Journal articles: '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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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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Mugge, A., R. P. Brandes, B. Heublein, C. Nolte, A. Haverich, and P. R. Lichtlen. "Endothelial dysfunction in heart transplanted patients with graft vasculopathy." European Heart Journal 16, suppl J (October 2, 1995): 78–83. http://dx.doi.org/10.1093/eurheartj/16.suppl_j.78.

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Saiura, Akio, Masataka Sata, Ken-ichi Hiasa, Shiro Kitamoto, Miwa Washida, Kensuke Egashira, Ryozo Nagai, and Masatoshi Makuuchi. "Antimonocyte Chemoattractant Protein-1 Gene Therapy Attenuates Graft Vasculopathy." Arteriosclerosis, Thrombosis, and Vascular Biology 24, no. 10 (October 2004): 1886–90. http://dx.doi.org/10.1161/01.atv.0000141045.49616.6f.

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Clemmensen, Tor Skibsted, Hans Eiskjær, Pernille B. Kofoed-Nielsen, Søren Høyer, and Steen Hvitfeldt Poulsen. "Case of Acute Graft Failure during Suspected Humoral Rejection with Preserved Ejection Fraction, but Severely Reduced Longitudinal Deformation Detected by 2D-Speckle Tracking." Case Reports in Transplantation 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/173589.

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This case displays limited utility of left ventricular ejection fraction to detect acute graft failure due to microvascular vasculopathy and suspected humoral rejection. Despite severe and progressive graft failure, clinically and by right heart catheterizations, left ventricular ejection fraction remained unchanged, indicating need of more reliable noninvasive methods for graft function surveillance. Global longitudinal strain relates to clinical heart failure, filling pressure, and cardiac index during suspected humoral rejection and microvascular dysfunction in this HTX patient. We suggest routine monitoring of graft function by global longitudinal strain as supplement to routine left ventricular ejection fraction and diastolic Doppler measurements.

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Ljubas Macek, Jana, Bosko Skoric, Maja Cikes, Marijan Pasalic, Zeljko Baricevic, Jure Samardzic, Ivo Planinc, and Davor Milicic. "Graft vasculopathy, rejection and mortality predictors in heart transplant patients." Cardiologia Croatica 9, no. 5-6 (May 22, 2014): 233. http://dx.doi.org/10.15836/ccar.2014.233.

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Kearney, S., A. J. Fulton, M. F. McMullin, and E. McKenna. "POC07 Central nervous graft-vs-host disease causing intracranial vasculopathy." Journal of Neurology, Neurosurgery & Psychiatry 81, no. 11 (October 22, 2010): e36-e36. http://dx.doi.org/10.1136/jnnp.2010.226340.77.

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Mahesh, Balakrishnan, Hon-Sing Leong, K. Sukumaran Nair, Ann McCormack, Padmini Sarathchandra, and Marlene L. Rose. "Autoimmunity to Vimentin Potentiates Graft Vasculopathy in Murine Cardiac Allografts." Transplantation 90, no. 1 (July 2010): 4–13. http://dx.doi.org/10.1097/tp.0b013e3181dfa694.

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17

Baran, D. A., S. Kaplan, S. Lubitz, I. Galin, S. Alvi, R. Correa, M. Courtney, et al. "Graft vasculopathy: comparison of cyclosporine and tacrolimus over 15 + years." Journal of Heart and Lung Transplantation 23, no. 2 (February 2004): S164. http://dx.doi.org/10.1016/j.healun.2003.11.363.

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18

Yamamoto, Tetsufumi, Masataka Sata, Daiju Fukuda, and Shinichi Takamoto. "The Angiotensin II Type 1 Receptor Blocker Candesartan Attenuates Graft Vasculopathy." Journal of Surgical Research 132, no. 1 (May 2006): 62–68. http://dx.doi.org/10.1016/j.jss.2005.07.011.

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Roldán, C., S. Mirabet, V. Brossa, E. Moltó, L. Lopez, Y. Alvaro, E. Sole, J. M. Padró, C. Gelpí, and E. Roig. "Correlation of Immunological Markers With Graft Vasculopathy Development in Heart Transplantation." Transplantation Proceedings 44, no. 9 (November 2012): 2653–56. http://dx.doi.org/10.1016/j.transproceed.2012.09.048.

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20

Nagumo, Sakura, Emanuele Gallinoro, Alessandro Candreva, Takuya Mizukami, Giovanni Monizzi, Monika Kodeboina, Sofie Verstreken, et al. "Vessel Fractional Flow Reserve and Graft Vasculopathy in Heart Transplant Recipients." Journal of Interventional Cardiology 2020 (July 14, 2020): 1–7. http://dx.doi.org/10.1155/2020/9835151.

