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Journal articles on the topic 'Intimal hyperplasia'

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Published: 4 June 2021
Last updated: 10 March 2023

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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 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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2

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

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3

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 (March 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. Candesartan, at doses of 50, 100, and 500 µg/kg/day, was delivered via an Alzet pump placed in the abdomen one week prior to aortic injury. There was no attenuation of the hyperplastic response of the aortic wall. However, at 50 µg/kg/day the rate of reendothelialisation was significantly increased. These data suggest that candesartan may exhibit pleiotropic effects on vascular wound healing, in addition to the well-known effect of attenuating the development of intimal hyperplasia.
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4

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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5

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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6

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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7

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 (January 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 placebo or varying regimens of clopidogrel, including chronic, pre-CEA bolus, chronic plus pre-CEA bolus, and chronic plus post-CEA bolus; a homocystine diet was used to elevate both plasma homocysteine and the degree of intimal hyperplasia. Platelet aggregation, platelet activity, and intimal hyperplasia were then assessed. Platelet aggregation was not decreased with chronic clopidogrel; however, it was decreased with pre-CEA bolus clopidogrel. Similarly, platelet activity was not inhibited by chronic clopidogrel but was inhibited by pre-CEA and chronic plus pre-CEA bolus clopidogrel. Neither chronic, pre-CEA bolus, chronic plus pre-CEA bolus, nor chronic plus post-CEA bolus clopidogrel resulted in a decrease in intimal hyperplasia. Although pre-CEA bolus clopidogrel resulted in a decrease in both platelet aggregation and activity, it was unable to decrease the development of intimal hyperplasia at any dose. Additional factors must therefore contribute to the pathologic development of intimal hyperplasia.
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8

Aydin, Unal, Murat Ugurlucan, Funda Gungor, Sedat Ziyade, Bekir Inan, Maciej Banach, Yusuf Kalko, and Tahsin Yasar. "Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model." Angiology 60, no. 3 (September 15, 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 total and low-density lipoprotein cholesterol levels ( P = .012 and P = .001, respectively), intima—media ratio ( P = .002), and intimal smooth muscle cell accumulation ( P < .05) in group 1. Luminal narrowing in animals in group 1 was significantly lower than that in animals in groups 2 and 3, but was higher than in animals in group 4 ( P = .009). Conclusions Atorvastatin suppresses intimal hyerplasia and aids in intimal regeneration by lowering blood lipids and intimal smooth muscle cell accumulation.
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9

Brody, Jerome I., and Nancy J. Pickering. "Pathobiology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (November 1989): 585–87. http://dx.doi.org/10.1016/0741-5214(89)90154-7.

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10

Haudenschild, Christian C. "Morphology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (November 1989): 591–92. http://dx.doi.org/10.1016/0741-5214(89)90157-2.

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11

Levitt, Adam B., Keith Robinson, Eric Wellons, Kin Man Lai, Jian Hua Cui, Brian Gannon, and David Rosenthal. "Prevention of intimal hyperplasia." Cardiovascular Radiation Medicine 5, no. 1 (January 2004): 34–37. http://dx.doi.org/10.1016/j.carrad.2004.03.002.

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12

Davies, M. G., and P. O. Hagen. "Pathobiology of intimal hyperplasia." British Journal of Surgery 81, no. 9 (September 1994): 1254–69. http://dx.doi.org/10.1002/bjs.1800810904.

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13

Sottiurai, V. S. "Can Intimal Hyperplasia and Distal Anastomotic Intimal Hyperplasia be Controlled and Prevented?" Annals of Vascular Surgery 21, no. 3 (May 2007): 289–91. http://dx.doi.org/10.1016/j.avsg.2007.03.001.

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14

Saroyan, R. M., M. P. Roberts, J. T. Light, I. L. Chen, M. Y. Vaccarella, D. J. Bang, P. Kvamme, et al. "Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (May 1, 1992): H1449—H1457. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1449.

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Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1449-H1457, 1992. The recovery of prostacyclin (prostaglandin I2, PGI2) synthesis and endothelium-derived relaxing factor (EDRF) activity, as demonstrated by acetylcholine (ACh)-induced relaxation, by rabbit aorta was examined up to 8 wk after balloon catheter-induced injury. Following injury, basal 6-keto-PGF1 alpha formation was decreased acutely; however, after 3 wk it was not different from control. Arachidonic acid-stimulated 6-keto-PGF1 alpha formation was decreased, returning to control levels at 3 and 8 wk for thoracic and abdominal aorta, respectively. ACh-induced relaxation did not return to control levels over the 8-wk study. Initiation of reendothelialization with a layer of hyperplastic endothelial cells overlying subendothelial fibrosis and intimal hyperplasia were present at 2-3 wk. Intimal hyperplasia appeared 2 wk after injury and progressed throughout the period of the study. These data indicate that following balloon catheter-induced injury the formation of both PGI2 and EDRF is reduced and that recovery follows a differential time course. In addition, the recovery of PGI2 formation did not coincide with the attenuation of intimal hyperplasia, whereas the relationship between EDRF formation and intimal hyperplasia is uncertain.
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15

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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16

Osgood, Michael J., Charles R. Flynn, Padmini Komalavilas, and Colleen Brophy. "Cell-permeant peptide inhibitors of vasospasm and intimal hyperplasia." Vascular 21, no. 1 (October 26, 2012): 46–53. http://dx.doi.org/10.1258/vasc.2011.201203.

