Human Epicardial Adipose Tissue Is a Source of Inflammatory Mediators

Human Epicardial Adipose Tissue Is a Source of Inflammatory Mediators

November 18, 2003 | Tomasz Mazurek, MD*, LiFeng Zhang, PhD*, Andrew Zalewski, MD; John D. Mannion, MD; James T. Diehl, MD; Hwyda Arafat, MD, PhD; Lea Sarov-Blat, PhD; Shawn O'Brien, PhD; Elizabeth A. Keiper, BS; Anthony G. Johnson, MD; Jack Martin, MD; Barry J. Goldstein, MD, PhD; Yi Shi, MD, PhD
This study investigates the expression of inflammatory mediators in epicardial and subcutaneous adipose tissues in patients with critical coronary artery disease (CAD). The researchers collected paired samples of epicardial and subcutaneous adipose tissues from 42 patients undergoing elective coronary artery bypass grafting (CABG) surgery. They found significantly higher levels of inflammatory mediators, including chemokine (monocyte chemotactic protein [MCP]-1) and cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α), in epicardial adipose tissue compared to subcutaneous adipose tissue. This proinflammatory activity was observed regardless of clinical variables such as diabetes, body mass index, or chronic use of statins or ACE inhibitors/angiotensin II receptor blockers. Microarray analysis confirmed a broad inflammatory reaction in epicardial adipose tissue. Additionally, epicardial adipose tissue showed the presence of inflammatory cell infiltrates, including T lymphocytes, macrophages, and mast cells. The findings suggest that epicardial adipose tissue is a significant source of inflammatory mediators in high-risk cardiac patients, and current therapies do not effectively reduce local inflammatory signals.This study investigates the expression of inflammatory mediators in epicardial and subcutaneous adipose tissues in patients with critical coronary artery disease (CAD). The researchers collected paired samples of epicardial and subcutaneous adipose tissues from 42 patients undergoing elective coronary artery bypass grafting (CABG) surgery. They found significantly higher levels of inflammatory mediators, including chemokine (monocyte chemotactic protein [MCP]-1) and cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α), in epicardial adipose tissue compared to subcutaneous adipose tissue. This proinflammatory activity was observed regardless of clinical variables such as diabetes, body mass index, or chronic use of statins or ACE inhibitors/angiotensin II receptor blockers. Microarray analysis confirmed a broad inflammatory reaction in epicardial adipose tissue. Additionally, epicardial adipose tissue showed the presence of inflammatory cell infiltrates, including T lymphocytes, macrophages, and mast cells. The findings suggest that epicardial adipose tissue is a significant source of inflammatory mediators in high-risk cardiac patients, and current therapies do not effectively reduce local inflammatory signals.
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