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Relevant bibliographies by topics / Intimal hyperplasia

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Academic literature on the topic 'Intimal hyperplasia'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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Journal articles on the topic "Intimal hyperplasia"

1

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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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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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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Koshy, Prakash, Amanda Self, Philip J. Kadowitz, Vivian A. Fonseca, and Dennis B. McNamara. "Effects of low-dose candesartan on the rate of re-endothelialisation following vascular wound healing." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (2001): S81—S83. http://dx.doi.org/10.1177/14703203010020011401.

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The wound healing response of the vascular wall to injury involves re-endothelialisation of the denuded luminal surface and thickening of the intimal area (intimal hyperplasia), as expressed by the intimal-to-medial area ratio (I/M). Candesartan, at doses of 1 mg/kg/day or higher, has been reported to attenuate the intimal hyperplastic response. We tested the hypothesis that candesartan, at doses lower than those associated with attenuation of intimal hyperplasia, may affect re-endothelialisation. New Zealand White rabbits were subjected to balloon catheter injury to the thoracic aorta. Candes

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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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Shiroma, H., and A. Kusaba. "Ultrastructural Features of Progressive Intimal Hyperplasia at the Distal End-to-Side Anastomosis of Vein Grafts." Cardiovascular Surgery 4, no. 3 (1996): 393–98. http://dx.doi.org/10.1177/096721099600400327.

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The features of intimal hyperplasia at the distal end-to-side anastomosis of arterially implanted autovein bypass grafts in dogs were examined using light and transmission electron microscopy. The bypass grafting was done under conditions of reduced blood flow with an abnormal flow wave and high peripheral resistance. Anastomotic intimal hyperplasia was evident 14 to 31 days after implantation, then gradually increased, particularly at the toe portion of the anastomosis. From 6 to 12 months after implantation, the intimal hyperplasia was excessively increased and severe luminal stenosis had de

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O'Malley, M. K. "Intimal hyperplasia." European Journal of Vascular Surgery 6, no. 4 (1992): 343–45. http://dx.doi.org/10.1016/s0950-821x(05)80277-4.

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8

Aydin, Unal, Murat Ugurlucan, Funda Gungor, et al. "Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model." Angiology 60, no. 3 (2008): 370–77. http://dx.doi.org/10.1177/0003319708321102.

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Introduction Vascular intimal hyperplasia is associated with increased mortality and morbidity. The authors investigated the effects of atorvastatin on vascular intimal hyperplasia. Materials and methods Rats were divided into 4 groups. Groups 1, 2, and 3 had experimental aortic injury and received intraperitoneal injection of atorvastatin, solvent, or 0.9% NaCl, respectively. Group 4 was a nonintervention (laparotomy only) control group. Animals were sacrificed after 3 weeks. Blood samples and injured aortic segment were analyzed. Results Atorvastatin administration significantly lowered tota

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Karasu, Aykut, Yılmaz Güler, Soner Büyükkınacı, and Halil Toplamoğlu. "Deneysel Karotis Endarterektomide “Abciximab”ın Restenozis Üzerine Etkisi." Sinir Sistemi Cerrahisi Dergisi 1, no. 1 (2008): 12–19. https://doi.org/10.54306/sscd.2008.43.

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Objective: Thrombosis and intimal hyperplasia occuring after carotid endarterectomy cause restonosis. By preventing activation of platelets and neointimal hyperplasia, carotid thrombosis and intimal hyperplasia can be impeded. In this study we applied platelet gpIIa/gpIIIb receptor blocker abciximab on rat vessel walls and examined its effect on intimal hyperplasia. Methods: Abciximab was produced at mammiferous cell culture as fab portion of 7E3 monoclonal antibody. It inhibits platelet aggregation by binding glicoprotein IIa/IIIb receptor on platelet. It also inhibits intimal hyperplasia by

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Bledsoe, Shelly L., Aliza T. Brown, Joseph A. Davis, Hongjiang Chen, John F. Eidt, and Mohammed M. Moursi. "Effect of Clopidogrel on Platelet Aggregation and Intimal Hyperplasia following Carotid Endarterectomy in the Rat." Vascular 13, no. 1 (2005): 43–49. http://dx.doi.org/10.1258/rsmvasc.13.1.43.