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Outcomes from vein graft bypass are limited by graft failure, leading causes of which include intimal hyperplasia and vasospasm. intimal hyperplasia remains the most common cause of graft failure, but no therapeutic modalities have been shown to prevent intimal hyperplasia in humans. The small heat shock proteins are a class of naturally occurring proteins in vascular smooth muscle. These proteins have an integral role in maintenance of vascular tone and in cellular defense against various stressors. Transduction domains have enabled intracellular therapeutic delivery of peptide analogs of heat shock proteins, as well as peptide inhibitors of the kinases that phosphorylate these proteins. These cell-permeant peptides have been shown to prevent vasospasm and intimal hyperplasia in vitro. Since vascular bypass using vein grafts is analogous to autologous organ transplantation, ex vivo treatment of the vein graft with cell-permeant peptide inhibitors of vasospasm and intimal hyperplasia prior to implantation provides a unique opportunity for targeted treatment of the graft to improve patency.
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17

Hui, David. "Intimal Hyperplasia in Murine Models." Current Drug Targets 9, no. 3 (March 1, 2008): 251–60. http://dx.doi.org/10.2174/138945008783755601.

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18

HOOD, PHYLLIS B. "An Overview of Intimal Hyperplasia." Radiology 180, no. 2 (August 1991): 378. http://dx.doi.org/10.1148/radiology.180.2.378.

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19

Mills, B., T. Robb, and DF Larson. "Intimal hyperplasia: slow but deadly." Perfusion 27, no. 6 (June 29, 2012): 520–28. http://dx.doi.org/10.1177/0267659112452316.

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20

Rose, Marlene L. "Interferon-γ and Intimal Hyperplasia." Circulation Research 101, no. 6 (September 14, 2007): 542–44. http://dx.doi.org/10.1161/circresaha.107.160911.

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21

Lee, Samuel, and Richard T. Lee. "Mechanical Stretch and Intimal Hyperplasia." Arteriosclerosis, Thrombosis, and Vascular Biology 30, no. 3 (March 2010): 459–60. http://dx.doi.org/10.1161/atvbaha.109.201509.

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22

Lemson, M. S., J. H. M. Tordoir, M. J. A. P. Daemen, and P. J. E. H. M. Kitslaar. "Intimal Hyperplasia in Vascular Grafts." European Journal of Vascular and Endovascular Surgery 19, no. 4 (April 2000): 336–50. http://dx.doi.org/10.1053/ejvs.1999.1040.

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23

Greisler, Howard P. "Vascular prosthesis/healing/intimal hyperplasia." Journal of Vascular Surgery 20, no. 1 (July 1994): 131–32. http://dx.doi.org/10.1016/0741-5214(94)90193-7.

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24

LaMuraglia, Glenn M. "Pharmacologic suppression of intimal hyperplasia." Journal of Vascular Surgery 20, no. 6 (December 1994): 1010–11. http://dx.doi.org/10.1016/0741-5214(94)90247-x.

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25

Gibbons, Gary H. "Restenosis: Remodeling Versus Intimal Hyperplasia." Journal of Vascular and Interventional Radiology 7, no. 1 (January 1996): 55–62. http://dx.doi.org/10.1016/s1051-0443(96)70027-1.

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26

Newby, Andrew C., and Alla B. Zaltsman. "Molecular mechanisms in intimal hyperplasia." Journal of Pathology 190, no. 3 (February 2000): 300–309. http://dx.doi.org/10.1002/(sici)1096-9896(200002)190:3<300::aid-path596>3.0.co;2-i.

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27

Bundens, W. P., and Y. Wolf. "The etiology of intimal hyperplasia." Medical Hypotheses 43, no. 5 (November 1994): 343–46. http://dx.doi.org/10.1016/0306-9877(94)90114-7.

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28

Hariri, R. J., D. R. Alonso, D. P. Hajjar, D. Coletti, and M. E. Weksler. "Aging and arteriosclerosis. I. Development of myointimal hyperplasia after endothelial injury." Journal of Experimental Medicine 164, no. 4 (October 1, 1986): 1171–78. http://dx.doi.org/10.1084/jem.164.4.1171.