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Background. Cardiac allograft vasculopathy (CAV) remains the Achilles’ heel of long-term survival after heart transplantation (HTx). The severity and extent of CAV is graded with conventional coronary angiography (COR) which has several limitations. Recently, vessel“It is very important for the corresponding author to have a linked ORCID (Open Researcher and Contributor ID) account on MTS. To register a linked ORCID account, please go to the Account Update page (http://mts.hindawi.com/update/) in our Manuscript Tracking System and after you have logged in click on the ORCID link at the top of the page. This link will take you to the ORCID website where you will be able to create an account for yourself. Once you have done so, your new ORCID will be saved in our Manuscript Tracking System automatically.”"?> fractional flow reserve (vFFR) derived from COR has emerged as a diagnostic computational tool to quantify the functional severity of coronary artery disease. Purpose. The present study assessed the usefulness of vFFR to detect CAV in HTx recipients. Methods. In HTx patients referred for annual check-up, undergoing surveillance COR, the extent of CAV was graded according to the criteria proposed by the international society of heart and lung transplantation (ISHLT). In addition, three-dimensional coronary geometries were constructed from COR to calculate pressure losses using vFFR. Results. In 65 HTx patients with a mean age of 53.7 ± 10.1 years, 8.5 years (IQR 1.90, 15.2) years after HTx, a total number of 173 vessels (59 LAD, 61 LCX, and 53 RCA) were analyzed. The mean vFFR was 0.84 ± 0.15 and median was 0.88 (IQR 0.79, 0.94). A vFFR ≤ 0.80 was present in 24 patients (48 vessels). HTx patients with a history of ischemic cardiomyopathy (ICMP) had numerically lower vFFR as compared to those with non-ICMP (0.70 ± 0.22 vs. 0.79 ± 0.13, p=0.06). The use of vFFR reclassified 31.9% of patients compared to the anatomical ISHLT criteria. Despite a CAV score of 0, a pathological vFFR ≤ 0.80 was detected in 8 patients (34.8%). Conclusion. The impairment in epicardial conductance assessed by vFFR in a subgroup of patients without CAV according to standard ISHLT criteria suggests the presence of a diffuse vasculopathy undetectable by conventional angiography. Therefore, we speculate that vFFR may be useful in risk stratification after HTx.

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Yamamoto, Tetsufumi, Masataka Sata, Daiju Fukuda, and Shinichi Takamoto. "The angiotensin II type 1 receptor blocker valsartan attenuates graft vasculopathy." Basic Research in Cardiology 100, no. 1 (October 20, 2004): 84–91. http://dx.doi.org/10.1007/s00395-004-0489-0.

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Yuan, Xueli, Jesus Paez-Cortez, Isabela Schmitt-Knosalla, Francesca D'Addio, Bechara Mfarrej, Michela Donnarumma, Antje Habicht, et al. "A novel role of CD4 Th17 cells in mediating cardiac allograft rejection and vasculopathy." Journal of Experimental Medicine 205, no. 13 (December 1, 2008): 3133–44. http://dx.doi.org/10.1084/jem.20081937.

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T-bet plays a crucial role in Th1 development. We investigated the role of T-bet in the development of allograft rejection in an established MHC class II–mismatched (bm12 into B6) model of chronic allograft vasculopathy (CAV). Intriguingly, and in contrast to IFN-γ−/− mice that are protected from CAV, T-bet−/− recipients develop markedly accelerated allograft rejection accompanied by early severe vascular inflammation and vasculopathy, and infiltration by predominantly IL-17–producing CD4 T cells. Concurrently, T-bet−/− mice exhibit a T helper type 1 (Th1)–deficient environment characterized by profound IFN-γ deficiency, a Th2 switch characterized by increased production of interleukin (IL) 4, IL-5, IL-10, and IL-13 cytokines, as well as increased production of the proinflammatory cytokines IL-6, IL-12p40, and IL-17. Neutralization of IL-17 inhibits accelerated allograft rejection and vasculopathy in T-bet−/− mice. Interestingly, CD4 but not CD8 T cell deficiency in T-bet−/− mice affords dramatic protection from vasculopathy and facilitates long-term graft acceptance. This is the first study establishing that in the absence of Th1-mediated alloimmune responses, CD4 Th17 cells mediate an aggressive proinflammatory response culminating in severe accelerated allograft rejection and vasculopathy. These results have important implications for the development of novel therapies to target this intractable problem in clinical solid organ transplantation.

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Reich, Heidi J., Jon A. Kobashigawa, Tamar Aintablian, Danny Ramzy, Michelle M. Kittleson, and Fardad Esmailian. "Effects of Older Donor Age and Cold Ischemic Time on Long-Term Outcomes of Heart Transplantation." Texas Heart Institute Journal 45, no. 1 (February 1, 2018): 17–22. http://dx.doi.org/10.14503/thij-16-6178.

