Skeletonized GEA had sufficient lumen diameter with excellent graft flow and early patency even when used as a sequential graft. Estimated glomerular filtration rate correlates significantly with intimal hyperplasia.
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Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 1P1 (January 1996): 229–33. http://dx.doi.org/10.1177/02841851960371p147.

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Purpose: This experimental study was designed to investigate the effect of irradiation in prevention of intimal hyperplasia. Material and Methods: Twenty rabbits were divided into 4 groups, which were irradiated with 2, 5, 10, and 20 Gy, respectively. The intima of both femoral arteries was injured by air-drying, and irradiation was performed on the unilateral side. The contralateral femoral artery served as a control. Angiograms as well as histologic specimens were obtained 1 month later. Results: Marked intimal hyperplasia was observed in all control sites. There were no significant differences in thickness of intimal hyperplasia between irradiated and control sites in groups irradiated with 2 and 5 Gy. However, in the 10-Gy- and 20-Gy-irradiated groups, intimal hyperplasia of the irradiated site was significantly suppressed. Medial thinning and dilation of the lumen were observed in the 20-Gy-irradiated group. Conclusion: Radiation may prevent intimal hyperplasia. Further investigation of the optimal dose, timing of irradiation, and long-term patency of irradiated vessels may be needed.
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ARPA, Abdurrahman, and Pınar AYDIN OZTURK. "Histopathological effects of nimodipine and pentoxifylline on the vessel wall in end-to-end anastomoses in rat carotid arteries." Journal of Experimental and Clinical Medicine 39, no. 3 (August 30, 2022): 879–83. http://dx.doi.org/10.52142/omujecm.39.3.54.

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When reperfusion following ischemia occurs, oxygen returns to the ischemic tissue, increasing free oxygen radicals and inducing paradox secondary damage. Before infarction, revascularization may influence the morbidity rate. Successful revascularization is not always achieved due to stenosis incidence, proliferation of smooth muscle cells, and intimal hyperplasia. This study compares the effects of nimodipine that prevents vasospasm and pentoxifylline, which stimulates growth factors and reduces collagen synthesis on intimal hyperplasia. Eighteen randomly selected Sprague-Dawley rats were divided into three groups: Group 1, the control group; Group 2, intraperitoneally administered nimodipine; Group 3, orally administered pentoxifylline. Their right-sided carotid arteries were used for anastomosis and the left-sided ones for the control. After a 7-day treatment, both the right and left carotid arteries were removed. In the biopsy, the lumen’s area and diameter, thickness of tunica media thickness, thrombus, edema, intimal hyperplasia, vessel wall injury, and inflammation were analyzed. Pentoxifylline was effective in preventing intimal hyperplasia and tunica intima was similar to that in untreated carotid arteries. However, nimodipine inhibited intimal hyperplasia, but it was not as effective as pentoxifylline. The effects of pentoxifylline after anastomosis should be further assessed in vasoprotective treatment taking into account its efficacy against intimal hyperplasia.
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Qian, Kun, Li Feng, Yujie Sun, Bowen Xiong, Yi Ding, Panting Han, Hailun Chen, Xiao Chen, Ling Du, and Yuxue Wang. "Overexpression of Salusin-α Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model." BioMed Research International 2018 (July 12, 2018): 1–9. http://dx.doi.org/10.1155/2018/8973986.

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Inhibiting vascular endothelial foam is the focus of clinical attention. Using SonoVue (an ultrasound contrast agent), the salusin-α gene was transfected into the arterial intima of an atherosclerotic rabbit model induced by a high-fat diet in this study. Subsequently the model of blood lipid indexes, the pathological structure of the intima, and changes in molecules regulating atherosclerosis were investigated. The high-density lipoprotein C and apolipoprotein A values in the salusin-α gene overexpression (P) group were higher than those in the salusin-α gene interference (RP) group (P < 0.05), whereas the total cholesterol, low-density lipoprotein C, and apolipoprotein B values were reversed. Rabbits in the P group showed significantly thinner vascular intimal thickness than that of other experimental groups (P < 0.05). The expression of positive regulators of atherosclerosis (ABCA1, ABCG1) was higher in the P group than that in the RP group (P < 0.05), and the opposite effect was observed for negative regulators (ACAT1, CD36). Thus, our results showed that the overexpression of salusin-α gene inhibited the proliferation of the vascular intima, thereby throwing some light on understanding the mechanism how salusin-α gene expression interfered with the foaming of vascular intimal cells.
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Kachlik, David, Vaclav Baca, Petr Fara, Alois Lametschwandtner, Bernd Minnich, Vladimir Musil, Bohuslav Sosna, Josef Stingl, Zdenek Straka, and Marek Setina. "Blood vessels of the normal and pathologically changed wall of the human vena saphena magna." Open Medicine 3, no. 4 (December 1, 2008): 475–81. http://dx.doi.org/10.2478/s11536-008-0047-5.