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Old Fischer 344 rats are more susceptible to vascular lesions after arterial endothelial injury than are young animals. Thus, 20-26-mo-old Fischer 344 rats developed greater and more persistent intimal proliferative lesions than did 2-5-mo-old rats after aortic endothelial denudation. 3 d after deendothelialization, intimal thickness was increased two-fold in both old and young animals. However, 14 d after endothelial injury, intimal thickness had increased nearly five times in old animals, but had regressed to normal in young animals. Intimal thickness of young aortic grafts transplanted into young recipients did not differ significantly from adjacent host aorta or autotransplanted aortic segments 6 wk after surgery. In contrast, intimal thickness of old grafts transplanted into young recipients was eight times greater than adjacent young host aorta 6 wk after surgery. The density of cell nuclei in the intima of old grafts was also much greater than that in young grafts. Thus, in two experimental models of vascular injury, old rats have consistently had greater myointimal hyperplasia than young rats. The increased proliferative response of aortic smooth muscle cells after vascular injury of old animals may contribute to the increased prevalence of vascular disease with age.
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29

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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30

Galarza-Delgado, D. Á., J. R. Azpiri-López, I. J. Colunga-Pedraza, D. E. Flores Alvarado, O. Ilizaliturri Guerra, P. F. Frausto Lerma, A. Pérez Villar, M. A. Reyes Soto, I. C. Zárate Salinas, and A. C. Garza Acosta. "AB1212 PREVALENCE OF CAROTID SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH PSORIATIC ARTHRITIS VS RHEUMATOID ARTHRITIS: A CASE CONTROL STUDY." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1897. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5197.

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Background:Rheumatic diseases such as Psoriatic Arthritis (PsA) and Rheumatoid Arthritis (RA) are associated with increased morbidity and mortality, mainly due to cardiovascular causes. Cardiovascular outcomes in patients with PsA and RA cannot be completely explained by traditional cardiovascular risk factors, suggesting that the systemic inflammation that characterizes these diseases may have an important role on accelerated atherosclerosis.1Objectives:To compare carotid intima-media thickness (cIMT) and asymptomatic carotid plaque (CP) prevalence, between patients with PsA, RA and controls.Methods:Cross-sectional observational study. Seventy patients, aged 35-75 years, with PsA and RA who fulfilled the CASPAR and ACR/EULAR 2010 classification criteria, respectively, who were active on a cardio-rheuma preventive clinic were recruited, matched with 70 healthy controls. All groups underwent a noninvasive examination using B-mode ultrasonography of the right and left common carotid artery. CP was defined as a focal narrowing ≥0.5 mm of the surrounding lumen or cIMT ≥1.2 mm; hyperplasia of the carotid intima was defined as cIMT ≥ 0.9 mm to 1.1 mm. Descriptive data were analyzed by continuous and categorical variables. Continuous variables with normal distribution are shown as mean ± standard deviation (SD), and non-normal distribution as median and quartiles (25q-75q). ANOVA, Kruskal Wallis,X2and Mann-Whitney U were used to compared data. Apvalue ≤0.05 was considered statistically significant. Statistical analysis was done using SPSS version 24 (IBM Corp., Armonk, NY, USA).Results:Clinical and demographic characteristics are shown in Table 1. The global prevalence of carotid atherosclerosis was 25.7% and 38.6% in RA and PsA respectively, and 27.1% in controls (p=0.170). Intimal hyperplasia was found in 20%, 12.9% and 0% in RA, PsA and controls (p=0.001), respectively (Table 2).Table 1.Clinical and demographic characteristicsRAn=70PsAn=70Controlsn=70PvalueGender Male9 (12.9%)31 (44.4%)11 (15.7%)<0.001 Female61 (87.1%)39 (55.7%)59 (84.3%)Age, years54.51±9.65753.1±10.8753.54±7.48NSBody Mass Index, BMI, kg/m228.99 (25.95-32.34)29.04 (26.23-31.92)27.44 (24.98-30.95)NSComorbidities Diabetes Mellitus11 (15.7%)14 (20%)8 (11.4%)NS Hypertension24 (34.3%)27 (38.6%)15 (21.4%)NS Dyslipidemia19 (27.1%)30 (42.9%)18 (25.7%)NS Active smoker7 (10%)16 (22.9%)15 (21.4%)NSDisease duration Duration, years8.45 (3.34-15.88)5 (2.75-8)-0.005Statins9 (12.9%)12 (17.1%)10 (14.3%)NSTable 2.Ultrasonographic characteristicsRAn=70PsAn=70Controlsn=70PvalueRight CIMT, mm0.8 (0.6-1.1)0.6 (0.5-0.9)0.6 (0.5-0.8)<0.001Left CIMT, mm0.8 (0.6-0.9)0.6 (0.5-0.7)0.6 (0.5-1.2)0.002Any Hyperplasia14 (20%)9 (12.9%)00.001Right intimal hyperplasia7 (10%)5 (7.1%)00.021Left intimal hyperplasia13 (18.6%)2 (2.9%)0<0.001Any plaque18 (25.7%)27 (38.6%)19 (27.1%)NSConclusion:This study shows the high prevalence of asymptomatic atherosclerosis in RA and PsA compared to general population. Even though it was shown a higher prevalence of CP in PsA, subclinical atherosclerosis in RA patients may have an increased clinical significance. The presence of carotid plaque between groups was not statistically significant. We observed increased prevalence of carotid intimal hyperplasia in RA and PsA compared with age-matched controls. We emphasize the value of ultrasonography in the detection of early atherosclerosis lesions.References:[1]Wah-Suarez, M. I., et.al. (2019). Carotid ultrasound findings in rheumatoid arthritis and control subjects: A case-control study.International Journal of Rheumatic Diseases,22(1), 25–31.Disclosure of Interests:None declared
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31