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Using older donor hearts in cardiac transplantation may lead to inferior outcomes: older donors have more comorbidities that reduce graft quality, including coronary artery disease, hypertension, diabetes mellitus, and dyslipidemia. Shorter cold ischemic times might overcome the detrimental effect of older donor age. We examined the relationship between donor allograft age and cold ischemic time on the long-term outcomes of heart transplant recipients. rom 1994 through 2010, surgeons at our hospital performed 745 heart transplantations. We retrospectively classified these cases by donor ages of <50 years (younger) and ≥50 years (older), then by cold ischemic times of <120 min (short), 120 to 240 min (intermediate), and >240 min (long). Endpoints included recipient and graft survival, and freedom from cardiac allograft vasculopathy, nonfatal major adverse cardiac events, and rejection. For intermediate ischemic times, the 5-year recipient survival rate was lower when donors were older (70% vs 82.6%; P=0.02). This was also true for long ischemic times (69.8% vs 87.6%; P=0.09). For short ischemic times, we found no difference in 5-year recipient or graft survival rates (80% older vs 85.6% younger; P=0.79), in freedom from nonfatal major adverse cardiac events (83.3% vs 91.5%; P=0.46), or in freedom from cardiac allograft vasculopathy (50% vs 70.6%; P=0.66). Rejection rates were mostly similar. Long-term graft survival in heart transplantation patients with older donor allografts may improve when cold ischemic times are shorter.

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Shahzad, Khurram, Martin Cadeiras, Kotaro Arai, Dmitry Abramov, Elizabeth Burke, and Mario C. Deng. "Unexplained Graft Dysfunction after Heart Transplantation—Role of Novel Molecular Expression Test Score and QTc-Interval: A Case Report." Cardiology Research and Practice 2010 (2010): 1–5. http://dx.doi.org/10.4061/2010/230810.

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In the current era of immunosuppressive medications there is increased observed incidence of graft dysfunction in the absence of known histological criteria of rejection after heart transplantation. A noninvasive molecular expression diagnostic test was developed and validated to rule out histological acute cellular rejection. In this paper we present for the first time, longitudinal pattern of changes in this novel diagnostic test score along with QTc-interval in a patient who was admitted with unexplained graft dysfunction. Patient presented with graft failure with negative findings on all known criteria of rejection including acute cellular rejection, antibody mediated rejection and cardiac allograft vasculopathy. The molecular expression test score showed gradual increase and QTc-interval showed gradual prolongation with the gradual decline in graft function. This paper exemplifies that in patients presenting with unexplained graft dysfunction, GEP test score and QTc-interval correlate with the changes in the graft function.

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Ostriker, Allison C., Yi Xie, Raja Chakraborty, Ashley J. Sizer, Yalai Bai, Min Ding, Wen-Liang Song, Anita Huttner, John Hwa, and Kathleen A. Martin. "TET2 Protects Against Vascular Smooth Muscle Cell Apoptosis and Intimal Thickening in Transplant Vasculopathy." Circulation 144, no. 6 (August 10, 2021): 455–70. http://dx.doi.org/10.1161/circulationaha.120.050553.

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Background: Coronary allograft vasculopathy (CAV) is a devastating sequela of heart transplant in which arterial intimal thickening limits coronary blood flow. There are currently no targeted therapies to prevent or reduce this pathology that leads to transplant failure. Vascular smooth muscle cell (VSMC) phenotypic plasticity is critical in CAV neointima formation. TET2 (TET methylcytosine dioxygenase 2) is an important epigenetic regulator of VSMC phenotype, but the role of TET2 in the progression of CAV is unknown. Methods: We assessed TET2 expression and activity in human CAV and renal transplant samples. We also used the sex-mismatched murine aortic graft model of graft arteriopathy (GA) in wild-type and inducible smooth muscle–specific Tet2 knockout mice; and in vitro studies in murine and human VSMCs using knockdown, overexpression, and transcriptomic approaches to assess the role of TET2 in VSMC responses to IFNγ (interferon γ), a cytokine elaborated by T cells that drives CAV progression. Results: In the present study, we found that TET2 expression and activity are negatively regulated in human CAV and renal transplant samples and in the murine aortic graft model of GA. IFNγ was sufficient to repress TET2 and induce an activated VSMC phenotype in vitro. TET2 depletion mimicked the effects of IFNγ, and TET2 overexpression rescued IFNγ-induced dedifferentiation. VSMC-specific TET2 depletion in aortic grafts, and in the femoral wire restenosis model, resulted in increased VSMC apoptosis and medial thinning. In GA, this apoptosis was tightly correlated with proliferation. In vitro, TET2-deficient VSMCs undergo apoptosis more readily in response to IFNγ and expressed a signature of increased susceptibility to extrinsic apoptotic signaling. Enhancing TET2 enzymatic activity with high-dose ascorbic acid rescued the effect of GA-induced VSMC apoptosis and intimal thickening in a TET2-dependent manner. Conclusions: TET2 is repressed in CAV and GA, likely mediated by IFNγ. TET2 serves to protect VSMCs from apoptosis in the context of transplant vasculopathy or IFNγ stimulation. Promoting TET2 activity in vivo with systemic ascorbic acid reduces VSMC apoptosis and intimal thickening. These data suggest that promoting TET2 activity in CAV may be an effective strategy for limiting CAV progression.

