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Joren C Madsen - One of the best experts on this subject based on the ideXlab platform.
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b cell clonal expansion within immune infiltrates in human cardiac Allograft Vasculopathy
American Journal of Transplantation, 2020Co-Authors: Michael M Givertz, Carolina Moore, Baoshan Gao, Krishna M Roskin, Elenarodica Vasilescu, Linda J Addonizio, Joren C MadsenAbstract:Cardiac Allograft Vasculopathy (CAV) is associated with intragraft B cell infiltrates. Here, we studied the clonal composition of B cell infiltrates using 4 graft specimens with CAV. Using deep sequencing, we analyzed the immunoglobulin heavy chain variable region repertoire in both graft and blood. Results showed robust B cell clonal expansion in the graft but not in the blood for all cases. Several expanded B cell clones, characterized by their uniquely rearranged complementarity-determining region 3, were detected in different locations in the graft. Sequences from intragraft B cells also showed elevated levels of mutated rearrangements in the graft compared to blood B cells. The number of somatic mutations per rearrangement was also higher in the graft than in the blood, suggesting that B cells continued maturing in situ. Overall, our studies demonstrated B cell clonal expansion in human cardiac Allografts with CAV. This local B cell response may contribute to the pathophysiology of CAV through a mechanism that needs to be identified.
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depletion of t regulatory cells promotes natural killer cell mediated cardiac Allograft Vasculopathy
Transplantation, 2014Co-Authors: Tsutomu Hirohashi, Catharine M Chase, P Dellapelle, Divya Sebastian, Evan Farkesh, Robert B Colvin, P S Russell, Alessandro Alessandrini, Joren C MadsenAbstract:Background A role for NK cells in cardiac Allograft Vasculopathy (CAV) was suggested by our earlier observation that CAV arises even in the absence of detectable anti-donor T or B cell reactivity in parental to F1 mouse heart grafts. However, prevention of CAV in this setting required the depletion of both NK and CD4+ T cells.
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international society for heart and lung transplantation working formulation of a standardized nomenclature for cardiac Allograft Vasculopathy 2010
Journal of Heart and Lung Transplantation, 2010Co-Authors: Mandeep R Mehra, J A Kobashigawa, Joren C Madsen, Randall C Starling, Maria G Crespoleiro, Anne I Dipchand, Stephan M Ensminger, N E Hiemann, Jayan Parameshwar, Patricia A UberAbstract:The development of cardiac Allograft Vasculopathy remains the Achilles heel of cardiac transplantation. Unfortunately, the definitions of cardiac Allograft Vasculopathy are diverse, and there are no uniform international standards for the nomenclature of this entity. This consensus document, commissioned by the International Society of Heart and Lung Transplantation Board, is based on best evidence and clinical consensus derived from critical analysis of available information pertaining to angiography, intravascular ultrasound imaging, microvascular function, cardiac Allograft histology, circulating immune markers, non-invasive imaging tests, and gene-based and protein-based biomarkers. This document represents a working formulation for an international nomenclature of cardiac Allograft Vasculopathy, similar to the development of the system for adjudication of cardiac Allograft rejection by histology.
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viral infection induces de novo lesions of coronary Allograft Vasculopathy through a natural killer cell dependent pathway
American Journal of Transplantation, 2009Co-Authors: Jay A Graham, Joren C Madsen, Tsutomu Hirohashi, Catharine M Chase, Robert B Colvin, Robert A Wilkinson, Jay A Fishman, P S RussellAbstract:Viral infections including those due to cytomegalovirus have been associated with accelerated cardiac Allograft Vasculopathy (CAV) in clinical trials and some animal models. Evidence demonstrating a direct causal relationship between such infections and de novo formation of coronary vascular lesions is lacking. Heterotopic murine cardiac transplants were performed in a parental to F1 combination in animals lacking both T- and B-lymphocytes (RAG−/−). Coronary Vasculopathy developed almost exclusively in the presence of recipient infection with lymphocytic choriomeningitis virus but not in uninfected controls. This process was also dependent upon the presence of natural killer (NK) cells as depletion of NK cells abrogated the process. These data show that a viral infection in its native host, and not previously implicated in the production of CAV, can contribute to the development of advanced coronary vascular lesions in cardiac allotransplants in mice. These data also suggest that virus-induced CAV can develop via an NK-cell-dependent pathway in the absence of T- and B-lymphocytes.