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AbstractThe vascular supply of the wall of human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass or surgery of the varices, and material from cadavers. Under physiological conditions, the wall of vena saphena magna is supplied by delicate system of vasa vasorum, organized in a form of feeding vessels branched into an irregular loose adventitial mesh and continuing further as a microcirculatory network supplying the two outer thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on heavy varicose veins. Slight increase of vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or with vein thrombophlebitis intimal hyperplasia, degradation of media and thrombosis, were found. Apparent massive increase of vasa vasorum growing into the whole media, hyperplastic intima and into the organizing thrombi, were regularly observed. The increase of vasa vasorum is a part of the complex of pathophysiological reactions of the vein wall on the hypoxia developing during the most serious pathological changes, and not as the primary varicogenic factor. The vascular supply of the wall of the human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass grafting or surgery of varices, as well as materials from cadavers. Under physiological conditions the wall of vena saphena magna is supplied by a delicate system of vasa vasorum. It is organized in a form of feeding vessels branched into an irregular loose adventitial mesh, which continues further as a microcirculatory network supplying the outer two thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on severe varicose veins. A slight increase of the vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or vein thrombophlebitis, intimal hyperplasia, degradation of media and thrombosis, were found. It was regularly observed that there was an apparent, massive increase of the vasa vasorum growing into the entire media, hyperplastic intima, and into the organizing thrombi. The increase of the vasa vasorum is due to the pathophysiological reaction of the vein wall as a result of hypoxia, which develops during the most serious pathological changes. The increase is not the primary varicogenic factor.
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Vazquez-Padron, Roberto I., Juan C. Duque, Marwan Tabbara, Loay H. Salman, and Laisel Martinez. "Intimal Hyperplasia and Arteriovenous Fistula Failure: Looking Beyond Size Differences." Kidney360 2, no. 8 (June 3, 2021): 1360–72. http://dx.doi.org/10.34067/kid.0002022021.

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AbstractThe development of venous intimal hyperplasia (IH) has been historically associated with failure of arteriovenous fistulas (AVFs) used for hemodialysis. This long-standing assumption, made on the basis of histologic observations, has been recently challenged by clinical studies indicating that the size of the intima by itself is not enough to explain stenosis or AVF maturation failure. Irrespective of this lack of association, IH is present in most native veins and fistulas, is prominent in many patients, and suggests a role in the vein that may not be reflected by its dimensions. Therefore, the contribution of IH to AVF dysfunction remains controversial. Using only clinical data and avoiding extrapolations from animal models, we critically discuss the biologic significance of IH in vein remodeling, vascular access function, and the response of the venous wall to repeated trauma in patients receiving hemodialysis. We address questions and pose new ones such as the following: What are the factors that contribute to IH in preaccess veins and AVFs? Do cellular phenotypes and composition of the intima influence AVF function? Are there protective roles of the venous intima? This review explores these possibilities, with hopes of rekindling a critical discussion about venous IH that goes beyond thickness and AVF outcomes.
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Mitra, Amit K., Michael G. Del Core, and Devendra K. Agrawal. "Cells, cytokines and cellular immunity in the pathogenesis of fibroproliferative vasculopathies." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (August 1, 2005): 701–15. http://dx.doi.org/10.1139/y05-080.

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Atherosclerosis and restenosis are the result of vascular injury followed by an inflammatory and fibroproliferative response that involves a large number of growth factors, cytokines, and cellular elements. Platelet activation and leukocyte recruitment into the arterial intima play a crucial role, initiating a whole spectrum of reactions leading to vascular smooth muscle cell hyperplasia and intimal migration. The roles of macrophages and lymphocytes and mast cells as mediators of inflammation and immune response is discussed, as are the roles of growth factors and cytokines. New light on the 'old' problems will help us to devise newer and better therapeutic strategies to combat these clinical entities.Key words: atherosclerosis, cellular immunity, cytokines, growth factors, intimal hyperplasia, mast cells, restenosis, vasculopathies.
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Dissertations / Theses on the topic "Intima Hyperplasia"

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Rösler, Stefan K. "Die Hämodynamik von femoro-cruralen Bypasanastomosen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2007. http://dx.doi.org/10.18452/15739.