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Koglin, Jörg, Troels Glysing-Jensen, and Mary E. Russell. "Immune sources of TGF-βI protect against graft vasculopathy: Graft vascular remodeling in TGF-βI-deficient mice." Transplantation 65, Supplement (May 1998): 175. http://dx.doi.org/10.1097/00007890-199805131-00385.

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Koglin, J??rg, Troels Glysing-Jensen, and Mary E. Russell. "Immune sources of TGF-??1 protect against graft vasculopathy: Graft vascular remodeling in TGF-??1-deficient mice." Transplantation 65, no. 12 (June 1998): S99. http://dx.doi.org/10.1097/00007890-199806270-00406.

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Shevchenko, A. O., E. A. Nikitina, and I. Yu Tunyaeva. "Hypertension in cardiac transplant recipients." Russian Journal of Transplantology and Artificial Organs 19, no. 2 (June 23, 2017): 114–25. http://dx.doi.org/10.15825/1995-1191-2017-2-114-125.

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Hypertension is a common syndrome in adult and pediatric cardiac transplant recipients affecting the great majority of patients. Elevated blood pressure is a major potentially modifiable risk factor associated with cardiac graft failure, vasculopathy, arrhythmias, stroke, renal failure and premature death. This review discusses the magnitude of the problem, its distinct mechanisms, and certain issues of prevention and treatment of post-transplant hypertension.

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Hasegawa, Tomomi, Koichiro Iwanaga, Donald E. Hultquist, Hui Liao, Scott H. Visovatti, and David J. Pinsky. "Suppression of nitrosative and oxidative stress to reduce cardiac allograft vasculopathy." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H1007—H1016. http://dx.doi.org/10.1152/ajpheart.00498.2008.

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Oxidant injury occurs when an organ is severed from its native blood supply and then reperfused and continues during subsequent periods of immune attack. Experiments here test the hypothesis that an antioxidant given only in the peri-reperfusion period protects against not only oxidative but also nitrosative stress, leading to reduced vasculopathy long after cardiac allotransplantation. Experiments were performed using a murine heterotopic cardiac transplantation model. An antioxidant, in the form of intraperitoneal high-dose riboflavin, was given to recipients during the initial 3 days after transplantation. Antioxidant-treated mice showed significantly longer graft survival than control mice. At 4 h after transplantation, antioxidant treatment significantly reduced graft lipid peroxidation and oxidized DNA and preserved antioxidant enzyme activity. At day 6 posttransplantation, the redox-sensitive transcription factor nuclear factor-κB and inducible nitric oxide synthase were significantly reduced following antioxidant treatment, with concomitant reduction of nitrotyrosine. Despite the limited duration of antioxidant treatment, both acute and chronic rejection were significantly suppressed. In vitro experiments confirmed suppression of nitrosative and oxidative stress and cardiomyocyte damage in antioxidant-treated cardiac allografts. Collectively, antioxidant administration during the initial 3 days after transplantation significantly reduces nitrosative and oxidative stress in cardiac allografts, modulates immune responses, and protects against vasculopathy.

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Rodriguez, Rose J., Linda J. Addonizio, Jacqueline M. Lamour, Seema Mital, Ralph Mosca, Lori J. West, Jenny C. Nova, and Daphne T. Hsu. "Pediatric Heart Transplantation across ABO Blood Type Barriers: A Case Study." Progress in Transplantation 15, no. 2 (June 2005): 161–65. http://dx.doi.org/10.1177/152692480501500209.

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Heart transplantation with ABO blood type–incompatible donors has historically been contraindicated because of the high risk of an immediate hyperacute humoral graft rejection. The immature neonatal immune system presents an immunologic window that allows for breaching the ABO barrier before the natural development of anti-ABO antibodies. Information from a small series of neonates has demonstrated similar survival rates and posttransplant outcomes compared to ABO-compatible transplantations. In the posttransplant period, particular attention is placed on the surveillance of graft-specific antibody production and monitoring for immunologic signs and symptoms of early graft vasculopathy. This article presents a case study of a neonate with congenital heart disease who underwent one of the first successful ABO-incompatible heart transplantations in the United States.