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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Van der Geest, K., F. Borg, K. Wolfe, W. A. Schmidt, R. Luqmani, and B. Dasgupta. "FRI0195 ULTRASONOGRAPHIC HALO SCORE ASSOCIATES WITH INTIMAL HYPERPLASIA IN GIANT CELL ARTERITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 680.3–681. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2963.

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Background:We have recently developed a novel ultrasonographic Halo Score to quantify the extent of vascular inflammation in GCA [1]. High Halo Scores were associated with a high rate of ocular ischaemia among patients with GCA. Earlier studies have shown that GCA patients with intimal hyperplasia in their temporal artery biopsy (TAB) are at the highest risk of neuro-ophthalmic, ischaemic complications [2,3]. We therefore questioned whether the ultrasonographic Halo Score might be linked to the presence of intimal hyperplasia in patients with GCA.Objectives:To investigate the relationship between the ultrasonographic Halo Score and intimal hyperplasia.Methods:This is a prospective study including 92 patients suspected of having GCA, who underwent both ultrasound of temporal/axillary arteries and TAB at diagnosis. Ultrasonographic halo counts and Halo Scores were determined [1]. An experienced pathologist determined whether or not the TAB findings were consistent with GCA. TABs were systematically evaluated for the presence of a transmural infiltrate and intimal hyperplasia. Multiple linear regression analysis was performed with either halo counts or Halo Scores as the dependent variable. Predictive variables included the presence of a transmural TAB infiltrate, intimal hyperplasia and male sex.Results:The TAB was consistent with GCA in 27 patients. The TAB revealed transmural inflammation in 18 patients and giant cells in 24 patients. Intimal hyperplasia was found in 20 patients with a positive TAB. Patients with a positive TAB showed higher halo counts and Halo Scores than patients with a negative TAB. Overall, patients with a positive TAB and intimal hyperplasia presented with the highest halo counts and Halo Scores (Figure). Among patients with a positive TAB, only intimal hyperplasia and male sex were predictive of higher halo counts and Halo Scores in the multiple linear regression analysis. Ocular ischaemia was present in 14% of patients with a positive TAB without intimal hyperplasia. However, 40% of patients with a positive TAB and intimal hyperplasia suffered from ocular ischaemia.Conclusion:The ultrasonographic Halo Score is strongly influenced by the presence of intimal hyperplasia, a TAB feature that associates with cranial ischemic complications in patients with GCA [2,3].References:[1]van der Geest KSM, Borg F, Kayani A, Paap D, Gondo P, Schmidt W, et al. Novel ultrasonographic Halo Score for giant cell arteritis: assessment of diagnostic accuracy and association with ocular ischaemia. Annals of the Rheumatic Diseases 2020 Jan 3.[2]Makkuni D, Bharadwaj A, Wolfe K, Payne S, Hutchings A, Dasgupta B. Is intimal hyperplasia a marker of neuro-ophthalmic complications of giant cell arteritis? Rheumatology (Oxford, England) 2008 Apr;47(4):488-490.[3]Kaiser M, Weyand CM, Bjornsson J, Goronzy JJ. Platelet-derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis. Arthritis and Rheumatism 1998 Apr;41(4):623-633.FigureDisclosure of Interests:Kornelis van der Geest Speakers bureau: Roche (2019), Frances Borg: None declared, Konrad Wolfe: None declared, Wolfgang A. Schmidt Grant/research support from: GSK, Novartis, Roche, Sanofi, Consultant of: GSK, Novartis, Roche, Sanofi, Chugai, Raashid Luqmani Grant/research support from: Arthritis UK, the Medical Research Council, the University of California San Francisco/Oxford Invention Fund, the Canadian Institutes of Health Research, The Vasculitis Foundation, GSK, Consultant of: GSK, Medpace, MedImmune, Roche, Bhaskar Dasgupta Grant/research support from: Roche, Consultant of: Roche, Sanofi, GSK, BMS, AbbVie, Speakers bureau: Roche
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33

Allon, Michael, Silvio H. Litovsky, Yingying Zhang, Ha Le, Alfred K. Cheung, and Yan-Ting Shiu. "Association of Preexisting Arterial Intimal Hyperplasia with Arteriovenous Fistula Outcomes." Clinical Journal of the American Society of Nephrology 13, no. 9 (August 23, 2018): 1358–63. http://dx.doi.org/10.2215/cjn.13431217.