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Die moderne Gefäßchirurgie bedient sich bei hohen Stadien der pAVK, spezieller Gefäßrekonstruktionen in Form von distalen End-zu-Seit-Gefäßanastomosen. Das langfristige Versagen der Gefäßanastomose hängt primär von der Entstehung einer subendothelialen Intimahyperplasie (IH) ab. Diese IH-Gebiete befinden sich je nach Anastomosengeometrie im Gebiet der Hauben- und Fersenzone sowie am Boden der Anastomose. // Mit Hilfe der Particle Image Velocimetry-Technik wird eine Taylor-Patch-, eine Miller-Cuff-Anastomose und eine femoro-crurale Patch-Prothese bezüglich ihrer Flussmuster sowie ihrer hämodynamischen Eigenschaften wie Geschwindigkeit, Scherstress und Rotation in z-Richtung (Vorticity) untersucht. // In einem hydrodynamischen Kreislaufmodell werden elastische, transparente Silikonmodelle der Anastomosen hergestellt und mit einem blutanalogen Newtonschen Fluid (Glycerol-Wasser-Gemisch) unter Simulation der femorocruralen Druckkurve, pulsatil bei Variation der Strömungsbedingung perfundiert. Der periphere Widerstand beträgt 0,5 mmHg/ml/min (PRU) und die Phasenverschiebung -12 Grad (zwischen Druck- und Flusskurve). // Die Flussmuster variieren zwischen den unterschiedlichen Ausstromverhältnissen erheblich. Bei den unterschiedlichen Flussstärken hingegen ähneln sich die Flussmuster. Alle drei Modelle zeigen ausgeprägte Flussseparationszonen im Hauben- und Fersengebiet sowie geometrieabhängig auch eine Stagnationszone am Boden. Diese Bereiche wiesen die geringsten Fluidgeschwindigkeiten, deutlich unter normalem Wandscherstressniveau liegende Scherstressverhältnisse sowie geringe Vorticitywerte auf. Im Bereich der Übergangszonen finden sich hohe Scherstress- sowie Vorticitywerte. Geschwindigkeitsunterschiede des Fluids zeigten sich im Bereich der Ausstromsegmente. Variable Stressverteilungen zeigen sich auch innerhalb der Separationszonen. Eine Erklärung für die unterschiedlich beschriebenen Offenheitsraten der drei Anastomosenformen wird durch diese Arbeit nicht gefunden.
Modern vascular surgery uses special termino-lateral anastomoses for treating high levels of peripheral arterial disease (PAD). Long term stenoses and occlusions of vascular anastomoses mostly depend on the development of subendothelial myointimal hyperplasia (MIH). There are characteristic areas within the anastomoses, where this process can be examined: The heel, the tow and the floor zone. // This examination observes local hemodynamics like velocity, shear stress and vorticity (rotation in z-direction) and flow patterns of a Taylor-Patch-, a Miller-Cuff-Anastomosis and a feroro-crural patch prothesis (FCPP) with the usage of a Particle Image Velocimetry. In a hydrodynamic circulation model various elastic, transparent silicon phantoms of termino-lateral anastomoses are perfused with a Newton fluid blood analogon (glycerol-water mixture) while simulating the femorocrural pressure curve in a pulsatile manner under variation of the flow conditions. The outflow resistance is 0.5 mmHg/ml/min (PRU, peripheral resistance units) and a phase shift of -12° between flow and pressure curve is simulated. // The flow patterns differed extremely in accordance of the various outflow ratios. Using different flow intensity, the flow patterns are very similar. // All three anastomoses show characteristic heel and toe separation zones. In the FCPP centre a stagnation zone on the floor can not be examined. Shear stress inside the flow separations was significantly lower than normal wall shear stress. High shear stress levels were found inside the transition zones between flow separation and high velocity mainstream. An explanation for the different stenoses and occlusions time of the three different anastomoses can not be found.
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Lima, Paulo Roberto da Silva. "Estudo comparativo da hiperplasia miointimal pós-angioplastia na artéria ilíaca externa de coelhos, com aterosclerose induzida, tratados com Allium sativum e colostazol." Universidade Federal de Alagoas, 2015. http://www.repositorio.ufal.br/handle/riufal/2098.