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Shirasawa, Bungo, Kimikazu Hamano, Hiroshi Ito, Hidenori Gohra, Tomoe Katho, Yoshihiko Fujimura, and Kensuke Esato. "Can Low-dose Irradiation of Donor Hearts before Transplantation Inhibit Graft Vasculopathy?" Japanese Journal of Cardiovascular Surgery 28, no. 1 (1999): 30–33. http://dx.doi.org/10.4326/jjcvs.28.30.

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Garlicki, M. "May preservation solution affect the incidence of graft vasculopathy in transplanted heart?" Journal of Heart and Lung Transplantation 22, no. 1 (January 2003): S76. http://dx.doi.org/10.1016/s1053-2498(02)00683-6.

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Kanitakis, J., G. Karayannopoulou, P. Petruzzo, and M. Lanzetta. "Graft Vasculopathy May Affect the Skin of Vascularized Composite Allografts Undergoing Rejection." Transplantation 98 (July 2014): 410. http://dx.doi.org/10.1097/00007890-201407151-01356.

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Gelpi, C., C. Roldan, S. Mirabet, V. Brossa, L. Lopez, A. Mendez, J. M. Padro, and E. Roig. "475 Correlation of Immunological Markers with Graft Vasculopathy Development in Heart Transplantation." Journal of Heart and Lung Transplantation 31, no. 4 (April 2012): S167. http://dx.doi.org/10.1016/j.healun.2012.01.486.

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Barrett, Helen L., Karin Lust, Narelle Fagermo, Leonie K. Callaway, and Lee Minuzzo. "Moyamoya disease in pregnancy: maintenance of maternal blood pressure." Obstetric Medicine 5, no. 1 (December 8, 2011): 32–34. http://dx.doi.org/10.1258/om.2011.110046.

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Moyamoya disease is a rare cerebrovascular occlusive disorder characterized by stenosis in the circle of Willis with the development of a compensatory circulation. It has been associated with significant morbidity in pregnancy including intracranial haemorrhage, ischaemic stroke and epilepsy. We present the case of a 26-year-old woman with a previous diagnosis of moyamoya vasculopathy with bilateral superficial temporal to middle cerebral artery bypass grafting. During the second trimester, she developed significant neurological symptoms related to postural hypotension in the presence of a stenosis of the right-sided graft. The hypotension was treated with fludrocortisone therapy with improvement in blood pressure and symptoms. Moyamoya vasculopathy poses unique challenges to obstetric care. This is the first report of use of fludrocortisone for maintenance of blood pressure during pregnancy in this condition.

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Ludwig, Bernd, Johanna Schneider, Daniela Föll, and Qian Zhou. "Antibody-mediated rejection with detection of de novo donor-specific anti-human leucocyte antigen Class II antibodies 3 years after heart transplantation: a case report." European Heart Journal - Case Reports 4, no. 1 (January 25, 2020): 1–4. http://dx.doi.org/10.1093/ehjcr/ytz246.

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Abstract Background Antibody-mediated rejection (AMR) in cardiac transplantation may manifest early within the first weeks after transplantation but also late after months to years following transplantation resulting in mild heart failure to cardiogenic shock. While patients with early cardiac AMR are less affected and seem to have survival rates comparable to transplant recipients without AMR, late cardiac AMR is frequently associated with graft dysfunction, fulminant forms of cardiac allograft vasculopathy, and a high mortality rate. Nevertheless, AMR of cardiac allografts remains difficult to diagnose and to treat. Case summary We report the case of a 47-year-old male patient with late AMR of the cardiac allograft 3 years after heart transplantation. Antibody-mediated rejection was confirmed by endomyocardial biopsy and the presence of donor-specific antibodies (DSA). The patient was treated with high dose of prednisolone, plasmapheresis, intravenous Gamma Globulin, rituximab, immunoadsorption, and bortezomib. Under this treatment regimen left ventricular ejection fraction and pro B-type natriuretic peptide recovered, and the patient improved to New York Heart Association Class I. Currently, 3 years after the diagnosis of cardiac AMR, graft function continues to be nearly normal, and there is no evidence for transplant vasculopathy. Discussion This case illustrates that AMR can occur at any time after transplantation. Although graft function fully recovered after treatment in our patient, the level of DSA remained high, suggesting that DSA may not be a reliable parameter to determine the intensity and duration of the therapy.

