AI Summary & Key Takeaways
AI InsightConclusion: Our study shows that both peri-arterial and atrial EAT inflammation significantly increase in patients with CAD, suggesting that inflammation in EAT may have a significant relationship with the CAD’s pathogenesis.
📌 3 Key Takeaways
Abstract
Objectives: In this study, we aimed to investigate the potential relationship between inflammation of the epicardial adipose tissue (EAT) and coronary artery disease (CAD). Patients and methods: Between September 2017 and March 2018, a total of 38 patients (31 males, 7 females; mean age: 55 years; range, 46 to 64 years) who underwent elective open heart surgery were prospectively analyzed. The patients were divided into two groups according to the procedure type as those without CAD (n=15) and those with CAD (n=23) as the control group. The CAD group underwent isolated coronary artery bypass grafting, while the control group underwent open heart surgery and had normal coronary arteries as assessed by coronary angiography. The EAT samples were taken intraoperatively from peri-arterial and right atrial appendage in the CAD patients, while the samples were taken from only right atrial appendage in the control group. Specimens were stained and the presence and amount of inflammatory cell infiltrates were examined. More than 50 inflammatory cell counts in the pathological examination were accepted as significant inflammation. Results: The mean white blood cell (7.5±2.3 vs. 7.1±2.2, respectively; p=0.842) and mean C-reactive protein (0.4±1.0 vs. 0.5±0.8, respectively; p=0.755) values were similar in both groups. In the CAD group, inflammatory cell infiltration in the atrium was more frequent than the control group (43% vs. 6.6%, respectively; p=0.036). Peri-arterial infiltration was also high similar with RAA in the CAD group. Conclusion: Our study shows that both peri-arterial and atrial EAT inflammation significantly increase in patients with CAD, suggesting that inflammation in EAT may have a significant relationship with the CAD’s pathogenesis.