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Intimal hyperplasia is associated with graft failure and vascular sutures in the first year after surgery and in postangioplasty restenosis. Allium sativum (common garlic) lowers cholesterol and has antioxidant effects; it also has antiplatelet and antitumor properties and, therefore, has great potential to reduce or inhibit intimal hyperplasia of the arteries. Attempts have been made to inhibit intimal hyperplasia of the arteries with cilostazol and other drugs. Therefore, it is important to address the following research question: what is the difference between the mean of post-angioplasty myointimal thickening in the iliac artery of rabbits treated with A. sativum and that treated with cilostazol? Our objective is to determine the mean difference of post-angioplasty myointimal hyperplasia in the external iliac artery of rabbits with induced atherosclerosis, and compare the outcome between treatment with A. sativum and treatment with cilostazol. This is a randomized preclinical trial study conducted in experimental animals. We used female New Zealand rabbits (Oryctolagus cuniculus), submitted to an atherosclerotic diet and angioplasty of the external iliac artery. The animals were divided into the following groups (n = 10 each) according to treatment: group A, A. sativum, 800 μg⋅kg-1⋅day-1, orally; group C, cilostazol, 50 mg/day, orally; group S, 10 mL of 0.9% physiological saline solution, orally. Our primary variable is the difference of the mean myointimal hyperplasia. The secondary variable is the mean plate thickness of the arterial wall. Complementary data include frequency of limb ischemia, limb loss frequency, frequency of hematoma or bruising, frequency of infection, frequency of bleeding, frequency of animal death, and mean of lipid levels. The sample size was arbitrated in 30 rabbits. Statistical analysis was performed by using ANOVA and Tukey tests, as well as the χ2 test. We calculated the 95% confidence interval (CI) for each point estimate, and the P value was set as < 0.05. Group S had a mean hyperplasia rate of 35.74% (95% CI, 31.76–39.71%); group C, 16.21% (95% CI, 13.36–19.05%); and group A, 21.12% (95% CI, 17.26–25.01%); P < 0.0001. In conclution the Allium sativum quite as effective in inhibiting myointimal hyperplasia compared with those treated with cilostazol.
A hiperplasia intimal está relacionada à falha de enxertos e suturas vasculares no primeiro ano pós-cirurgia e nas reestenoses pós-angioplastia. O Allium sativum (alho comum) reduz o colesterol e tem efeito antioxidante, antiplaquetário e antitumoral; logo havia grande possibilidade de reduzir ou inibir a hiperplasia da íntima das artérias, a qual sua inibição vem sendo tentada com o Cilostazol e outros tratamentos. Sendo assim é relevante responder a pergunta de pesquisa: qual a diferença de média de hiperplasia miointimal pós-angioplastia na artéria ilíaca de coelhos tratados com Allium sativum comparada aos tratados com Cilostazol? O objetivo é determinar a diferença de média de hiperplasia miointimal pós-angioplastia na artéria ilíaca externa de coelhos com aterosclerose induzida e tratados com Allium sativum comparada aos tratados com Cilostazol. O estudo foi um ensaio pré-clínico aleatório em animais de experimentação por 35 dias. Os animais foram coelhos fêmeas (Oryctolagus cuniculus), da linhagem Nova Zelandia, submetidos à dieta ateroslcerótica e à angioplastia da artéria ilíaca externa direita. Os animais foram divididos em: Grupo A (n=10) coelhos tratados com a Allium sativum (800 μg/kg/dia), em doses diárias, por via oral. Grupo C (n=10): coelhos tratados com Cilostazol em doses diárias de 50 mg/dia, por via oral. Grupo S (n= 10) coelhos tratados com 10 mL de soro fisiológico 0,9%, por via oral, que foi nosso controle negativo. A variável primária foi a diferença de frequência da média de hiperplasia miointimal. Variáveis secundárias: a média de espessura da placa na parede arterial. Dados complementares: a frequência isquemia do membro, a frequência de perda do membro, a frequência de hematoma ou equimose, a frequência de infecção, a frequência de sangramento, a frequência de morte do animal e a média dos níveis lipídicos. O tamanho da amostra foi arbitrado em 30 coelhos. A análise estatística foi realizada com o teste ANOVA, Qui-quadrado e Tukey. Foi calculado o intervalo de confiança de 95% para cada ponto estimado. Os resultados foram: grupo S teve um índice médio de hiperplasia de 35,74% IC de 95% (31,76% a 39,71%); grupo C teve um índice médio de hiperplasia de 16,21% IC de 95% (13,36% a 19,05%); grupo A teve um índice médio de hiperplasia de 21,12% IC de 95% (17,26% a 25,01%); com P < 0,0001. Sendo assim, o Allium sativum tem a mesma eficácia na inibição da hiperplasia miointimal comparada aos tratados com Cilostazol
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PRANDI, FRANCESCA. "Identification of early pathophysiological events underlying venous coronary bypass stenosis by a mechano-biology approach." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/50493.

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Saphenous vein graft disease represents an unresolved problem in coronary artery bypass grafting. After surgery, progressive modification in the vein wall occurs, leading to occlusion of the graft lumen. This process, called intima hyperplasia, involves the participation of vein-resident cells as well as the recruitment of vein-extrinsic cells. Arterial wall strain has recently emerged as one of the factor that can contribute to the pathogenesis of the vein graft disease. Therefore, in collaboration with Department of Bioengineering, Politecnico di Milano we developed a culture system for the ex vivo pressure stimulation of vein segments. This new ex vivo vein culture system is able to reproduce the wall strain typical of the arterial circulation. The ex vivo vein culture system (ECVS) adopted in this project has been validated and proved as a valuable, reliable, easy handling and versatile tool for studying arterial pressure events triggered in VGD. The biological data achieved confirm an important contribution of the arterial-like wall strain in SV structural and biochemical changes, activation of vessel resident cells and in the expression of molecular signals involved in the pathogenesis of IH. Using this system, we found that either venous- or arterial-specific pressure regimens induced vein pro-pathologic commitment involving upregulation of Matrix Metallo-Proteases 2/9, and induction of microRNAs-21/146a/221. By contrast, arterial-like pressure caused a significant morphological rearrangement of the vein, a suppression of Tissue Inhibitor of Metallo Protease-1, an enhanced expression of TGF-β1 and BMP-2 mRNAs and, finally, the upregulation of microRNAs-138/200b/200c. In coronary-pressure stimulated vessels, the density of the adventitial vasa vasorum was significantly increased. This was accompanied by an increased presence of cells co-expressing NG2, CD44 and SM22α markers in the adventitia, identifying them as multipotent mesenchymal cells/smooth muscle cells progenitors with a pericyte origin. An increase in Histone H3 Lysine 4 methylation and histone H4 Lysines 9/16 acetylation levels was finally found in adventitial cells and vasa vasorum. The present findings suggest a mechanistic role of the arterial-like pulsatile pressure in reinforcement of SV-resident cells pro-pathologic commitment in vein bypass failure, by activation of mechanical-dependent transcriptional circuitries and of pericyte-derived cells located in the vessel adventitia. The ultimate goal of this project is to find a treatment that can prevent, avoid or reduce the incidence of the vein graft disease in patients subjected to bypass surgery with saphenous vein. This treatment could include one or more targets identified in this work focusing on the early stage of the pathological adaptation of the SV to the new hemodynamic environment.
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Chen, Changyi. "Intimal hyperplasia in endarterectomized arteries." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25393.