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Cleaver, Jonathan, Mario Teo, Shelley Renowden, Keith Miller, Harsha Gunawardena, and Philip Clatworthy. "Sneddon Syndrome: A Case Report Exploring the Current Challenges Faced with Diagnosis and Management." Case Reports in Neurology 11, no. 3 (December 16, 2019): 357–68. http://dx.doi.org/10.1159/000503955.

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Sneddon syndrome (SS) is a rare medium-vessel vasculopathy which characteristically presents with livedo racemosa (LR) and complications such as strokes. This case report describes a female presenting acutely with a stroke and, initially, no evidence of LR. Her antiphospholipid antibodies were negative, and her neuroimaging revealed multiple territory strokes with extensive vasculopathy and fragile neo-formed vessel collateralisation. She had progressive memory loss and multiple transient ischaemic attacks on a background of established infarctions. SS should be considered in any idiopathic medium-vessel vasculopathy despite the absence of LR. Medical therapy can be challenging and the importance of antiphospholipid status in risk stratifying anticoagulation against antiplatelet therapy is discussed with a proposed rheumatology management strategy. The medical option of hydroxychloroquine should be considered in all patients in view of its anti-thrombotic properties and efficacy in diseases such as systemic lupus erythematosus and antiphospholipid syndrome with the suggestion that SS may be a forme fruste of these diseases. Neurosurgical options should be considered for recurrent transient neurological symptoms. For our patient, this included an extracranial to intracranial bypass via a radial artery graft for haemodynamic stroke management confirmed on SPECT imaging. The traditional hallmark of SS has previously been LR. This case highlights an atypical presentation stressing the importance of diagnostic vigilance in a patient with an idiopathic medium-vessel vasculopathy, together with balancing the medical risk of antiplatelet therapy, anticoagulation and thrombolysis whilst revealing possible neurosurgical options in select SS patients.

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Koloskova, N. N., V. N. Poptsov, V. М. Zakharevich, I. I. Muminov, N. P. Mozheyko, O. E. Gichkun, Е. А. Nikitina, et al. "Gender aspects of incidence of antibody-mediated rejection and allograft vasculopathy events after heart transplantation." Russian Journal of Transplantology and Artificial Organs 21, no. 1 (May 18, 2019): 17–22. http://dx.doi.org/10.15825/1995-1191-2019-1-17-22.

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Abstract. Despite improvements in immunosuppressive therapy, antibody-mediated rejection (AMR) remains one of the most important risk factors for poor prognosis for survival of recipients, cardiac graft dysfunction, and cardiac allograft vasculopathy (CAV) after heart transplantation.Aim: to assess the incidence of case of antibodymediated rejection and cardiac allograft vasculopathy depending on the gender of the patients who underwent heart transplantation in our Center from January 2010 to December 2017.Methods. The median observation was 42 months. The study comprised 606 patients (84 [14%] women) who underwent heart transplantation in 2010 to 2017. We analyzed all the episodes of antibody-mediated rejection, which were diagnosed by the results of endomyocardial biopsies.Results. We comparing the total incidence of antibody-mediated rejection and we are found significant differences among men and women who underwent heart transplantation (p < 0.05), the survival rate during the first year after heart transplantation was 95 and 92%, respectively. The incidence of antibody-consistent rejection was significantly higher among women who had a history of pregnancy and/or use of mechanical circulatory support systems (UNOS status 1A) in the pre-transplantation history (p < 0.05), and we also found significant differences in the incidence of cardiac allograft vasculopathy in women diagnosed with AMR (p < 0.05). The survival rate among women within a year after the diagnosis of AMR is 83% compared to 96% of the recipients free from AMR.Conclusions. Women are at higher risk for AMR after heart transplantation and it increases their risk for cardiac allograft vasculopathy. Females recipients may more frequent myocardial control biopsies and a personalized approach in prescribing immunosuppressive therapy. Women-recipients of transplanted heart should undergo These measures will help to identify in time the development of antibodymediated rejection and reduce the incidence of cardiac allograft vasculopathy after heart transplant.

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WAHLERS, T., H. FIEGUTH, M. JURMANN, J. ALBES, B. HAUSEN, S. DEMERTZIS, H. SCHAFERS, P. OPPELT, H. BORST, and A. MUGGE. "Graft coronary vasculopathy in cardiac transplantation — evaluation of risk factors by multivariate analysis." European Journal of Cardio-Thoracic Surgery 10, no. 1 (1996): 1–5. http://dx.doi.org/10.1016/s1010-7940(96)80258-2.

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Mirabet, S., C. Gelpí, C. Roldán, V. Brossa, C. A. Mendoza, L. Lopez, E. Molto, et al. "Assessment of Immunological Markers as Mediators of Graft Vasculopathy Development in Heart Transplantation." Transplantation Proceedings 43, no. 6 (July 2011): 2253–56. http://dx.doi.org/10.1016/j.transproceed.2011.06.044.