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Background and objectivesPreoperative arterial function is associated with arteriovenous fistula (AVF) development. Because arterial pathology may correlate with its function, preexisting arterial intimal hyperplasia may be associated with AVF development.Design, setting, participants, & measurementsVascular specimens obtained from 125 patients (with minimal 2 mm arterial diameter and 2.5 mm venous diameter) undergoing AVF creation were quantified for arterial intimal hyperplasia, arterial medial fibrosis, arterial microcalcification, and venous intimal hyperplasia. A 6-week postoperative ultrasound quantified AVF diameter, blood flow, and stenosis. Clinical AVF maturation was assessed using a predefined protocol. In a prospective cohort study design, we investigated the association of preexisting arterial intimal hyperplasia with the postoperative AVF diameter, blood flow, stenosis, and clinical maturation failure, after controlling for baseline demographics, comorbidities, and preoperative vein diameter. Additional analyses evaluated whether other vascular pathologies interacted with arterial intimal hyperplasia in affecting AVF outcomes.ResultsThe median intimal thickness of the native artery was 22.0 μm (interquartile range, 14.8–37.1 μm). The median postoperative AVF diameter was 4.8 (interquartile range, 3.7–6.8) mm, blood flow was 796 (interquartile range, 413–1036) ml/min, and stenosis was present in 37 out of 98 patients with ultrasound data (38%). AVF nonmaturation occurred in 37 out of 125 patients (30%). Preexisting arterial intimal thickness was not significantly associated with AVF blood flow (−12 ml/min; 95% confidence interval [95% CI], −55 to 30 ml/min), diameter (−0.04 mm; 95% CI, −0.21 to 0.14 mm), stenosis (odds ratio, 0.93; 95% CI, 0.75 to 1.14), or clinical maturation failure (odds ratio, 1.07; 95% CI, 0.90 to 1.28), all per 10 μm increase. There was no significant interaction of preexisting arterial intimal thickness and postoperative AVF outcomes with arterial medial fibrosis, arterial microcalcification, or venous intimal hyperplasia.ConclusionsPreexisting arterial intimal hyperplasia is not associated with the 6-week AVF blood flow, diameter or stenosis, or clinical maturation when the preoperative arterial diameter is ≥2 mm.
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34

Kemahli, Mustafa Baris, Tugra Gencpinar, Huseyin Dursun, Cagatay Bilen, Pinar Akokay, Serdar Bayrak, and Abidin Cenk Erdal. "Effects Of Rivaroxaban And Apixaban On Intimal Hyperplasia In Rabbits." Turkish Journal of Vascular Surgery 31, no. 3 (November 15, 2022): 148–56. http://dx.doi.org/10.9739/tjvs.2022.09.03.

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Aim: Intimal hyperplasia causes vascular occlusion and its optimal treatment is unknown. In this study, we evaluated the effectiveness of Apixaban and Rivaroxaban treatment for preventing intimal hyperplasia in rabbits. Material and Methods: The rabbits (n = 15) were randomly divided into three groups. Reanastomoses are applied to the carotid artery. All groups received 100 U/kg heparin sodium during the operation period. Group A (n = 5) as a control group had no medication. Group B (n = 5) was given Rivaroxaban 3 mg/kg/day. In-group C (n = 5) Apixaban was administered per orally 10 mg/kg. At the end of the treatment on the 28th day, carotid artery specimens were excised and evaluated histologically. Results: Increased intima thickness was observed in the control group than the drug groups (P=0.019, P=0.007). It was found that there was no difference between groups in terms of lumen diameter, lumen area, tunica media area and tunica media thickness. There was difference between groups in terms of caspase 3 or TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) staining (p<0.05). Conclusion: Apixaban and Rivaroxaban may have protective efficacy against intimal hyperplasia after vascular surgical intervention.
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35

Zhang, Dechuan, Tieying Yin, Feifei Du, Dingyuan Du, Lili Tan, Hans Gregersen, and Guixue Wang. "EVALUATION OF INTIMAL HYPERPLASIA AND THROMBOSIS AFTER IMPLANTATION OF PLATELET GLYCOPROTEIN IIIa MONOCLONAL ANTIBODY-ELUTING STENT IN NEW ZEALAND WHITE RABBIT AORTA OR ILIAC ARTERIES." Biomedical Engineering: Applications, Basis and Communications 27, no. 05 (October 2015): 1550046. http://dx.doi.org/10.4015/s1016237215500465.