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Jackson, Andrew John. "Cellular aspects of intimal hyperplasia formation." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2417/.

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Introduction: 12,000 infrainguinal bypass grafts are performed annually in the UK. Despite improvements in surgical technique, outcomes remain suboptimal: 20% of above knee grafts require intervention to maintain patency by 3 years. Only antiplatelet agents have been demonstrated thus far to improve graft survival. 80% of graft failure is as a result of intimal hyperplasia, an inflammatory process characterised by the proliferation and migration of vascular smooth muscle cells. Toll Like Receptors (TLR), part of the innate immune system, have been implicated in atherosclerosis formation but not investigated in a model of infrainguinal graft failure. When a vein is used as a conduit for infrainguinal bypass graft it has been exposed to ischaemic and hypoxic conditions: preliminary data has demonstrated that ischaemic vascular smooth muscle cell explants are hyperproliferative. Phospholipase C γ (PLC γ) is a signalling pathway with potential links to innate immune pathways and pathways induced by hypoxia and ischaemia. Methods: Human vein tissue was obtained from patients undergoing amputation and coronary artery bypass surgery and used for immunohistochemistry and to obtain vascular smooth muscle cells by explant method. Immunohistochemistry was used to determine the presence of TLR4 and PLC γ in human vein tissue. Specific TLR Ligands were used to determine the functional response of TLR’s in vascular smooth muscle cells as measured by Interleukin 8 ELISA. Radiolabelled Thymidine incorporation was used to measure proliferation of vascular smooth muscle cells in response to TLR4 activation, hypoxia and PLC γ inhibition. Results: TLR4 was demonstrated to be present in human vein tissue, and functionally active in human vascular smooth muscle cells. Furthermore stimulation with the specific ligand of TLR4 caused enhanced proliferation of vascular smooth muscle cells. Hypoxia (5% and 10% Oxygen) significantly enhanced proliferative responses of vascular smooth muscle cells. PLC γ was demonstrated to be present in human vein tissue, and inhibition, using U73122 in vascular smooth muscle cells reduced proliferation. Conclusion: TLR activation and hypoxia appear to enhance the proliferative responses of human vascular smooth muscle cells, a key cellular pathway of intimal hyperplasia formation and infrainguinal graft failure. Inhibition of PLC γ reduces proliferative responses. Further research is required to confirm that PLC γ is a key common pathway mediating enhances of proliferation caused by TLR activation and hypoxia.
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Religa, Piotr. "Development of intimal hyperplasia in transplant arteriosclerosis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-448-8/.

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Porter, Karen Elizabeth. "An investigation into human vein graft intimal hyperplasia." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/34203.

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The most common cause of vein bypass graft failure in the postoperative period of 1 month to 1 year is stenosis, which occurs in up to 30% of arterial reconstructions. This thesis investigates the intimal hyperplasia underlying such lesions using a laboratory model. The first chapter reviews the current literature regarding vein graft stenoses and is followed in Chapter 2 by a brief introduction to tissue and organ culture and their usefulness as investigative research tools. Before embarking on a study of a pathological condition, Chapter 3 studies the structure of the "normal" long saphenous vein in patients undergoing arterial surgery. A degree of intimal thickening was identified in the majority of the veins in this population, the possible causes of which are discussed. The fourth chapter describes and validates an organ culture of human saphenous vein to study the vascular biology of vein graft intimal hyperplasia. Since smooth muscle cell proliferation is a pivotal event in the development of such lesions, a reliable and reproducible method of assessing proliferation was required and is described in Chapter 5. Chapter 6 investigates the effect of endothelial denudation on the development of intimal thickening, and an organ coculture study described in Chapter 7 positively identifies a soluble paracrine mediator produced by the endothelium which can promote intimal hyperplasia. The following chapters utilise variations of the coculture method to further define the precise role played by the endothelium. Chapter 8 demonstrates that isolated, cultured endothelial cells do not promote intimal thickening in denuded veins, suggesting that the normal anatomical location of endothelial cells overlying smooth muscle cells in the vein wall may be important. Chapter 9 therefore describes the development of a method to reseed endothelial cells onto denuded vein segments in order to observe whether the development of intimal hyperplasia can be restored. This proved not to be the case, possibly because the process of culturing had phenotypically altered the endothelial cells, thereby rendering them incapable of producing their paracrine factor. However, a number of other hypotheses and methods by which they could be investigated, are also discussed. The main drawback of human saphenous vein organ culture is that it is a no-flow system. There is considerable evidence in the literature to show that haemodynamics modify the normal and pathological structure and function of blood vessels. Chapter 10 therefore describes the development of an in vitro flow model of saphenous vein graft intimal hyperplasia in an attempt to model the in vivo situation more closely. The final chapter summarises the data presented in this thesis, draws conclusions, and examines prospects for future research in this field.
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Mellander, Stefan. "On cellular sources for intimal hyperplasia after vascular interventions /." Göteborg : Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/4440.

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Kanjickal, Deenu George. "Perivascular Drug Delivery Systems for the Inhibition of Intimal Hyperplasia." University of Akron / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=akron1133715441.

