# Potential Inflammatory Mediators in Pericardial Fluids of Patients With Coronary Artery Diseases and Their Association With Plasma Biomarkers

## TL;DR

This study explores inflammatory markers in pericardial fluid and blood of heart disease patients, finding higher levels in fluid and potential for new biomarkers.

## Contribution

The study identifies pericardial fluid as a potential source of novel biomarkers for coronary artery disease through analysis of specific inflammatory mediators.

## Key findings

- IL-33 and fetuin A protein levels were significantly higher in pericardial fluid compared to plasma.
- CK-18 levels were similar in plasma and pericardial fluid.
- Strong positive correlations were found between CK-18 and both IL-33 and fetuin A in pericardial fluid.

## Abstract

The aim of this study was to determine the gene expression and protein levels of interleukin‐33 (IL‐33), fetuin A and cytokeratin 18 (CK‐18) in the pericardial fluid (PF) and plasma of patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting (CABG). The CAD patients (mean age: 73.4 years) were enrolled. The IL‐33, fetuin A, and CK‐18 protein levels in pericardial fluid (PF) and plasma of patients with CAD were measured by ELISA, while IL‐33 and Fetuin A gene expressions were analysed via quantitative reverse transcription‐PCR (qRT‐PCR). The IL‐33 protein level in PF was significantly higher than plasma (PF: 57.09 ng/L; Plasma: 50.15 ng/L; p < 0.05). Similarly, the fetuin A protein levels were significantly elevated in PF compared to plasma (PF: 1060.53 mg/L; Plasma: 725.85 mg/L; p < 0.05). However, gene expression levels (ΔCt values) for IL‐33 and fetuin A were significantly higher in plasma than in PF (p < 0.05). The CK‐18 protein levels were comparable between plasma and PF (p > 0.05). Strong positive correlations were observed between CK‐18 and IL‐33 (r = 0.127, p < 0.001) and between CK‐18 and fetuin A (r = 0.096, p < 0.001) in PF. The IL‐33, fetuin A, and CK‐18 levels in PF are predicted to have the potential to be used as a source of biomarkers for CAD. Although the collection of PF samples requires an invasive procedure, the proximity of PF to the heart tissue makes it a valuable source for understanding cardiac pathophysiology. These findings highlight the potential diagnostic and therapeutic utility of PF biomarkers in patients with CAD.