Changes in Plasma Levels of VEGF-C and Endothelin-1 During the First Post-Transplant Year Are Predictive of Cardiac Allograft Vasculopathy: Results From the CTOT-05 Study.

2014 ◽  
Vol 98 ◽  
pp. 878 ◽  
Author(s):  
K. Daly ◽  
R. Starling ◽  
B. Armstrong ◽  
D. Ikle ◽  
N. Bridges ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Post Transplant ◽  
Endothelin 1

Circulating C-type natriuretic peptide is increased in orthotopic cardiac transplant recipients and associated with cardiac allograft vasculopathy

2000 ◽  
Vol 99 (5) ◽  
pp. 467-472 ◽  
Author(s):  
Martin G. BUCKLEY ◽  
Geraint H. JENKINS ◽  
Andrew G. MITCHELL ◽  
Magdi H. YACOUB ◽  
Donald R. J. SINGER
Keyword(s):  
Heart Transplantation ◽  
Plasma Levels ◽  
Healthy Subjects ◽  
Cardiac Transplantation ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Cardiac Transplant ◽  
Transplant Recipients ◽  
Allograft Vasculopathy ◽  
Post Transplant

C-type natriuretic peptide (CNP) is a potent, endothelial-derived relaxant and growth-inhibitory factor. Accelerated vascular disease is an important cause of morbidity in cardiac transplant recipients, and endothelial dysfunction is now well recognized in patients with cardiovascular disease. CNP has not previously been investigated following cardiac transplantation. We therefore studied plasma levels of immunoreactive CNP in patients early and late after heart transplantation, compared with levels in healthy subjects. We measured CNP in extracted human plasma using an antibody against human CNP-(1–22). CNP levels were significantly elevated in 13 cardiac recipients 2 weeks post-transplant [2.64±0.26 pmol/l (mean±S.E.M.)] compared with those in the normal healthy subjects (0.62±0.04 pmol/l; n = 20, P < 0.001). Plasma levels of CNP were also significantly elevated in a second group of established cardiac transplant recipients (1.15±0.07 pmol/l; n = 46) studied 1–13 years post-transplant when compared with the healthy subjects (P < 0.001). In the group studied later after transplantation, CNP levels were significantly associated with systolic blood pressure (P < 0.05) and were higher in patients with angiographic post-transplant coronary artery disease (P = 0.032). In conclusion, these findings clearly demonstrate that CNP is elevated soon after cardiac transplantation and remains raised in patients even several years post-transplant. CNP may be important as a circulating or local hormone involved in vascular contractile function and in the pathophysiology of cardiac allograft vasculopathy following heart transplantation.

Post-transplant increase in soluble human leukocyte antigen-G associated with non-severe cardiac allograft vasculopathy

2013 ◽  
Vol 74 (3) ◽  
pp. 318-324 ◽  
Author(s):  
R.M. Blanco-García ◽  
M.R. López-Álvarez ◽  
I.P. Garrido ◽  
G. Salgado-Cecilia ◽  
J.A. Campillo ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Leukocyte Antigen ◽  
Post Transplant ◽  
Human Leukocyte Antigen G

Abstract 17120: Association of Endotoxemia and Endothelin-1 With Development of Cardiac Allograft Vasculopathy After Heart Transplantation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lorenzo Braghieri ◽  
Bruno Bohn ◽  
Giulio Mondellini ◽  
Azka Javaid ◽  
Andrea J Kim ◽  
...  
Keyword(s):  
Median Time ◽  
Subsequent Development ◽  
Endothelial Damage ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Blood Collection ◽  
Allograft Vasculopathy ◽  
Entire Cohort ◽  
Endothelin 1 ◽  
Increased Risk

