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Relevant bibliographies by topics / Graft vasculopathy

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Academic literature on the topic 'Graft vasculopathy'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Graft vasculopathy"

1

Ii, Masaaki, and Douglas W. Losordo. "Transplant Graft Vasculopathy." Circulation 108, no. 25 (December 23, 2003): 3056–58. http://dx.doi.org/10.1161/01.cir.0000108160.88358.65.

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2

Hamano, Kimikazu, Hisashi Bashuda, Hiroshi Ito, Bungo Shirasawa, Kou Okumura, and Kensuke Esato. "Graft Vasculopathy and Tolerance: Does the Balance of Th Cells Contribute to Graft Vasculopathy?" Journal of Surgical Research 93, no. 1 (September 2000): 28–34. http://dx.doi.org/10.1006/jsre.2000.5967.

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Kaufman, C. L., R. Ouseph, B. Blair, J. E. Kutz, T. M. Tsai, L. R. Scheker, H. Y. Tien, et al. "Graft Vasculopathy in Clinical Hand Transplantation." American Journal of Transplantation 12, no. 4 (February 11, 2012): 1004–16. http://dx.doi.org/10.1111/j.1600-6143.2011.03915.x.

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Sakhovsky, S. A., N. N. Koloskova, A. Yu Goncharova, and B. L. Mironkov. "Intravascular visualization methods in estimating vasculopathy of a transplanted heart." Russian Journal of Transplantology and Artificial Organs 21, no. 1 (May 18, 2019): 165–68. http://dx.doi.org/10.15825/1995-1191-2019-1-165-168.

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One of the pathognomonic signs of сardiac allograft vasculopathy is concentric intimal hyperplasia, which can be assessed by intravascular imaging techniques. Early detection of cardiac graft vasculopathy and timely correction of immunosuppressive therapy can help slow the pathological process and, as a result, increase the functional survival of the heart graft. Recently, the method of intravascular optical coherence tomography, which improves the accuracy of the assessment of the layers of the vascular wall and is considered as an alternative to intravascular ultrasound, is becoming more and more common. This review focuses on the importance of modern methods of intravascular imaging in the early diagnosis of cardiac graft vasculopathy and the identification of predictors of this disease.

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Hsu, D. T., J. M. Lamour, R. Korsin, S. Mital, J. Nova, R. Rodriguez, and L. J. Addonizio. "Long term incidence of graft vasculopathy in children." Journal of Heart and Lung Transplantation 21, no. 1 (January 2002): 173. http://dx.doi.org/10.1016/s1053-2498(01)00763-x.

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Kaplon, R. J., S. R. Kapadia, N. G. Smedira, T. Buda, M. Goormastic, E. M. Tuzcu, and P. M. McCarthy. "Does LVAD bridging-to-transplantation increase graft vasculopathy?" Journal of Heart and Lung Transplantation 18, no. 1 (January 1999): 63. http://dx.doi.org/10.1016/s1053-2498(99)80123-5.

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Bushell, Andrew. "TGF-?? AND GRAFT VASCULOPATHY: WHERE TO FROM HERE?" Transplantation 73, no. 10 (May 2002): 1534–36. http://dx.doi.org/10.1097/00007890-200205270-00002.

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8

Sucher, Robert, Theresa Hautz, Elisabeth Mohr, Maximilian Mackowitz, Vanessa Mellitzer, Christina Steger, Benno Cardini, et al. "Sodium Sulfite Exacerbates Allograft Vasculopathy and Affects Tryptophan Breakdown in Murine Heterotopic Aortic Transplantation." Oxidative Medicine and Cellular Longevity 2019 (April 8, 2019): 1–11. http://dx.doi.org/10.1155/2019/8461048.