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macrophage depletion suppresses cardiac Allograft Vasculopathy in mice
American Journal of Transplantation, 2007Co-Authors: William H Kitchens, Robert B Colvin, P S Russell, C M Chase, Shuichiro Uehara, Lynn D Cornell, Joren C MadsenAbstract:Cardiac Allograft Vasculopathy (CAV) is a major source of late posttransplant mortality. Although numerous cell types are implicated in the pathogenesis of CAV, it is unclear which cells actually induce the vascular damage that results in intimal proliferation. Because macrophages are abundant in CAV lesions and are capable of producing growth factors implicated in neointimal proliferation, they are leading end-effector candidates. Macrophages were depleted in a murine heterotopic cardiac transplant system known to develop fulminant CAV lesions. C57BL/6 hearts were transplanted into (C57BL/6 x BALB/c)F(1) recipients, which then received anti-macrophage therapy with intraperitoneal carrageenan or i.v. gadolinium. Intraperitoneal carrageenan treatment depleted macrophages by 30-80% with minimal effects upon T, B or NK cells as confirmed by flow cytometry and NK cytotoxicity assays. Carrageenan treatment led to a 70% reduction in the development of CAV, as compared to mock-treated controls (p = 0.01), which correlated with the degree of macrophage depletion. Inhibition of macrophage phagocytosis alone with gadolinium failed to prevent CAV. Macrophages may represent the end-effector cells in a final common pathway towards CAV independent of T-cell or B-cell alloreactivity and exert their injurious effects through mechanisms related to cytokine/growth factor production rather than phagocytosis.
Donna Mancini - One of the best experts on this subject based on the ideXlab platform.
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letter by clerkin et al regarding article importance of routine antihuman leukocyte antibody monitoring de novo donor specific antibodies are associated with rejection and Allograft Vasculopathy after heart transplantation
Circulation, 2018Co-Authors: Kevin J Clerkin, Maryjane Farr, Donna ManciniAbstract:We read the article by Wong et al with interest and congratulate the authors for their addition to the literature regarding de novo donor specific antihuman leukocyte antigen antibodies (dnDSA) following heart transplantation.1 DSA have been shown to be detrimental following heart transplantation, leading to increased cellular rejection, cardiac Allograft Vasculopathy, antibody mediated rejection (AMR), and mortality.2–4 We recently reported our experience with a prospective cohort of …
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detection and imaging of cardiac Allograft Vasculopathy
Jacc-cardiovascular Imaging, 2013Co-Authors: Ari Pollack, Donna Mancini, Tamim Nazif, Giora WeiszAbstract:Cardiac Allograft Vasculopathy (CAV) is an important cause of morbidity and mortality among cardiac transplant recipients. CAV occurs in approximately 30% of patients by 5 years and 50% by 10 years, and is a major cause of graft loss and death. Early detection of CAV is important because it may allow alterations in medical therapy before progression to the stage that revascularization is required. This has led to routine screening for CAV in transplant recipients, traditionally by invasive coronary angiography (ICA). Recent advances in imaging technology, specifically intravascular ultrasound, now also permit detection of subangiographic CAV. Noninvasive stress testing and multislice coronary computed tomography angiography have been investigated as noninvasive alternatives to routine ICA. However, currently available noninvasive tests remain limited with respect to their sensitivity and specificity for CAV. Given the multiple available diagnostic modalities, no consensus definition for the classification of CAV has been widely accepted, although new guidelines that rely heavily on ICA have recently been published by the International Society of Heart and Lung Transplantation. This review summarizes imaging modalities that are utilized in the diagnosis and surveillance of CAV and explores newer imaging techniques that may play a future role.
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cardiac Allograft Vasculopathy advances in understanding its pathophysiology prevention and treatment
Current Opinion in Cardiology, 2004Co-Authors: Sean Pinney, Donna ManciniAbstract:PURPOSE OF REVIEW To discuss the current understanding of the pathogenesis, natural history, and diagnosis of cardiac Allograft Vasculopathy, and to outline new preventive and treatment strategies. RECENT FINDINGS The central event in the development of Allograft Vasculopathy is the inflammatory response to immune or nonimmune-mediated endothelial damage. This response is characterized by the release of inflammatory cytokines, upregulation of cell-surface adhesion molecules, and the subsequent binding of leukocytes. Once induced, vascular smooth muscle cells proliferate and migrate from the media to form a neointima. Circulating progenitor cells are recruited to sites of arterial injury where they may then differentiate into smooth muscle cells. Because of its diffuse nature, Allograft Vasculopathy is best detected by intravascular ultrasound. Noninvasive tests, such as dobutamine echocardiography, are gaining in favor. Although the only definitive treatment is retransplantation, the immunosuppressant rapamycin can limit disease progression. Its synthetic derivative, everolimus, effectively prevented intimal hyperplasia in de novo transplant recipients. SUMMARY These advances have provided hope that Allograft Vasculopathy may finally be manageable.
