Article Text

Secretory products of epicardial adipose tissue in association with obesity and coronary artery disease
  1. K Karastergiou1,
  2. NC Ogston2,
  3. JC Kaski1,
  4. V Mohamed-Ali2,
  5. M Jahangiri1
  1. 1St George’s University of London, London, UK
  2. 2University College London, London, UK


Introduction Secretory products of adipose tissue (adipokines), especially of the epicardial depot that surrounds the coronary arteries, may affect vascular homeostasis. The majority of these adipokines are detrimental to the vessel wall, with the exception of adiponectin, which is anti-inflammatory and anti-atherogenic. Therefore, we set out to investigate whether obesity and/or coronary artery disease (CAD) are associated with alterations in epicardial adipokines.

Methods Fasting blood samples and epicardial and subcutaneous fat samples were collected from white, non-diabetic patients undergoing cardiac surgery with or without CAD (CAD group, n  =  44 and control group, n  =  22). Both groups were subdivided into lean and obese subgroups (body mass index ⩽27 kg/m2 and >27 kg/m2, respectively). Leptin, adiponectin and IL-6 levels were determined in serum and supernatant of adipose tissue organ cultures (0.1 g/ml of serum-free media for 24 h at 37°C/5% CO2) by two-site ELISA. Data are presented as median (interquartile range).

Results Epicardial fat secreted significantly higher amounts of leptin (0.56 (0.22–1.1) vs 0.13 (0.06–0.45) ng/g per hour), adiponectin (55.7 (37.0–91.0) vs 35.8 (23.8–67.8) ng/g per hour) and IL-6 (1.99 (1.22–3.75) vs 0.57 (0.32–1.16) ng/g per hour) compared with thoracic subcutaneous tissue, all p<0.001. Obesity and CAD were associated with suppressed epicardial adiponectin release. Thus, lean/control patients had significantly higher epicardial adiponectin (111.5 (66.2–182.9) ng/g per hour) compared with obese/control (55.2 (38.1–105.5) ng/g per hour, p = 0.05), lean/CAD (44.7 (33.3–91.0) ng/g per hour, p = 0.007) and obese/CAD patients (48.8 (35.4–87.9) ng/g per hour, p<0.001). No additive effect of obesity and CAD was noted. Epicardial adiponectin also correlated with high-density lipoprotein cholesterol (r  =  0.36, p = 0.03) and triglycerides (r  =  −0.356, p = 0.03). Subcutaneous and systemic adiponectin followed similar trends. Epicardial leptin and IL-6 levels were not associated with either obesity or CAD.

Conclusion The release of adiponectin, an anti-inflammatory mediator, by epicardial adipose tissue is suppressed in the presence of obesity and CAD. The release of leptin and IL-6 remained unaltered. Whether these changes can have pathophysiological consequences in the neighbouring myocardium and coronary arteries should be addressed in future studies.

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