Introduction: Cardiac allograft vasculopathy (CAV) is a leading cause of death after heart transplant (HT). Inflammation is a known cardiovascular risk factor, with gut derived endotoxemia potentially instigating this process, leading to endothelial damage. Our prior work showed that elevation of biomarkers of inflammation (endothelin-1 (ET-1)) and endotoxemia (lipopolysaccharide (LPS)) persists after HT. We investigated the association of LPS and ET-1 with subsequent development of CAV. Methods: Pts who met the following criteria were included: i) blood sampling ≥6 mo post-HT; ii) no evidence of CAV at the time of sampling. Pts were followed up to 2.3y after sampling. Cox-PH was used to regress freedom from CAV on LPS and ET-1 (≤ vs >median), time from HT to sampling (≤ vs >1y), interaction among variables. Results: 33 HT pts enrolled, mean age 57±11y; 70% male; median time post-HT 1.96(0.5-3.7)y. 17(52%) pts developed CAV at 0.7(0.6-1)y following blood collection. Baseline characteristics of pts who developed CAV vs not were similar, except for longer median time post-HT in pts who developed CAV: 2.4(0.7-5.3) vs 1.05(0.5-2.7)y, p=0.1. Median LPS and ET-1 for the entire cohort were 0.34(0.28-0.45) EU/ml and 1.83(1.26-2.72) pg/ml. Pts with >median LPS or ET-1 values trended towards higher risk of developing CAV: HR 1.79(0.66, 4.85), p=0.3 ( Fig.1A ); HR 2.05(0.71, 5.92), p=0.2 ( Fig.1B ). No association was observed between time post-HT and CAV: HR=0.87 comparing ≤ vs. >1y, p=0.8. Pts with both >median LPS and ET-1 levels (n=7) were at significantly higher risk of CAV: HR 2.96(1.06, 8.27), p=0.039, compared to others ( Fig.1C ). When examining pts sampled within the first year of HT (N=14), pts with >median LPS (N=5) were at particularly increased risk of CAV: HR 9.71(0.97, 96.9), p=0.05, while pts with >median ET-1 were not. Conclusions: Elevated LPS and ET-1 synergistically associate with increased CAV risk post-HT. Further studies are warranted to validate these findings.

scholarly journals Value of the First Post-Transplant Biopsy for Predicting Long-Term Cardiac Allograft Vasculopathy (CAV) and Graft Failure in Heart Transplant Patients

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e36100 ◽  
Author(s):  
Carlos A. Labarrere ◽  
John R. Woods ◽  
James W. Hardin ◽  
Gonzalo L. Campana ◽  
Miguel A. Ortiz ◽  
...  
Keyword(s):  
Heart Transplant ◽  
Graft Failure ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Post Transplant ◽  
Transplant Patients ◽  
Transplant Biopsy

scholarly journals Association of Endothelin-1 With Accelerated Cardiac Allograft Vasculopathy and Late Mortality Following Heart Transplantation

2019 ◽  
Vol 25 (2) ◽  
pp. 97-104 ◽  
Author(s):  
Rushi V. Parikh ◽  
Kiran Khush ◽  
Vedant S. Pargaonkar ◽  
Helen Luikart ◽  
David Grimm ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Late Mortality ◽  
Endothelin 1

scholarly journals Gene Expression Signatures of Peripheral Blood Mononuclear Cells during the Early Post-Transplant Period in Patients Developing Cardiac Allograft Vasculopathy

2010 ◽  
Vol 2010 ◽  
pp. 1-13 ◽  
Author(s):  
Khurram Shahzad ◽  
Martin Cadeiras ◽  
Sarfaraz Memon ◽  
Barry Zeeberg ◽  
Tod Klingler ◽  
...  
Keyword(s):  
Gene Expression ◽  
At Risk ◽  
Expression Profiles ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Diagnostic Methods ◽  
Differentially Expressed ◽  
Allograft Vasculopathy ◽  
Post Transplant ◽  
Patients At Risk

Background. Cardiac allograft vasculopathy (CAV) is a major cause of graft loss and death after heart transplantation. Currently, no diagnostic methods are available during the early post-transplant period to accurately identify patients at risk of CAV. We hypothesized that PBMC gene expression profiles (GEP) can identify patients at risk of CAV.Methods. We retrospectively analyzed a limited set of whole-genome PBMC microarrays from 10 post-transplant patients who did (n=3) or did not (n=7) develop advanced grade CAV during their long-term follow-up. We used significance analysis of microarrays to identify differentially expressed genes and High-Throughput GoMiner to assess gene ontology (GO) categories. We corroborated our findings by retrospective analysis of PBMC real-time PCR data from 33 patients.Results. Over 300 genes were differentially expressed (FDR < 5%), and 18 GO-categories including “macrophage activation”, “Interleukin-6 pathway”, “NF-KappaB cascade”, and “response to virus” were enriched by these genes (FDR < 5%). Out of 8 transcripts available for RT-PCR analysis, we confirmed 6 transcripts (75.0%) including FPRL1, S100A9, CXCL10, PRO1073, and MMP9 (P<.05).Conclusion. Our pilot data suggest that GEP of PBMC may become a valuable tool in the evaluation of patients at risk of CAV. Larger prospectively designed studies are needed to corroborate our hypothesis.

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