Richard J Rodeheffer - One of the best experts on this subject based on the ideXlab platform.
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combined heart and liver transplant attenuates cardiac Allograft Vasculopathy compared with isolated heart transplantation
Transplantation, 2013Co-Authors: Yan Topilsky, Naveen L Pereira, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, Brooks S Edwards, A L Clavell, Richard J Rodeheffer, Robert P FrantzAbstract:Cardiac Allograft Vasculopathy (CAV) remains the leading cause morbidity and mortality in heart transplant recipients. (1, 2) Attempts at combined liver and renal transplantation against a positive cross-match (3–6) suggest that the liver graft protect the subsequent renal transplant from damage due to circulating pre-formed antibodies. Numerous reports suggest that any “multi-organ” transplant that includes more than the heart is associated with less cardiac rejection and CAV. (7–11) The experience with combined heart and liver transplant is small and limited mainly to patients with familial amyloidosis (FA), an autosomal-dominant disease. We have reported our single-center experience of combined heart and liver transplantation (H+Liver Tx) (12) in which we found no significant CAV in any of the H+Liver Tx patients by using routine angiography while in the comparable isolated heart transplant (HTx) group, angiographic CAV was diagnosed in 38% of patients. Based on these initial observations, we used serial coronary 3D volumetric IVUS to precisely delineate the occurrence and rate of progression of the CAV in patients with combined heart and liver transplant.
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donor specific antibodies to class ii antigens are associated with accelerated cardiac Allograft Vasculopathy a three dimensional volumetric intravascular ultrasound study
Transplantation, 2013Co-Authors: Yan Topilsky, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, Brooks S Edwards, A L Clavell, Manish J Gandhi, Laurie Voit, Richard J RodehefferAbstract:Background Although a link between donor-specific antibodies against human leukocyte antigens type II (DSA II+) and transplant glomerulopathy has been clearly established, its role in cardiac Allograft Vasculopathy (CAV) is unclear.
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sirolimus as primary immunosuppression attenuates Allograft Vasculopathy with improved late survival and decreased cardiac events after cardiac transplantation
Circulation, 2012Co-Authors: Yan Topilsky, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, A L Clavell, Richard J Rodeheffer, Brooks Sayre Edwards, Naveen Luke Pereira, Robert P FrantzAbstract:Background—We retrospectively analyzed the potential of sirolimus as a primary immunosuppressant in the long-term attenuation of cardiac Allograft Vasculopathy progression and the effects on cardiac-related morbidity and mortality. Methods and Results—Forty-five cardiac transplant recipients were converted to sirolimus 1.2 years (0.2, 4.0) after transplantation with complete calcineurin inhibitor withdrawal. Fifty-eight control subjects 2.0 years (0.2, 6.5 years) from transplantation were maintained on calcineurin inhibitors. Age, sex, ejection fraction, and time from transplantation to baseline intravascular ultrasound study were not different (P>0.2 for all) between the groups; neither were secondary immunosuppressants and use of steroids. Three-dimensional intravascular ultrasound studies were performed at baseline and 3.1 years (1.3, 4.6 years) later. Plaque index progression (plaque volume/vessel volume) was attenuated in the sirolimus group (0.7±10.5% versus 9.3±10.8%; P=0.0003) owing to reduced pla...