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Sivanesan, Sharmila. "Correlating geometry, haemodynamics and intimal hyperplasia in radiocephalic arteriovenous fistulae." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337127.

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Books on the topic "Intima Hyperplasia"

1

Oskar, Klotz. Concerning compensatory hyperplasia of the intima. [S.l: s.n., 1995.

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B, Dobrin Philip, ed. Intimal hyperplasia. Austin: R.G. Landes Co., 1994.

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Davenport, Kathryn. Drug delivery coatings for nitinol stents to prevent intimal hyperplasia. Birmingham: University of Birmingham, 2002.

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Pharmacologic suppression of intimal hyperplasia. Austin, Tex: R.G. Landes, 1993.

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Lamuraglia, G. Photodynamic Therapy of Intimal Hyperplasia. Chapman & Hall, 1997.

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Cheema, Asim N. Arterial repair after balloon angioplasty and stenting: Role of extracellular matrix and adventitial microvessels in the development of intimal hyperplasia and restenosis. 2004.

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Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ‎ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
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Book chapters on the topic "Intima Hyperplasia"

1

Tanner, Felix C., and Thomas F. Lüscher. "Pathophysiology of Intimal Hyperplasia." In Radiology of Peripheral Vascular Diseases, 29–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-56956-2_4.

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Purcell, Seth T., Shruti Rao, and Ruth L. Bush. "Understanding Intimal Hyperplasia Biology in Hemodialysis Access." In Hemodialysis Access, 245–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40061-7_28.

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Sheng, Neha, and Brittany Mead. "Hemodynamics, Atherosclerosis, Intimal Hyperplasia, and Wound Healing." In The Vascular Surgery In-Training Examination Review (VSITE), 59–73. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24121-5_5.

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Grazioli, Luigi, Barbara Frittoli, Roberta Ambrosini, Martina Bertuletti, and Francesca Castagnoli. "Hepatic Hemangioma, Focal Nodular Hyperplasia, and Hepatocellular Adenoma." In Imaging of the Liver and Intra-hepatic Biliary Tract, 3–48. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39021-1_1.

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McNamara, Dennis B., Harmeet Aurora, Brenda Bedi, Thomas Osgood, Raphael Santiago, I.-L. Chen, Philip J. Kadowitz, and Donald L. Akers. "Nitric Oxide: An Endogenous Inhibitor of Balloon Catheter-Induced Intimal Hyperplasia." In Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide, 175–80. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1903-4_21.

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Wu, Jiacheng, and Kevin W. Cassel. "Observer-Based Feedback Control of a Mathematical Model of Intimal Hyperplasia." In 2013 Proceedings of the Conference on Control and its Applications, 184–90. Philadelphia, PA: Society for Industrial and Applied Mathematics, 2013. http://dx.doi.org/10.1137/1.9781611973273.25.

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Geary, Randolph L., and Stephen M. Schwartz. "Intimal Hyperplasia is the Wrong Target: Restenosis as a Failure of Remodeling." In Arterial Remodeling: A Critical Factor in Restenosis, 199–230. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6079-1_11.

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Landymore, R. W., M. A. MacAulay, B. Sheridan, and C. Cameron. "Eicosapentaenoic Acid, Persantine, and Aspirin for the Prevention of Vein Graft Intimal Hyperplasia." In Coronary Artery Surgery in the Nineties, 179. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-45622-0_35.

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Choi, Eric T., Niraj Sehgal, Shaping Sun, Jeffrey Trachtenberg, Una S. Ryan, and Allan D. Callow. "A Novel Approach to Preventing Intimal Hyperplasia: Inhibition of Smooth Muscle Cell Migration with Enalapril." In Modern Vascular Surgery, 28–40. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2632-1_3.

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Thankam, Finosh G., Victoria E. D. Wilson, and Devendra K. Agrawal. "Preclinical Models of Intimal Hyperplasia and Restenosis to Predict Clinical Events and Develop Novel Therapies." In Biomedical Translational Research, 427–45. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4345-3_26.

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Conference papers on the topic "Intima Hyperplasia"

1

Richardson, William J., Dennis D. van der Voort, and James E. Moore. "A Device to Subject Cells to Longitudinal Stretch Gradients on a Tube In Vitro." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80941.

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In the US, cardiovascular disease accounts for more than 800,000 deaths and an economic burden of nearly $300 billion per year. A major pathology afflicting the cardiovascular system is atherosclerosis, characterized by intraluminal plaque formation, producing a stenosis and obstructing flow. Balloon angioplasty, often coupled with the implantation of either a bare-metal or drug-eluting stent, has become a standard treatment of atherosclerosis. However, the host tissue’s response to stenting is frequently maladaptive, leading to intimal hyperplasia via smooth muscle cell (SMC) division and migration to the intima, and increased matrix protein synthesis, all contributing to restenosis of the vessel.
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Wang, Gui-xue, Chao-jun Tang, Dang-heng Wei, Lu-shan Liu, Li Yang, and Lin-Hong Deng. "The Change of Local Wall Shear Stress Accelerates Intima Hyperplasia and Atherosclerosis." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.128.