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Since the percutaneous coronary intervention (PCI) was first introduced into China in 1984, this procedure has become widely accepted as an important step in coronary revascularization. This study aims to evaluate intimal hyperplasia and thrombosis after implantation of platelet glycoprotein IIIa monoclonal antibody (mAb)-eluting stent in the New Zealand white rabbit abdominal aorta or iliac artery by comparing CT angiography and pathological experiments. The antibody-eluting stents were prepared by the passive absorption method. Arterial intima in the stented segment and 0.5 cm adjacent to the stented site were observed and analyzed by scanning electron microscopy (SEM) and cross-sectional staining. Endothelialization and thrombosis on the stent surface were visualized by CT angiography and three-dimensional (3D) reconstruction technique in animals surviving from 1 to 12 weeks. Compared to stainless steel stents, the surface of antibody-eluting stents was covered with a complete endothelial layer after four weeks. Both CT angiography and pathological results showed intimal hyperplasia (p < 0.05) after 12 weeks. Therefore, pathological methods are the goldern standard for evaluation of intimal hyperplasia while CT angiography has a higher specificity in demonstrating the intimal changes after stent implantation for 12 weeks. The mAb-eluting stent has the potential to prevent thrombosis formation due to the interaction of stent with blood, and decreases the stenosis ratio by inhibiting neointima proliferation.
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36

Nakagawa, H., K. Kichikawa, K. Takayama, M. Sakamoto, T. Wada, T. Taoka, A. Fukusumi, S. Iwasaki, H. Uchida, and T. Sakaki. "Palmaz Stent Deployment for Subclavian and Brachiocephalic Arterial Occlusive Disease." Interventional Neuroradiology 7, no. 1_suppl (December 2001): 49–52. http://dx.doi.org/10.1177/15910199010070s106.

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Palmaz stent deployment is a useful method for subclavian and brachiocephalic arterial occlusive disease. We evaluated restenosis or intimal thickening after Palmaz stent deployment for nine lesions of subclavian or brachiocephalic arterial occlusive disease focusing on stent diameter, atheroma thickness near the stent, and degree of coverage for the lesion. Follow up DSA and IVUS at 5–14 months (mean 9) after therapy showed no significant changes in the size or shape of the stent itself. There were two lesions of thin in-stent intimal hyperplasia and five lesions of thick hyperplasia. There was no close relationship between intimal hyperplasia and stent diameter or atheroma size (relative thickness). There was some relationship between the degree of coverage of the lesion by the stent and degree of intimal hyperplasia, but to determine statistical significance, accumulation of a greater number of cases is necessary.
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37

Pyo, Robert, Yuichiro Sato, Nigel Mackman, and Mark Taubman. "Mice deficient in tissue factor demonstrate attenuated intimal hyperplasia in response to vascular injury and decreased smooth muscle cell migration." Thrombosis and Haemostasis 92, no. 09 (2004): 451–58. http://dx.doi.org/10.1160/th04-02-0122.

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SummaryTissue factor (TF) is the primary initiator of the coagulation cascade and is thought to play a key role in the generation of arterial thrombosis. Recent studies have suggested that TF mediates inflammatory processes in the arterial wall and may be an important regulator of intimal hyperplasia. We have employed genetically engineered mice (mTF−/−/hTF+) with markedly diminished TF activity (≈1% normal levels) to examine the role of TF in mediating the response to arterial injury. mTF−/−/hTF+ displayed a marked reduction in intimal hyperplasia (46% decrease in intimal area, 60% decrease in intimal/medial ratio) in response to femoral artery injury when compared to wild type controls. The decreased intimal hyperplasia seen in low TF mice was noted in a model of vascular injury not associated with significant thrombosis, suggesting that it may be mediated by non-procoagulant properties of TF. Smooth muscle cells from mTF−/−/hTF+ mice grew normally in response to serum, but exhibited a marked defect in cell migration in a modified Boyden chamber assay. In contrast, there was no difference in platelet derived growth factorinduced migration, suggesting that the effect of TF on smooth muscle cell migration is agonist dependent. These data suggest that TF may mediate intimal hyperplasia by regulating smooth muscle cell migration.
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38

Kleinert, Leigh B., James B. Hoying, and Stuart K. Williams. "The Neointima Formed in Endothelial Cell Sodded ePTFE Vascular Grafts Results from Both Cellular-Hyperplasia and Extracellular-Hypertrophy." Cell Transplantation 5, no. 4 (July 1996): 475–82. http://dx.doi.org/10.1177/096368979600500406.

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Endothelial cell transplantation onto polymeric vascular grafts results in the formation of a neointima. The formation of this neointima is often suggested to result from a chronic cellular hyperplasia where the terms intimal hyperplasia and intimal thickening are used interchangeably. While the formation of a midgraft neointima in sodded grafts involves a level of cell proliferation, the synthesis and deposition of extracellular matrix proteins is also a ubiquitous observation in these grafts. To assess the composition of midgraft neointima in sodded grafts, a morphometric method was developed to provide a differential quantitation of the cellular-hyperplastic and extracellular-hypertrophic elements of intimal thickening. The formed neointima on microvessel endothelial cell sodded and control (noncell-treated) ePTFE vascular grafts was quantified after 3, 12, and 52 wk of graft implantation in a canine carotid artery model. Midgraft sections of grafts were evaluated for both intimal thickness (IT) and cell density per unit volume and quantified using a PC-based image analysis program. Sodded grafts explanted at 3 wk exhibited an average neointimal cell density (3 × 109 cells/cm3; IT 30 μm) equivalent to cell densities observed in normal arterial media. After 12 wk the mean cell density approached a hyperplastic value (3.7 × 109 cells/cm3; IT 76 μm), while grafts explanted after 52 wk exhibited a mean cell density (2.8 × 109 cells/cm3; IT 30 μm) similar to 3-wk values. Control grafts that received no cells exhibited no midgraft cellular coverage. These results indicate that neointima formation in the midgraft region of sodded grafts occurred via mechanisms involving both a cellular hyperplasia and an extracellular hypertrophy. Differential responses occur presumably due to localized differences in cellular proliferation and cellular biosynthetic activity.
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39

Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 2 (1996): 229–33. http://dx.doi.org/10.3109/02841859609173451.

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40

Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 2 (January 1996): 229–33. http://dx.doi.org/10.1080/02841859609173451.

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41

Giddens, Don P. "Hemodynamic Factors and Anastomotic Intimal Hyperplasia." Journal of Vascular and Interventional Radiology 10, no. 7 (July 1999): 975–77. http://dx.doi.org/10.1016/s1051-0443(99)70163-6.

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42

Mylonaki, Ioanna, Elisabeth Allain, Francesco Strano, Eric Allémann, Jean-Marc Corpataux, Paolo Meda, Olivier Jordan, et al. "Evaluating intimal hyperplasia under clinical conditions." Interactive CardioVascular and Thoracic Surgery 27, no. 3 (March 30, 2018): 427–36. http://dx.doi.org/10.1093/icvts/ivy101.

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43

Salame, MY, RS More, NJ Samani, and DP deBono. "The Plasminogen Activators in Intimal Hyperplasia." Clinical Science 93, s37 (August 1, 1997): 30P. http://dx.doi.org/10.1042/cs093030pa.

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44

Hanratty, Colm G., Melanie Murrell, Levon M. Khachigian, Philip S. Tsao, and Michael R. Ward. "Low flow promotes instent intimal hyperplasia." Atherosclerosis 177, no. 2 (December 2004): 269–74. http://dx.doi.org/10.1016/j.atherosclerosis.2004.07.016.

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45

&NA;. "IL-10 reduces postinjury intimal hyperplasia." Inpharma Weekly &NA;, no. 1235 (April 2000): 8. http://dx.doi.org/10.2165/00128413-200012350-00018.

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46

Che Man, Rohaina, Nadiah Sulaiman, Mohamad Fikeri Ishak, Ruszymah Bt Hj Idrus, Mohd Ramzisham Abdul Rahman, and Muhammad Dain Yazid. "The Effects of Pro-Inflammatory and Anti-Inflammatory Agents for the Suppression of Intimal Hyperplasia: An Evidence-Based Review." International Journal of Environmental Research and Public Health 17, no. 21 (October 26, 2020): 7825. http://dx.doi.org/10.3390/ijerph17217825.

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Anti-atherogenic therapy is crucial in halting the progression of inflammation-induced intimal hyperplasia. The aim of this concise review was to methodically assess the recent findings of the different approaches, mainly on the recruitment of chemokines and/or cytokine and its effects in combating the intimal hyperplasia caused by various risk factors. Pubmed and Scopus databases were searched, followed by article selection based on pre-set inclusion and exclusion criteria. The combination of keywords used were monocyte chemoattractant protein-1 OR MCP-1 OR TNF-alpha OR TNF-α AND hyperplasia OR intimal hyperplasia OR neointimal hyperplasia AND in vitro. These keywords combination was incorporated in the study and had successfully identified 77 articles, with 22 articles were acquired from Pubmed, whereas 55 articles were obtained from Scopus. However, after title screening, only twelve articles meet the requirements of defined inclusion criteria. We classified the data into 4 different approaches, i.e., utilisation of natural product, genetic manipulation and protein inhibition, targeted drugs in clinical setting, and chemokine and cytokines induction. Most of the articles are working on genetic manipulation targeted on specific pathway to inhibit the pro-inflammatory factors expression. We also found that the utilisation of chemokine- and cytokine-related treatments are emerging throughout the years. However, there is no study utilising the combination of approaches that might give a better outcome in combating intimal hyperplasia. Hopefully, this concise review will provide an insight regarding the usage of different novel approaches in halting the progression of intimal hyperplasia, which serves as a key factor for the development of atherosclerosis in cardiovascular disease.
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Zhang, Bao-fu, Zi-heng Wu, Jie Deng, Hao-jie Jin, Wei-biao Chen, Sai Zhang, Xiu-jie Liu, Wan-tie Wang, and Xiang-tao Zheng. "M6A methylation-mediated elevation of SM22α inhibits the proliferation and migration of vascular smooth muscle cells and ameliorates intimal hyperplasia in type 2 diabetes mellitus." Biological Chemistry 403, no. 3 (December 7, 2021): 317–29. http://dx.doi.org/10.1515/hsz-2021-0296.