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Graft vasculopathy is the main feature of chronic rejection in organ transplantation, with oxidative stress being a major trigger. Inflammation-associated prooxidant processes may be controlled by antioxidants; however, interference with redox-regulated mechanisms is a complex endeavor. An essential feature of the cellular immune response is the acceleration of tryptophan (Trp) breakdown, leading to the formation of several bioactive catabolites. Long-term activation of this immunobiochemical pathway contributes to the establishment of a tolerogenic environment, thereby supporting allograft survival. Herein, the impact of the antioxidant sodium sulfite on the development of graft vasculopathy was assessed in murine aortic transplantation. Allogeneic (BALB/c to C57BL/6) heterotopic murine aortic transplantations were performed. Animals were left untreated or were treated with 10 μl of 0.1 M, of 0.01 M sodium sulfite, or of 0.1 M sodium sulfate, intraperitoneally once/day, until postoperative day (POD) 100. Grafts were assessed by histology, immunohistochemistry, and adhesion molecule gene expression. Serum concentrations of tryptophan and its catabolite kynurenine (Kyn) were measured. On day 100, graft vasculopathy was significantly increased upon treatment with 0.1 M sodium sulfite, compared to allogeneic untreated controls (p=0.004), which correlated with a significant increase ofα-smooth-muscle-actin, Vcam-1, and P-selectin. Serum Kyn concentrations increased in the allogeneic control group over time (p<0.05,POD≥50), while low-dose sodium sulfite treatment (0.01 M) treatment resulted in a decrease in Kyn levels over time (p<0.05,POD≥10), compared to the respective baselines (p<0.05). Longitudinal analysis of serum metabolite concentrations in the different treatment groups further identified an overall effect of sodium sulfite on Kyn concentrations. Antioxidative treatment may result in ambivalent consequences. Our data reveal that an excess of antioxidants like sodium sulfite can aggravate allograft vasculopathy, which further highlights the challenges associated with interventions that interfere with the complex interplay of redox-regulated inflammatory processes.

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Ambrosi, Pierre, Bernard Kreitmann, and Gilbert Habib. "Resting heart rate: A predictor of graft vasculopathy? Reply." International Journal of Cardiology 145, no. 3 (December 2010): 505. http://dx.doi.org/10.1016/j.ijcard.2009.12.007.

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Bowen, Theodore, Shawn A. Silver, and Cathy Sila. "Rapidly Progressive Intracranial Vasculopathy in Graft Versus Host Disease." Journal of Stroke and Cerebrovascular Diseases 28, no. 6 (June 2019): e73-e74. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2019.02.017.

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More sources

Dissertations / Theses on the topic "Graft vasculopathy"

1

Lieder, Anja. "The lymphocyte reconstituted severe combinmed immunodeficient mouse as a model of human allograft vasculopathy." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275269.

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2

Wang, Hui-Tzu Lin. "Estudo sequencial do perfil de expressão gênica em biópsias endomiocárdicas parafinadas: associação com rejeição humoral e vasculopatia do aloenxerto cardíaco." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/98/98131/tde-16032015-085220/.