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Intimal hyperplasia results in significant morbidity and mortality following vascular intervention. Both platelets and elevated homocysteine have been implicated in the development of intimal hyperplasia. We previously demonstrated that a locally applied antiplatelet agent decreases the development of intimal hyperplasia. We were therefore interested in a systemic antiplatelet agent, clopidogrel. We hypothesized that clopidogrel would decrease platelet aggregation and activity and intimal hyperplasia. Male Sprague-Dawley rats underwent carotid endarterectomy (CEA) and treatment with either pla

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Dissertations / Theses on the topic "Intimal hyperplasia"

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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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2

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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Favreau, John T. "Oscillatory wall strain reduction precedes arterial intimal hyperplasia in a murine model." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-dissertations/172.

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Cardiovascular diseases (CVD) remain the most common cause of death in the United States. Additionally, peripheral artery disease affects thousands of people each year. A major underlying cause of these diseases is the occlusion of the coronary or peripheral arteries due to arteriosclerosis. To overcome this, a number of vascular interventions have been developed including angioplasty, stenting, endarterectomies and bypass grafts. Although all of these methods are capable of restoring blood flow to the distal organ after occlusion, they are all plagued by unacceptably high restenosis rates. Wh

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Bastijanic, Jennifer M. "Multifunctional Biomimetic Modifications to Address Endothelialization and Intimal Hyperplasia in Vascular Grafts." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1428065969.

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Dunlop, Paul. "Clincial and laboratory aspects of intimal hyperplasia in lower limb bypass grafts." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/34332.

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This thesis examines aspects of intimal hyperplasia in infrainguinal bypass grafts. There are 3 introductory chapters. Chapter 1 describes the aetiology and treatment of lower limb vascular disease, with particular reference to atherosclerosis. Chapter 2 is a review of the literature regarding the vascular biology of intimal hyperplasia. Chapter 3 is a review of the techniques of cell and organ culture used in the study of vascular disorders. Chapter 4 is composed of four clinical studies of infrainguinal grafts performed at the Leicester Royal Infirmary. There is a prospective study of the lo

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Books on the topic "Intimal hyperplasia"

1

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

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2

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

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3

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

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Pharmacologic suppression of intimal hyperplasia. R.G. Landes, 1993.

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5

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

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6

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 "Intimal hyperplasia"

1

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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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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Esato, Kensuke, Nobuya Zempo, Masaki O-hara, Kentaroh Fujioka, Takayuki Kuga, and Hiroaki Takenaka. "Effects of Morphology of Distal Anastomosis Immediately After Surgery on Intimal Hyperplasia in Femoropopliteal Bypass Graft." In Modern Vascular Surgery. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2946-9_26.

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Conference papers on the topic "Intimal hyperplasia"

1

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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Tran-Son-Tay, Roger, Minki Hwang, Scott A. Berceli, C. Keith Ozaki, and Marc Garbey. "A Model of Vein Graft Intimal Hyperplasia." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353667.

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Ballyk, Peter D., Matadial Ojha, Colin Walsh, and Jagdish Butany. "Suture-Induced Intramural Stresses and Intimal Hyperplasia." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1190.

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Abstract Intimal hyperplasia is a major cause of outflow stenosis and thrombosis of prosthetic bypass grafts. In an end-to-side graft-artery anastomosis, the thickness of the early cellular lesion is greatest at the suture-line, where the distribution is roughly uniform around the junction (Bassiouny et al., 1992; Trubel et al., 1994). This distribution is difficult to explain on the basis of either hemodynamic or compliance mismatch factors alone since these effects are not uniformly distributed (Ojha, 1994; Ballyk et al., 1995).

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Harper, R. A., I. F. Lane, C. M. Backhouse, C. N. McCollum, and A. C. Meek. "PLATELET DEPOSITION AND PSEUDO-INTIMAL HYPERPLASIA IN PROSTHETIC VASCULAR GRAFTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643088.