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Abstract Abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by insulin resistance facilitates intimal hyperplasia of type 2 diabetes mellitus (T2DM) and N6-methyladenosine (m6A) methylation modification mediates the VSMC proliferation. This study aimed to reveal the m6A methylation modification regulatory mechanism. In this study, m6A demethylase FTO was elevated in insulin-treated VSMCs and T2DM mice with intimal injury. Functionally, FTO knockdown elevated m6A methylation level and further restrained VSMC proliferation and migration induced by insulin. Mechanistically, FTO knockdown elevated Smooth muscle 22 alpha (SM22α) expression and m6A-binding protein IGF2BP2 enhanced SM22α mRNA stability by recognizing and binding to m6A methylation modified mRNA. In vivo studies confirmed that the elevated m6A modification level of SM22α mRNA mitigated intimal hyperplasia in T2DM mice. Conclusively, m6A methylation-mediated elevation of SM22α restrained VSMC proliferation and migration and ameliorated intimal hyperplasia in T2DM.
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48

Light, J. T., J. A. Bellan, I. L. Chen, L. L. Longenecker, W. A. Murphy, D. H. Coy, P. J. Kadowitz, and D. B. McNamara. "Angiopeptin enhances acetylcholine-induced relaxation and inhibits intimal hyperplasia after vascular injury." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1265—H1274. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1265.

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The effects of the somatostatin analogue, angiopeptin (BIM-23014), on neoendothelial function, as evidenced by formation of prostaglandin (PG) I2 and by acetylcholine-induced relaxation (formation of endothelial-derived relaxing factor), were investigated in the rabbit aorta. A balloon catheter injury of the thoracic and abdominal aorta was induced in New Zealand White rabbits. Animals treated with angiopeptin for 2 or 4 wk were compared with untreated rabbits at 2 or 4 wk after the induction of injury, as well as to sham-operated controls. When the rabbits were killed, vascular rings were assessed for arachidonic acid-stimulated PGI2 formation, acetylcholine-induced relaxation, and the degree of intimal hyperplasia. Vascular rings from animals treated with angiopeptin exhibited enhanced acetylcholine-induced relaxation; however, angiopeptin treatment had no effect on arachidonic acid-stimulated PGI2 formation. Intimal hyperplasia in treated animals was reduced by 36%. Treatment with another somatostatin analogue, BIM-23030, did not enhance relaxation or inhibit intimal hyperplasia. These data suggest that treatment with angiopeptin may inhibit intimal hyperplasia in part by its beneficial effect on neoendothelial function.
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Asfar, Sami, Ali Shuaib, Fatemah Al-Otaibi, Sora S. Asfar, and Narayana Kilarkaje. "A New Technique to Induce Experimental Myointimal Hyperplasia." Medical Principles and Practice 27, no. 5 (2018): 415–19. http://dx.doi.org/10.1159/000492575.

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Background: Arterial myointimal hyperplasia (MIH) has a significant impact on the long-term outcomes of vascular procedures such as bypass surgery and angioplasty. In this study, we describe a new and innovative technique to induce MIH using a dental flossing cachet in Wistar rats. Methods: The intimal damage in the common carotid artery was induced by inserting the tip of the dental flossing cachet through the external carotid artery into the common carotid artery and turning it on for 3 rounds of 20 s each (n = 10). After 2 weeks, the rats were anesthetized and the common carotid arteries of the experimental side and the contralateral side (control) were harvested and preserved for histopathological studies. Results: The experimental carotid arteries showed significant intimal proliferation and thickening compared to the controls. The intima/media ratio of the experimental and normal (control) common carotid arteries were 1.274 ± 0.162 and 0.089 ± 0.023 (mean ± SEM), respectively (p < 0.001). Conclusion: This technique is simple, inexpensive, and highly reproducible and it induces sufficient MIH to study this phenomenon in animal models.
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Todorov, S. S., R. V. Sidorov, E. P. Talalaev, and I. F. Shlyk. "The role of glycosaminoglycanes in the development of intimal hyperplasia in the shunting of coronary arteries." Medical Herald of the South of Russia 9, no. 3 (October 1, 2018): 94–98. http://dx.doi.org/10.21886/2219-8075-2018-9-3-94-98.

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The article is devoted to the study of the role of glycosaminoglycans (hyaluronic acid, heparan sulfate derivatives, dermatan sulfate) in the genesis of intimal arterial hyperplasia. It is shown that these substances play important role in the structural reorganization of vessels, including the development of intimal hyperplasia of the arteries. Scientific works on the role of GAG in the genesis of intimal hyperplasia are based on experimental data. The authors draw attention to GAG involvement in cell-intercell nteractions of artery walls, including proliferation, migration, signal transduction of smooth muscle cells, endotheliocytes, platelets. Undoubtedly, attempts to create a 3D shunt with hyaluronate, atorvastatin can be used in the clinic for full and longterm use, which can prevent the development of restenosis of the arteries.
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