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acute cellular rejection and the subsequent development of Allograft Vasculopathy after cardiac transplantation
Journal of Heart and Lung Transplantation, 2009Co-Authors: Eugenia Raichlin, Walter K Kremers, A L Clavell, Richard J Rodeheffer, Robert P Frantz, Brooks Sayre Edwards, Naveen Luke Pereira, Richard C Daly, Christopher G A Mcgregor, Amir LermanAbstract:Background Cardiac Allograft Vasculopathy (CAV) is primarily immune-mediated. We investigated the role of cellular rejection in CAV development. Methods The study comprised 252 cardiac transplant recipients (mean age, 49.02 ± 17.05 years; mean follow-up, 7.61 ± 4.49 years). Total rejection score (TRS) based on the 2004 International Society of Heart and Lung Transplantation R grading system (0R = 0, 1R=1, 2R=2, 3R=3) and any rejection score (ARS; calculated as 0R=0, 1R=1, 2R=1; 3R=1, or the number of rejections of any grade) were normalized for the total number of biopsy specimens. CAV was defined as coronary stenosis of 40% or more and/or distal pruning of secondary side branches. Thirty-two patients had undergone 3-dimensional intravascular ultrasound (IVUS) at baseline and with virtual histology (VH) IVUS at 24 months. Results In univariate analysis, 6-month TRS (hazard ratio [HR], 1.9; 95% confidence interval [CI], 0.99–3.90, p = 0.05) and ARS (HR, 2.22; 95% CI, 1.01–4.95; p = 0.047) were associated with increased risk of CAV. In multivariate analysis, 6-month TRS (HR, 2.84; 95% CI, 1.44–6.91, p = 0.02) was significantly associated with increased risk of CAV onset. The 12- and 24-month rejection scores were not risk factors for the onset of CAV. By Kaplan-Meier analysis, 6-month TRS exceeding 0.3 was associated with a significantly shorter time to CAV onset ( p = 0.018). There was direct correlation ( r = 0.44, p = 0.012) between TRS at 6 months and the percentage of necrotic core demonstrated by VH-IVUS at 24 months. Conclusion Recurrent cellular rejection has a cumulative effect on the onset of CAV. The mechanism may be due to increased inflammation resulting in increased plaque burden suggesting a relationship between the immune basis of cellular rejection and CAV.
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conversion to sirolimus as primary immunosuppression attenuates the progression of Allograft Vasculopathy after cardiac transplantation
Circulation, 2007Co-Authors: Eugenia Raichlin, Walter K Kremers, A L Clavell, Richard J Rodeheffer, Robert P Frantz, Brooks Sayre Edwards, Amir Lerman, Zain I Khalpey, Charanjit S Rihal, Sudhir S KushwahaAbstract:Background— We investigated the potential of conversion to sirolimus (SRL) as a primary immunosuppressant in attenuating cardiac Allograft Vasculopathy progression. Methods and Results— Twenty-nine cardiac transplant recipients were converted to SRL 3.8±3.4 years after transplantation with complete calcineurin inhibitor (CNI) withdrawal. Secondary immunosuppressants (azathioprine or mycophenolate) and steroids remained unchanged. Forty patients (controls) 4.8±4.0 years from transplantation were maintained on CNIs. Three-dimensional intravascular ultrasound studies were performed at baseline and 12.1±2.6 months later. Mean plaque (media and intima) volume (PV) and plaque index (PI) (PV/vessel volume percent) increased significantly in the CNI group (1.28±2.86 mm3/mm, P=0.004; and 6±8%, P=0.0001) but not in the SRL group (0.1±1.13 mm3/mm, P=0.63; and 0.1±8%, P=0.94). In patients enrolled within 2 years after transplantation, the increases in PV (0.06±1.06 versus 1.77±1.65 mm3/mm; P=0.0081) and PI (0±9% vers...
A L Clavell - One of the best experts on this subject based on the ideXlab platform.
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effects of mtor inhibitor related proteinuria on progression of cardiac Allograft Vasculopathy and outcomes among heart transplant recipients
American Journal of Transplantation, 2021Co-Authors: Rabea Asleh, Naveen L Pereira, Brooks S Edwards, A L Clavell, Amir Lerman, Alexandros Briasoulis, John M Stulak, Hilmi Alnsasra, Takumi Toya, Richard C DalyAbstract:We have previously described the use of sirolimus (SRL) as primary immunosuppression following heart transplantation (HT). The advantages of this approach include attenuation of cardiac Allograft Vasculopathy (CAV), improvement in glomerular filtration rate (GFR), and reduced malignancy. However, in some patients SRL may cause significant proteinuria. We sought to investigate the prognostic value of proteinuria after conversion to SRL. CAV progression and adverse clinical events were studied. CAV progression was assessed by measuring the Δ change in plaque volume (PV) and plaque index (PI) per year using coronary intravascular ultrasound. Proteinuria was defined as Δ urine protein ≥300 mg/24 h at 1 year after conversion to SRL. Overall, 137 patients were analyzed (26% with proteinuria). Patients with proteinuria had significantly lower GFR (P = .005) but similar GFR during follow-up. Delta PV (P < .001) and Δ PI (P = .001) were significantly higher among patients with proteinuria after adjustment for baseline characteristics. Multivariate Cox regression analysis showed higher all-cause mortality (hazard ratio 3.8; P = .01) with proteinuria but similar risk of CAV-related events (P = .61). Our results indicate that proteinuria is a marker of baseline renal dysfunction, and that HT recipients who develop proteinuria after conversion to SRL have less attenuation of CAV progression and higher mortality risk.