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Ogawa, Yoko, Ichiro Manabe, Takayuki Shindo, Jun-ichi Suzuki, Isobe Mitsuaki, and Ryozo Nagai. "A synthetic retinoid, Am80, inhibits acute rejection and graft vasculopathy in cardiac transplantation." Vascular Pharmacology 45, no. 3 (September 2006): e17. http://dx.doi.org/10.1016/j.vph.2006.08.091.

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Nagumo, S., E. Gallinoro, A. Candreva, T. Mizukami, S. Verstreken, R. Dierckx, W. Heggermont, et al. "Virtual Fractional Flow Reserve in Heart Transplant Recipients with and without Graft Vasculopathy." Journal of Heart and Lung Transplantation 39, no. 4 (April 2020): S76—S77. http://dx.doi.org/10.1016/j.healun.2020.01.1294.

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Habibi, Shaghayegh, Eiman Ghaffarpasand, Fahimehalsadat Shojaei, Mahda Alihashemi, Farima Kahe, Farbod Zahedi Tajrishi, and Gerald Chi. "Prognostic Value of Biomarkers in Cardiac Allograft Vasculopathy following Heart Transplantation: A Literature Review." Cardiology 145, no. 11 (2020): 693–702. http://dx.doi.org/10.1159/000509630.

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Cardiac allograft vasculopathy (CAV), also known as cardiac transplant vasculopathy, is a major determinant of long-term survival among cardiac transplantation recipients. Histologically, CAV is featured by diffuse, concentric thickening of the vascular wall, and primarily affects large and small epicardial coronary arteries, intramyocardial arteries, and veins. Owing to graft denervation, CAV typically follows an insidious course, and patients may not experience classic angina symptoms but instead present with progressive heart failure or ventricular arrhythmias. Recent studies on biomarkers have furthered the knowledge concerning the prediction and prognosis of CAV. Given its association with metabolic, thrombotic, inflammatory, and immunologic markers, CAV is likely to represent a complex multifactorial process that involves both immune-mediated and non-immune-mediated pathways. In order to identify the high-risk patients that would benefit from early intervention, future research is warranted to examine the usefulness of a biomarker panel in CAV risk stratification.

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Mileva, Niya, Sakura Nagumo, Emanuele Gallinoro, Jeroen Sonck, Sofie Verstreken, Riet Dierkcx, Ward Heggermont, et al. "Validation of Coronary Angiography-Derived Vessel Fractional Flow Reserve in Heart Transplant Patients with Suspected Graft Vasculopathy." Diagnostics 11, no. 10 (September 24, 2021): 1750. http://dx.doi.org/10.3390/diagnostics11101750.

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Cardiac transplant-related vasculopathy remains a leading cause of morbidity and mortality in heart transplant (HTx) recipients. Recently, coronary angiography-derived vessel fractional flow reserve (vFFR) has emerged as a new diagnostic computational tool to functionally evaluate the severity of coronary artery disease. Although vFFR estimates have been shown to perform well against invasive FFR in atherosclerotic coronary artery disease, data on the use of vFFR in heart transplant recipients suffering from cardiac transplant-related arteriopathy are lacking. The aim of the presented study was to validate coronary angiography-derived vessel fractional flow reserve to calculate fractional flow reserve in HTx patients with and without cardiac transplant-related vasculopathy. A prospective, single center study of HTx patients referred for annual check-up, undergoing surveillance coronarography was conducted. Invasive FFR was measured using a motorized device at the speed of 1.0 mm/s in all three major coronary arteries. Angiography-derived pullback FFR was derived from the angiogram and compared with invasive FFR pullback curve. Overall, 18,059 FFR values were extracted from the FFR pullback curves from 23 HTx patients. The mean age was 59.3 ± 9.7 years, the mean time after transplantation was 5.24 years [IQR 1.20, 11.25]. A total of 39 vessels from 23 patients (24 LAD, 11 LCX, 4 RCA) were analyzed. Mean distal vFFR was 0.87 ± 0.14 whereas invasive distal FFR was 0.88 ± 0.17. An excellent correlation was found between invasive distal FFR and vFFR (r = 0.92; p < 0.001). The correlation of the pullback tracing was high, with a correlation coefficient between vFFR and invasive FFR pullback values of 0.72 (95% CI 0.71 to 0.73, p < 0.001). The mean difference between vFFR and invasive FFR pullback values was −0.01 with 0.06 of SD (limits of agreements −0.12 to 0.13). In HTx patients, coronary angiography-derived FFR correlates excellently with invasively measured wire-derived FFR. Therefore, angiography derived FFR could be used as a novel diagnostic tool to quantify the functional severity of graft vasculopathy.