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Platelet and fibrin accumulation in arterial grafts may cause pseudo-intimal hyperplasia and graft occlusion. The relationship between the rate of post-operative platelet accumulation and subsequent pseudo-intimal hyperplasia has been studied in prosthetic grafts implanted in greyhounds.The femoral artery in 30 greyhounds was replaced by a 6cm length of 6mm PTFE. Autologous 111In-platelet deposition over the graft was measured by probe and ratemeter for 7 days and radioactivity compared to the contralateral thigh. The daily increase in this ratio graft over reference was calculated as the Thro

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Ojha, Matadial, and Jagdish Butany. "Distal Anastomotic Intimal Hyperplasia in Human Aortocoronary Vein Grafts." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1319.

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Abstract Coronary artery bypass graft (CABG) surgery is a common way of treating the occlusive disease, atherosclerosis. However, these grafts tend to fail due to thrombosis from (i) surgical techniques and the diseased state of the native coronary artery a few months post-surgery[Lesperance et al., 1972; Campeau et al., 1975], and (ii) the development of intimal hyperplasia that acts a precursor for atherosclerosis and plaque rupture one or more years post-operatively [Grodin et al., 1979; Campeau et al., 1983]. Coronary vein grafts tend to occlude preferentially at the distal end-to-side ana

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Kopacz, Adrian M., Brandon J. Tefft, Shu Q. Liu, and Wing K. Liu. "Modeling of Endothelial Cell Adhesion Dynamics Modulated by Molecular Engineering." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13269.

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Vascular thrombosis, intimal hyperplasia, and atherosclerosis are common disorders affecting a very large portion of the human population. A potential reduction in these disorders will elicit a significant impact. It has been shown that endothelial cells play a critical role in protecting blood vessels against the formation of thrombosis and atherosclerosis. Hence, a successful endothelial cell lining of arterial constructs will prevent intimal hyperplasia in reconstructed arteries. However, in practice endothelial cells often detach from reconstructed arteries due to weak adhesion strength, h

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Ballyk, Peter D., Matadial Ojha, and Colin Walsh. "Comparing the Influence of Graft Angle on Peri-Anastomotic Wall and Fluid Mechanics." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0248.

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Abstract Distal anastomotic intimal hyperplasia (DAIH) can lead to outflow stenosis of vascular bypass grafts. In end-to-side graft-artery anastomoses, two separate regions of DAIH have been identified: (i) the suture line and (ii) the floor of the anastomosis across from the suture line (Bassiouny et al., 1992). Suture-line intimal thickening seems to be associated with post-surgical healing and influenced by graft-artery compliance mismatch (Trubel et al., 1994), while floor hyperplasia appears to be linked to fluid mechanical phenomena, such as temporal variations in wall shear stress (Ojha

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Ishibashi, Hiroyuki, Hyoun Park, Matadial Ojha, Shari Langdon, and Lowell Langille. "Shear-Induced Intimal Thickening on the Bed of an End-to-Side Anastomosis Model." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1321.

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Abstract The long-term failure of arterial bypass grafts and arteriovenous fistulae is often related to intimal hyperplasia that preferentially develops at the outflow or distal anastomosis. In studies using animal models, hyperplasia develops specifically around the suture line and on the bed across from the junction.

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Chesler, Naomi C., Nathan Brewton, and David N. Ku. "Alterations in Endothelial Permeability After Intravascular Intervention." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0178.

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Abstract Intravascular interventions such as balloon embolectomy are effective in removing arterial and venous thrombi and emboli but lead to endothelial injury. The clinical sequelae of this injury include intimal hyperplasia and renewed clot formation. Changes in endothelial permeability after intravascular intervention may influence the development of intimal hyperplasia. To assess the extent and type of injury engendered by the Fogarty embolectomy catheter, the permeability of the endothelium after sham embolectomy (catheter withdrawal in the absence of a thrombus or thrombus model) was me

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Ballyk, Peter D., Matadial Ojha, and Colin Walsh. "Axial Strain-Induced Stress Distributions at End-to-End and End-to-Side Graft-Artery Junctions: Clinical Implications." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1322.

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Abstract Suture-line intimal hyperplasia can lead to outflow stenosis of vascular bypass grafts. One prominent theory suggests that compliance mismatch between the graft and native vessel promotes suture-line hyperplasia, however, this theory has not yet been proven. Many studies have demonstrated that matching graft compliance to that of the artery leads to improved graft patency, but only a few have actually quantified the hyperplasia at compliant and non-compliant graft-artery junctions (Bassiouny et al., 1992; Trubel et al., 1994; Courtman, 1994).

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