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Carroll, Gráinne T., Paul D. Devereux, Anthony Callanan, Tim M. McGloughlin, and Michael T. Walsh. "The Influence of Realistic Arteriovenous (AV) Fistula Wall Shear Stress (WSS) on Endothelial Cell (EC) Gene Expression: A Correlation to Intimal Hyperplasia Development." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193248.

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The low patency rates of Arteriovenous (AV) fistulae are well documented in the literature [1]. Up to 90% of AV fistula morbidity is caused by stenotic lesion formation and the subsequent development of thrombosis in the Vascular Access (VA) junction [1]. The underlying pathology of these stenotic lesions is intimal hyperplasia (IH) which has been characterized by the degradation of the extra cellular matrix (ECM), migration and proliferation of smooth muscle cells (SMCs) and the infiltration of leukocytes and monocytes into the intima. IH primarily occurs in a number of key locations within the VA junction of AV fistulae which include the suture line of the anastomosis, on the floor of the vein opposite the VA junction and downstream of the anastomosis within the venous conduit of the AV fistula [2].
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4

Ballyk, Peter D., Matadial Ojha, and Colin Walsh. "Vein Cuffs May Improve Anastomotic Patency by Reducing Suture-Line Intramural Stresses." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0258.

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Abstract Intimal hyperplasia (IH) is an important complication of arterial bypass surgery which can ultimately lead to graft failure. The pathogenesis of IH involves the migration of smooth muscle cells from the media to the intima where they proliferate and secrete extracellular matrix. This results in a thickened vessel wall which may cause stenosis and/or thrombosis of the distal graft-artery junction. It has been shown that IH is a more significant problem in stiff synthetic grafts than in more compliant vein grafts (Bassiouny et al., 1992), and that synthetic grafts have a higher failure rate (Waiden et al., 1980). Consequently, autogenous vein (or artery) grafts are used clinically whenever possible. In cases where autogenous grafts are not long enough or not available (for e.g. if they have already been harvested or have been obliterated by disease), a vein cuff interposed between the distal end of a synthetic graft and the host artery can improve long term patency by reducing distal anastomotic IH (Miller et al., 1984; Suggs et al., 1988).
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Campbell, Triona, Reena Cole, and Michael O’Donnell. "Pressure Induced Strain at Femoral Artery Bypass Graft Junctions." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176342.

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Femoral or femoropopliteal artery bypass graft junctions have a predilection for failure due to restenosis. It has been clinically proven that vascular reconstructions tend to restenose within a short period of time [1]. Extensive studies have cited wall shear stresses as being primarily responsible and definite correlations between hydrodynamic stresses in the arterial wall and arterial disease have been shown [2,3]. However intensive investigations into wall shear stresses have lead to conflicting arguments on the proliferation and propagation of stenoses. It was concluded by Freidman [4] that the intima at sites exposed to relatively high or unidirectional shears thickened initially, but as time progressed the greatest thicknesses were ultimately achieved at sites exposed to lower or more oscillatory shear environments. A contradicting view was expressed by Nazemi [5] that low wall shear stress contributed to the onset of atherosclerotic plaque formation, whilst high wall shear stress encouraging plaque growth. A number of studies have however established a statistically significant correlation between pressure and intimal hyperplasia and concluded that blood pressure and not blood flow is the primary factor responsible for the localization of atherosclerosis [6–8].
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Dryjski, Maciej, Eileen Mikat, and Thorir D. Bjornsson. "IN VIVO POTENCY OF HEPARIN AND HEPARINOIDS TO INHIBIT RAT SMOOTH MUSCLE CELL PROLIFERATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644604.

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The final response of endothelial cell injury in the arterial wall is characterized by proliferation of smooth muscle cells (SMC) in the intima to form a fibro-musculo-elastic plaque. Recent in vivo and in vitro studies have shown that heparin can inhibit proliferation of SMC. These studies, however, have not elucidated the relationships between heparin dose or concentration and its in vivo antiproliferative response. In the present study, we investigated the potency of standard heparin (SH), low molecular weight heparin (LMWH) and a mixture of sulfated glycosaminoglycans (Organon 10172) with respect to the in vivo inhibition of SMC proliferation after endothelial cell injury. The injury was achieved by a short infusion of air into an isolated segment of the rat carotid artery. The drugs were administered by the AlzetR miniosmotic pumps for two weeks, at which time the animals were sacrificed and both carotid arteries were fixed in situ for light and transmission electron microscopy. The index of the intimal SMC proliferation was the maximum intima to media area (I/M) ratio. The control animals developed a marked intimal thickening (I/M: 0.97). The animals treated with 50 units/kg/hr of SH exhibited significantly less intimal hyperplasia (I/M: 0.10). With decreasing SH doses, there were increases in the I/M ratio (5 units/kg/hr, I/M: 0.44; 0.5 units/kg/hr, I/M: 0.75, and 0.05 units/kg/hr, I/M: 0.84). LMWH in doses of 50 units/kg/hr inhibited SMC proliferation as effectively as SH (I/M: 0.10), however, at doses of 15 units/kg/hr the I/M ratio was 0.55. The effect of Organon 10172 was significant at doses of 50 units/kg/hr (I/M: 0.04), but limited at doses of 15 units/kg/hr (I/M: 0.61). The APTT and anti-Xa levels were only slightly increased in the animals treated with 50 units/kg/hr of LMWH and Organon 10172, but unchanged in the animals receiving SH and the lower doses of LMWH and Organon 10172. It is concluded that SH, LMWH and Organon 10172 have significant antiproliferative effects upon SMC. The differences in the dose-response curves suggests more than one mechanism of action.
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Kute, Stephanie M., and David A. Vorp. "Regional Association of Biological and Hemodynamic Parameters in Distal End-to-Side Vascular Anastomoses Perfused Ex Vivo." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32513.