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Aggarwal, Ashim, Joseph Pyle, John Hamilton, and Geetha Bhat. "Early Cardiac Allograft Vasculopathy: Are the Viruses to Blame?" Case Reports in Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/734074.

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This paper describes a case of early (7 months after transplant) cardiac allograft vasculopathy. This-43-year-old (CMV positive, EBV negative) female patient underwent an orthotopic heart transplant with a (CMV negative, EBV positive) donor heart. She had a history of herpes zoster infection and postherpetic neuralgia in the past. The patient’s panel reactive antibodies had been almost undetectable on routine surveillance testing, and her surveillance endomyocardial biopsies apart from a few episodes of mild-to-moderate acute cellular rejection (treated adequately with steroids) never showed any evidence of humoral rejection. The postoperative course was complicated by multiple admissions for upper respiratory symptoms, and the patient tested positive for entero, rhino, and coronaviruses serologies. During her last admission (seven months postoperatively) the patient developed mild left ventricular dysfunction with an ejection fraction of 40%. The patient’s endomyocardial biopsy done at that time revealed concentric intimal proliferation and inflammation resulting in near-total luminal occlusion in the epicardial and the intramyocardial coronary vessels, suggestive of graft vasculopathy with no evidence of rejection, and the patient had a fatal ventricular arrhythmia.

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Anderson, Josephine L. C., Margot L. Poot, Hannah L. M. Steffen, Daan Kremer, Stephan J. L. Bakker, and Uwe J. F. Tietge. "The Framingham Risk Score Is Associated with Chronic Graft Failure in Renal Transplant Recipients." Journal of Clinical Medicine 10, no. 15 (July 26, 2021): 3287. http://dx.doi.org/10.3390/jcm10153287.

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Predicting chronic graft failure in renal transplant recipients (RTR) is an unmet clinical need. Chronic graft failure is often accompanied by transplant vasculopathy, the formation of de novo atherosclerosis in the transplanted kidney. Therefore, we determined whether the 10-year Framingham risk score (FRS), an established atherosclerotic cardiovascular disease prediction module, is associated with chronic graft failure in RTR. In this prospective longitudinal study, 600 well-characterised RTR were followed for 10 years. The association with death-censored chronic graft failure (n = 81, 13.5%) was computed. An extended Cox model showed that each one percent increase of the FRS significantly increased the risk of chronic graft failure by 4% (HR: 1.04, p < 0.001). This association remained significant after adjustment for potential confounders, including eGFR (HR: 1.03, p = 0.014). Adding the FRS to eGFR resulted in a higher AUC in a receiver operating curve (AUC = 0.79, p < 0.001) than eGFR alone (AUC = 0.75, p < 0.001), and an improvement in the model likelihood ratio statistic (67.60 to 88.39, p < 0.001). These results suggest that a combination of the FRS and eGFR improves risk prediction. The easy to determine and widely available FRS has clinical potential to predict chronic graft failure in RTR.

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Kang, Duk Hee, Shin Wook Kang, Hyeon Joo Jeong, Yu Seun Kim, Chul Woo Yang, and Richard J. Johnson. "Transplant Graft Vasculopathy: An Emerging Target for Prevention and Treatment of Renal Allograft Dysfunction." Yonsei Medical Journal 45, no. 6 (2004): 1053. http://dx.doi.org/10.3349/ymj.2004.45.6.1053.

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Paul, Leendert C. "Calcium channel blockers and angiotensin-converting enzyme inhibitors in the prevention of graft vasculopathy." Journal of Heart and Lung Transplantation 19, no. 5 (May 2000): 409–13. http://dx.doi.org/10.1016/s1053-2498(00)00072-3.

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Cantin, Bernard, Dening Zhu, Peizhong Wen, Shyam N. Panchal, Judith K. Gwathmey, Gerald M. Reaven, and Hannah A. Valantine. "Preferential involvement of larger vessels in a rat model of diabetes-induced graft vasculopathy." Journal of Heart and Lung Transplantation 21, no. 9 (September 2002): 1040–43. http://dx.doi.org/10.1016/s1053-2498(01)00401-6.

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Kwon, Murray H., Samantha Y. Wong, Abbas Ardehali, Hillel Laks, Zilu K. Zhang, Mario C. Deng, and Richard J. Shemin. "Primary graft dysfunction does not lead to increased cardiac allograft vasculopathy in surviving patients." Journal of Thoracic and Cardiovascular Surgery 145, no. 3 (March 2013): 869–73. http://dx.doi.org/10.1016/j.jtcvs.2012.09.037.

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Journal articles on the topic 'Graft vasculopathy'

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