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long term effects of aspirin on cardiac Allograft Vasculopathy progression and adverse outcomes after heart transplantation
Journal of the American College of Cardiology, 2020Co-Authors: Rabea Asleh, Byron H Smith, Walter K Kremers, Naveen L Pereira, Brooks S Edwards, Amir Lerman, Alexandros Briasoulis, Camden L Lopez, John M Stulak, A L ClavellAbstract:Enhanced platelet reactivity may play a role in the development and progression of cardiac Allograft Vasculopathy (CAV). The use of anti-platelet agents following heart transplantation (HT) has been inconsistent and although aspirin is often a part of the medication regimen after HT, limited
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combined heart and liver transplant attenuates cardiac Allograft Vasculopathy compared with isolated heart transplantation
Transplantation, 2013Co-Authors: Yan Topilsky, Naveen L Pereira, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, Brooks S Edwards, A L Clavell, Richard J Rodeheffer, Robert P FrantzAbstract:Cardiac Allograft Vasculopathy (CAV) remains the leading cause morbidity and mortality in heart transplant recipients. (1, 2) Attempts at combined liver and renal transplantation against a positive cross-match (3–6) suggest that the liver graft protect the subsequent renal transplant from damage due to circulating pre-formed antibodies. Numerous reports suggest that any “multi-organ” transplant that includes more than the heart is associated with less cardiac rejection and CAV. (7–11) The experience with combined heart and liver transplant is small and limited mainly to patients with familial amyloidosis (FA), an autosomal-dominant disease. We have reported our single-center experience of combined heart and liver transplantation (H+Liver Tx) (12) in which we found no significant CAV in any of the H+Liver Tx patients by using routine angiography while in the comparable isolated heart transplant (HTx) group, angiographic CAV was diagnosed in 38% of patients. Based on these initial observations, we used serial coronary 3D volumetric IVUS to precisely delineate the occurrence and rate of progression of the CAV in patients with combined heart and liver transplant.
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donor specific antibodies to class ii antigens are associated with accelerated cardiac Allograft Vasculopathy a three dimensional volumetric intravascular ultrasound study
Transplantation, 2013Co-Authors: Yan Topilsky, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, Brooks S Edwards, A L Clavell, Manish J Gandhi, Laurie Voit, Richard J RodehefferAbstract:Background Although a link between donor-specific antibodies against human leukocyte antigens type II (DSA II+) and transplant glomerulopathy has been clearly established, its role in cardiac Allograft Vasculopathy (CAV) is unclear.
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sirolimus as primary immunosuppression attenuates Allograft Vasculopathy with improved late survival and decreased cardiac events after cardiac transplantation
Circulation, 2012Co-Authors: Yan Topilsky, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, A L Clavell, Richard J Rodeheffer, Brooks Sayre Edwards, Naveen Luke Pereira, Robert P FrantzAbstract:Background—We retrospectively analyzed the potential of sirolimus as a primary immunosuppressant in the long-term attenuation of cardiac Allograft Vasculopathy progression and the effects on cardiac-related morbidity and mortality. Methods and Results—Forty-five cardiac transplant recipients were converted to sirolimus 1.2 years (0.2, 4.0) after transplantation with complete calcineurin inhibitor withdrawal. Fifty-eight control subjects 2.0 years (0.2, 6.5 years) from transplantation were maintained on calcineurin inhibitors. Age, sex, ejection fraction, and time from transplantation to baseline intravascular ultrasound study were not different (P>0.2 for all) between the groups; neither were secondary immunosuppressants and use of steroids. Three-dimensional intravascular ultrasound studies were performed at baseline and 3.1 years (1.3, 4.6 years) later. Plaque index progression (plaque volume/vessel volume) was attenuated in the sirolimus group (0.7±10.5% versus 9.3±10.8%; P=0.0003) owing to reduced pla...
Naveen L Pereira - One of the best experts on this subject based on the ideXlab platform.
