Relevant bibliographies by topics / Intima Hyperplasia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Intima Hyperplasia'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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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 proliferatin
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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 (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, thicke
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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 (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 contro
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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 (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
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Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 1P1 (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 differen
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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 (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 divi
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Kachlik, David, Vaclav Baca, Petr Fara, et al. "Blood vessels of the normal and pathologically changed wall of the human vena saphena magna." Open Medicine 3, no. 4 (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
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Qian, Kun, Li Feng, Yujie Sun та ін. "Overexpression of Salusin-α Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model". BioMed Research International 2018 (12 липня 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
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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 (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. Ther
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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 (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
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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 hämodyna
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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 m
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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
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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 no
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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
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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"

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Oskar, Klotz. Concerning compensatory hyperplasia of the intima. s.n., 1995.

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

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

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Pharmacologic suppression of intimal hyperplasia. 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 thromb
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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
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Book chapters on the topic "Intima Hyperplasia"

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Tanner, Felix C., and Thomas F. Lüscher. "Pathophysiology of Intimal Hyperplasia." In Radiology of Peripheral Vascular Diseases. 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. 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). Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24121-5_5.

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McNamara, Dennis B., Harmeet Aurora, Brenda Bedi, et al. "Nitric Oxide: An Endogenous Inhibitor of Balloon Catheter-Induced Intimal Hyperplasia." In Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide. 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. Society for Industrial and Applied Mathematics, 2013. http://dx.doi.org/10.1137/1.9781611973273.25.

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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. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39021-1_1.

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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. 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. 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. 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. 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"

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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 mig
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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 t
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Gonzalez-Gonzalez, V., D. A. Galarza-Delgado, I. J. Colunga-Pedraza, et al. "AB0659 ASSOCIATION OF PLASMA ATHEROGENIC INDEX WITH CAROTID INTIMA-MEDIA HYPERPLASIA IN PATIENTS WITH RHEUMATOID ARTHRITIS." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.264.

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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
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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] th
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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
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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 bi
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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 w
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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 bio
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