Structural Valve Deterioration Is Linked to Increased Immune Infiltrate and Chemokine Expression.
Sabin J BozsoJimmy J H KangRatnadeep BasuBenjamin AdamJason R B DyckGavin Y OuditMichael C MoonDarren H FreedJayan NagendranJeevan NagendranPublished in: Journal of cardiovascular translational research (2020)
We aim to investigate whether structural valve deterioration (SVD) of bioprosthetic xenogenic tissue heart valves (XTHVs) is associated with increased immune cell infiltration and whether co-expression of several chemokines correlates with this increase in immune infiltrate. Explanted XTHVs from patients undergoing redo valve replacement for SVD were obtained. Immunohistochemical, microscopic, and gene expression analysis approaches were used. XTHVs (n = 37) were obtained from 32 patients (mean 67.7 years) after a mean time of 11.6 years post-implantation. Significantly increased immune cellular infiltration was observed in the explanted SVD valves for all immune cell types examined, including T cells, macrophages, B cells, neutrophils, and plasma cells, compared to non-SVD controls. Furthermore, a significantly increased chemokine gradient in explanted SVD valves accompanied immune cell infiltration. These data suggest the development of SVD is associated with a significantly increased burden of immune cellular infiltrate correlated to the induction of a chemokine gradient around the XHTV, representing chronic immune rejection.Graphical abstract Proposed interaction between innate and adaptive immunity leading to the development of structural valve deterioration in xenogenic tissue heart valves.
Keyphrases
- aortic valve
- aortic valve replacement
- aortic stenosis
- transcatheter aortic valve replacement
- transcatheter aortic valve implantation
- mitral valve
- ejection fraction
- patients undergoing
- poor prognosis
- immune response
- end stage renal disease
- heart failure
- chronic kidney disease
- newly diagnosed
- atrial fibrillation
- induced apoptosis
- machine learning
- binding protein
- oxidative stress
- copy number
- left ventricular
- gene expression
- risk factors
- long non coding rna
- big data
- patient reported outcomes
- dna methylation
- drug induced