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effects of mtor inhibitor related proteinuria on progression of cardiac Allograft Vasculopathy and outcomes among heart transplant recipients
American Journal of Transplantation, 2021Co-Authors: Rabea Asleh, Naveen L Pereira, Brooks S Edwards, A L Clavell, Amir Lerman, Alexandros Briasoulis, John M Stulak, Hilmi Alnsasra, Takumi Toya, Richard C DalyAbstract:We have previously described the use of sirolimus (SRL) as primary immunosuppression following heart transplantation (HT). The advantages of this approach include attenuation of cardiac Allograft Vasculopathy (CAV), improvement in glomerular filtration rate (GFR), and reduced malignancy. However, in some patients SRL may cause significant proteinuria. We sought to investigate the prognostic value of proteinuria after conversion to SRL. CAV progression and adverse clinical events were studied. CAV progression was assessed by measuring the Δ change in plaque volume (PV) and plaque index (PI) per year using coronary intravascular ultrasound. Proteinuria was defined as Δ urine protein ≥300 mg/24 h at 1 year after conversion to SRL. Overall, 137 patients were analyzed (26% with proteinuria). Patients with proteinuria had significantly lower GFR (P = .005) but similar GFR during follow-up. Delta PV (P < .001) and Δ PI (P = .001) were significantly higher among patients with proteinuria after adjustment for baseline characteristics. Multivariate Cox regression analysis showed higher all-cause mortality (hazard ratio 3.8; P = .01) with proteinuria but similar risk of CAV-related events (P = .61). Our results indicate that proteinuria is a marker of baseline renal dysfunction, and that HT recipients who develop proteinuria after conversion to SRL have less attenuation of CAV progression and higher mortality risk.
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long term effects of aspirin on cardiac Allograft Vasculopathy progression and adverse outcomes after heart transplantation
Journal of the American College of Cardiology, 2020Co-Authors: Rabea Asleh, Byron H Smith, Walter K Kremers, Naveen L Pereira, Brooks S Edwards, Amir Lerman, Alexandros Briasoulis, Camden L Lopez, John M Stulak, A L ClavellAbstract:Enhanced platelet reactivity may play a role in the development and progression of cardiac Allograft Vasculopathy (CAV). The use of anti-platelet agents following heart transplantation (HT) has been inconsistent and although aspirin is often a part of the medication regimen after HT, limited
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response by wong et al to letter regarding article importance of routine antihuman leukocyte antibody monitoring de novo donor specific antibodies are associated with rejection and Allograft Vasculopathy after heart transplantation
Circulation, 2018Co-Authors: Ka L Wong, Byron H Smith, Walter K Kremers, Naveen L PereiraAbstract:We thank Clerkin et al for their interest in our study addressing the importance of routine monitoring for de novo donor–specific antibodies (dnDSA) not only in predicting cellular and antibody-mediated rejection (AMR) but also for the first time demonstrating its association with Allograft Vasculopathy detected by intravascular ultrasound.1 Our data were analyzed using a Cox regression survival analysis model accounting for the timing of dnDSA events when predicting subsequent incidence of AMR. In 2 previous studies cited by Clerkin, patients at time of transplant were classified according to posttransplant outcomes such as dnDSA or AMR. Statistical theory does not …
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combined heart and liver transplant attenuates cardiac Allograft Vasculopathy compared with isolated heart transplantation
Transplantation, 2013Co-Authors: Yan Topilsky, Naveen L Pereira, Eugenia Raichlin, Tal Hasin, Barry A Boilson, John A Schirger, Brooks S Edwards, A L Clavell, Richard J Rodeheffer, Robert P FrantzAbstract:Cardiac Allograft Vasculopathy (CAV) remains the leading cause morbidity and mortality in heart transplant recipients. (1, 2) Attempts at combined liver and renal transplantation against a positive cross-match (3–6) suggest that the liver graft protect the subsequent renal transplant from damage due to circulating pre-formed antibodies. Numerous reports suggest that any “multi-organ” transplant that includes more than the heart is associated with less cardiac rejection and CAV. (7–11) The experience with combined heart and liver transplant is small and limited mainly to patients with familial amyloidosis (FA), an autosomal-dominant disease. We have reported our single-center experience of combined heart and liver transplantation (H+Liver Tx) (12) in which we found no significant CAV in any of the H+Liver Tx patients by using routine angiography while in the comparable isolated heart transplant (HTx) group, angiographic CAV was diagnosed in 38% of patients. Based on these initial observations, we used serial coronary 3D volumetric IVUS to precisely delineate the occurrence and rate of progression of the CAV in patients with combined heart and liver transplant.