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O transplante cardíaco é a última opção terapêutica para pacientes portadores de insuficiência cardíaca grave. Apesar dos avanços na terapia imunossupressora, a rejeição continua sendo o principal obstáculo para o sucesso do transplante. No presente estudo, propõe-se avaliar o perfil de expressão gênica no tecido cardíaco. Com isso, espera-se contribuir para o melhor entendimento do processo de rejeição a nível molecular. Foram analisadas as amostras sequenciais (1, 3 e 6 meses, 1 e 2 anos pós-transplante) de biópsias endomiocárdicas em parafina de 63 indivíduos transplantados cardíacos. O diagnóstico de rejeição humoral foi realizado pela detecção de C3d e C4d do complemento na reação de imuno-histoquímica, e as expressões dos genes protetores (ADIPOR1, ADIPOR2, HMOXO-1, BCL2L1 e VEGF) e genes associados à inflamação (IL-6, TNF?, IFN?, TGF-?, AIF-1, NOS2, ICAM, VCAM e MCP-1); foram avaliadas pela reação em cadeia da polimerase quantitativa em tempo real (qPCR). As frequências de indivíduos positivos para C4d (28,6%) e vasculite (20,0%) foram significantemente maiores em relação ao teste de reatividade de anticorpos realizado nos receptores antes do transplante (6,3%). Houve mudança no perfil de expressão gênica no tecido cardíaco após o transplante, com aumento da expressão dos genes inflamatórios (AIF-1, TNF?, IL-6, NOS2 e VCAM) e diminuição da expressão dos genes protetores (ADIPOR1, ADIPOR2, BCL2L1 e VEGF). Além disso, as expressões dos genes ADIPOR1 e ADIPOR2 foram significantemente menores nos indivíduos positivos para C4d (p<0,001) e gene VEGF (p<0,001) no grupo com vasculite. Houve também uma correlação positiva entre a expressão do gene VEGF e ADIPOR1 (r=0,5688) e ADIPOR2 (r=0,5191). Por outro lado, a expressão aumentada do gene VCAM (p<0,001) foi detectada em todos os tipos de rejeição. Conclui-se que, depois do transplante, o sistema imune do receptor passou a reconhecer os antígenos do órgão transplantado. Com isso, ocorreu uma mudança no perfil de expressão gênica no enxerto cardíaco, caracterizada pela expressão aumentada dos genes inflamatórios e diminuição dos genes protetores. A expressão aumentada do gene VCAM associada à baixa expressão dos genes protetores: ADIPOR1, ADIPOR2, BCL2L1 e VEGF resultaram em maior gravidade da rejeição celular, humoral e vasculopatia do aloenxerto cardíaco.
Heart transplantation is the ultimate treatment for patients with severe heart failure. Despite advances in immunosuppressive therapy, rejection still remains the main obstacle to successful transplant. The purpose of this study is to evaluate the gene expression profile in cardiac tissue. With this we hope to contribute to a better understanding of the rejection process at the molecular level. Sequential samples (1, 3, and 6 months, 1 to 2 years post-transplant) endomyocardial biopsies paraffin of 63 heart transplant subjects were analyzed. The diagnosis of humoral rejection was performed by detection of C3d and C4d complement in immunohistochemistry and the expression of protective genes (ADIPOR1, ADIPOR2, HMOXO-1, and VEGF BCL2L1) and genes associated with inflammation (IL-6,TNF?, IFN?, TGF-?, AIF-1, NOS2, ICAM, VCAM and MCP-1); were evaluated by quantitative real-time polymerase chain reaction (qPCR). The frequency of individuals positive for C4d (28.6%) and vasculitis (20.0%) were significantly higher compared to antibodies reactivity test conducted in the recipients before transplantation (6.3%). There was a change in the gene expression profile in cardiac tissue after transplantation, with increased expression of inflammatory genes (AIF-1,TNF?, IL-6, NOS2, and VCAM) and a decreased expression of protective genes (ADIPOR1, ADIPOR2, BCL2L1, and VEGF). Furthermore, the expressions of ADIPOR1 and ADIPOR2 genes were significantly lower in C4d positive individuals (p<0,001), and VEGF (p<0,001) in the group with vasculitis. There was also a positive correlation between VEGF expression and ADIPOR1 (r=0.5688) and DIPOR2 (r=0.5191). Moreover, increased expression of VCAM (p<0,001) was detected in all types of rejection. We conclude that, after transplantation, the recipient\'s immune system began to recognize the antigens of the transplanted organ. Thus, a change in gene expression profile in cardiac graft is characterized by increased inflammatory genes and decreased expression of protective genes. Increased VCAM gene associated with lower expression of protective genes expression: ADIPOR1, ADIPOR2, BCL2L1 and VEGF resulted in increased severity of cellular and humoral rejection and cardiac allograft vasculopathy.

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3

Waezi, Narges. "Das Langzeitergebnis von Rattenaortentransplantaten nach protrahierter Kältekonservierung in der Gefäßprotektionslösung TiProtec®." Doctoral thesis, 2019. http://hdl.handle.net/11858/00-1735-0000-002E-E5AC-A.

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Books on the topic "Graft vasculopathy"

1

Torres, Río Aguilar, Luigi P. Badano, and Dimitrios Tsiapras. Cardiac transplant patients. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0050.

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Echocardiography has a pivotal role in the care of heart transplant (HT) recipients. This chapter discusses the use of echocardiographic techniques for the assessment of HT patients. In the early post-transplant period, echocardiography has demonstrated its utility to assess the normal and abnormal structural and physiological changes of the transplanted heart, as well as to detect complications such as graft failure. During follow-up, development of acute/chronic graft rejection and cardiac allograft vasculopathy remains the leading causes of mortality in HT recipients and the role of conventional and new echocardiographic techniques in detecting these complications is discussed. Finally, the role of stress echocardiography, which provides additional functional information to the anatomical data obtained with invasive coronary angiography and intravascular ultrasound, is highlighted. The last sections of the chapter are dedicated to the echocardiographic monitoring of endomyocardial biopsies and how to schedule serial echocardiograms during the follow-up of HT recipients.