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Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.
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8

Galvin, D. AJ, A. C. Meek, K. German, R. A. Harper, and C. N. McCollum. "CAROTID INTIMAL TRAUMA: A MODEL FOR PLATELET INTERACTIONS WITH DAMAGED ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643369.

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Radiolabelled platelet deposition on prosthetic arterial grafts may be used as a method to evaluate antithrombotic drugs but requires large animals or patients and involves artificial flow surfaces. A rabbit model has been developed to investigate platelet uptake following carotid intimal damage.Both carotid arteries of 10 NZW rabbits were exposed by midline incision and intimal damage inflicted by a 3-minute unilateral artery compression using the jaws from non-toothed dissecting forceps mounted on a G-clamp with compression screw. Twenty-four hours later, autologous platelets were labelled with llllndium by the method of Hawker et al [1], The carotid arteries were excised 40 hours later and radiolabelled platelet uptake counted in a well crystal and expressed as a percentage of the activity in 1ml of blood.Total counts (mean ± sem) in the non-traumatised artery were 2.6±0.35×103 which was similar to background at 2.0±0.07×103. Expressed per gm, radioactivity in the traumatised artery at 4.8±0.38×l05/gm was significantly higher than 2.6±0.43×105 in the undamaged carotid (p<0.01). Platelet uptake on the damaged endothelium, expressed as a percentage of the activity in 1ml of blood, at 55.1±9.8 was also significantly higher than 28.6±6.3 percent on the control artery (p<0.01).This inexpensive model allows the precise measurement of radiolabelled platelet uptake on damaged arterial intima and may therefore be used to evaluate antithrombotic drugs and investigate the role of platelets in arterial repair, intimal hyperplasia and the pathogenesis of atheroma.1. Hawker RJ, Hawker LM, Wilkinson AR. Indium labelled human platelets: Optimal method. Clin Sci 1980; 50: 243-248
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9

Berceli, Scott A., and Alexander W. Clowes. "Intimal Hyperplasia — Development and Regression in Response to Fluid Shear." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0381.

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Abstract The long-term success of autogenous and prosthetic bypass grafts is dictated by the development and subsequent progression of intimal hyperplasia. While recent advances in vascular biology continue to improve our understanding of the mechanisms which control this process, available clinical therapies which treat or slow its progression have yet to be identified. Among the factors which influence the development of intimal hyperplasia are the physical forces exposed to bypass conduits. As initially described by Glagov et al. (1988) and confirmed by multiple other investigators, the biology of the hyperplastic response is modulated by the imposed fluid shearing forces While our ability to modulate the local hemodynamics of bypass conduits is limited, an understanding of how these forces govern the healing response can serve as a basis for future pharmacological therapies. In our laboratory we have employed a primate model to understand the influence of shear stress on the development of intimal hyperplasia in PTFE grafts.
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10

Wingate, Kathryn, Yan Tan, Raphael Nemenoff, and Wei Tan. "Combined Effects of Nanofiber Matrix Elasticity and VEGF-A on the Differentiation of Mesenchymal Stem Cells Towards Mature Endothelial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80747.

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The potential of mesenchymal stem cell (MSC) in the treatment of vascular diseases is becoming increasingly recognized.[1] The use of MSC to produce a functional endothelium in synthetic vascular grafts is of particular interest as this would prevent common graft failures such as neointima hyperplasia and thrombus. Current attempts to produce a functional endothelial layer with endothelial cells (EC) have limited success due to the need for invasive surgery and the limited expansion capability these cells have in vitro.[2] MSC are a powerful cellular alternative as they are easily obtained through a bone marrow biopsy, have a large expansion capability in vitro, are multipotent, and thromboresistant. Individual factors such as matrix elasticity, matrix structure, growth factors, and mechanical stimulations have all been shown to contribute to MSC differentiation towards vascular phenotypes in vivo. However, the response of MSCs to the combined effects of these factors is not well characterized. Additionally, many experiments studying MSC differentiation are conducted on 2D substrates instead of simulating the 3D nanofiber matrix structure found in-vivo. Furthermore, little is known about the underlying cell signaling pathways that direct vascular differentiation. Currently, researchers have yet to achieve MSC differentiation into mature, functional endothelial cells, a critical step for regenerating healthy vascular tissue. We hypothesize that the combined effects of VEGF-A growth factor and a 3D matrix elasticity that mimicking the mechanochemical properties of in-vivo intima induce more complete MSC differentiation into EC expressing mature markers through the regulation of critical vascular signaling molecules such as MAPK/ERK and RhoA/Rock.
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