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Book chapters on the topic "Graft vasculopathy"

1

"radial artery graft ECA–MCA bypass 21 ECA–MCA Bypass with Radial Artery Graft." In Surgical Techniques in Moyamoya Vasculopathy, edited by Peter Vajkoczy. Stuttgart: Georg Thieme Verlag, 2019. http://dx.doi.org/10.1055/b-0039-172635.

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2

"Nonimmune Factors in the Etiology of Graft Coronary Arteriosclerosis." In Transplant-Associated Coronary Artery Vasculopathy, 128–38. CRC Press, 2001. http://dx.doi.org/10.1201/9781498718448-8.

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3

Gustafsson, Finn, and Kasper Rossing. "Heart transplantation." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Theresa McDonagh and Faiez Zannad, 165–82. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0010.

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Heart transplantation remains the treatment of choice for end-stage heart failure refractory to conventional treatment. Long-term outcome is excellent, and median survival currently exceeds 13 years. The main causes of death late after transplantation are cardiac allograft vasculopathy and cancer. Medical therapy after transplantation is complex, including immunosuppressive therapy to reduce the risk of graft rejection and prophylaxis against viral and protozoal infections, as well as adjunctive therapy to treat common comorbidities, for instance hypertension. Pharmacological therapy of comorbid conditions requires specific consideration to clinically important interactions with immunosuppressive drugs.

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Gustafsson, Finn, and Kasper Rossing. "Heart transplantation." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Theresa McDonagh, Joao Pedro Ferreira, and Faiez Zannad, 165–82. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0010_update_001.

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Heart transplantation remains the treatment of choice for end-stage heart failure refractory to conventional treatment. Long-term outcome is excellent, and median survival currently exceeds 13 years. The main causes of death late after transplantation are cardiac allograft vasculopathy and cancer. Medical therapy after transplantation is complex, including immunosuppressive therapy to reduce the risk of graft rejection and prophylaxis against viral and protozoal infections, as well as adjunctive therapy to treat common comorbidities, for instance hypertension. Pharmacological therapy of comorbid conditions requires specific consideration to clinically important interactions with immunosuppressive drugs.

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Macdonald, Peter, and Kumud Dhital. "HFrEF other treatment: transplantation." In ESC CardioMed, 1889–92. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0433.

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Almost 5000 heart transplants are performed around the world each year. Transplant numbers are limited by donor organ availability. Recent reports of successful heart transplantation from donation after circulatory death donors have provided hope that transplant numbers will increase in the coming years. While total transplant numbers have been relatively static over the last decade, there have been dramatic changes in donor and recipient characteristics over this time—particularly increasing donor and recipient age, increasing acceptance of donor and recipient co-morbidities, and increasing use of long-term mechanical circulatory support to bridge recipients to transplantation. These changes have been accompanied by an increased incidence of primary graft dysfunction. As a consequence, 1-year mortality remains substantial at 15% with most deaths occurring in the first month after transplantation. Other major causes of death within the first year are acute rejection and infection. Beyond the first year, survival is excellent. Median survival is 11 years from the time of transplant and 13 years for those who survive the first year. For paediatric recipients, median 1-year conditional survival ranges from 15 years to 21 years depending on the age group. The large majority of transplant recipients experience a dramatic improvement in quality of life with most returning to active roles in the community. Major causes of late morbidity and mortality are coronary allograft vasculopathy, malignancy, infection, and renal failure.

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"STAACA/MCA double bypasses, with long grafts 12 STAACA/MCA Double Bypasses with Long Grafts." In Surgical Techniques in Moyamoya Vasculopathy, edited by Peter Vajkoczy. Stuttgart: Georg Thieme Verlag, 2019. http://dx.doi.org/10.1055/b-0039-172626.

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Conference papers on the topic "Graft vasculopathy"

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Torkian, Pooya, Taraneh Faghihi, and Reza Talaie. "Relative Atherosclerotic Sparing of the External Iliac Artery: Possibility of a Less Vasculopathic Arterial Graft Target." In PAIRS Annual Meeting. Thieme Medical and Scientific Publishers Pvt. Ltd., 2019. http://dx.doi.org/10.1055/s-0041-1730565.

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