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Roles of human epicardial adipose tissue in coronary artery atherosclerosis
Xinzhong Chen1, Zhouyang Jiao, Lei Wang
1Department of Cardiovascular Surgery, Huazhong University of Science and Technology, Wuhan, China. xinzhongchen@yahoo.com.cn
Insights
Epicardial adipose tissue inflammation is linked to coronary artery disease (CAD). Lower adiponectin levels in CAD patients suggest its role in disease development.
Area of Science:
- Cardiovascular Research
- Metabolic Syndrome
- Inflammation Biology
Background:
- Epicardial adipose tissue (EAT) is metabolically active and influences coronary artery health.
- Adipocytokines secreted by EAT may play a role in the pathogenesis of coronary artery disease (CAD).
- Understanding the specific interactions between EAT and vascular disease is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the relationship between epicardial adipose tissue and coronary artery atherosclerosis.
- To compare adipocytokine levels and gene expression in patients with and without coronary artery disease.
- To elucidate the role of local inflammation in epicardial adipose tissue in CAD pathogenesis.
Main Methods:
- Comparative analysis of plasma adipocytokine levels (adiponectin, IL-10, TNF-α) using ELISA in 34 patients.
- Assessment of adiponectin and CD68 expression in epicardial and subcutaneous adipose tissue via RT-PCR and immunohistochemistry.
- Stratification of patients into non-coronary artery disease (Group I) and coronary artery disease (Group II) groups.
Main Results:
- Plasma adiponectin levels were significantly lower in the coronary artery disease group (Group II) compared to the non-coronary artery disease group (Group I).
- No significant differences were observed in plasma IL-10, TNF-α, total cholesterol, HDL-cholesterol, or LDL-cholesterol between the groups.
- Epicardial adipose tissue in Group II showed increased CD68+ cell infiltration and significantly lower adiponectin mRNA expression compared to subcutaneous adipose tissue and Group I.
Conclusions:
- Local inflammation within epicardial adipose tissue is implicated in the pathogenesis of coronary artery disease.
- Reduced adiponectin expression in epicardial adipose tissue may contribute to the development of atherosclerosis.
- Epicardial adipose tissue serves as a potential indicator and contributor to coronary artery disease progression.
Abstract:
This study examined the adipocytokine-vascular interactions and link between epicardial adipose tissue and coronary artery atherosclerosis. Thirty-four patients undergoing open heart surgery were chosen randomly, and divided into group I (non-coronary artery disease group) and group II (coronary artery disease group). Blood samples were taken through peripheral vein prior to surgery. Plasma levels of a panel of proteins (adiponectin, IL-10, TNF-α) were detected by using ELISA. Epicardial adipose tissue was taken near the proximal tract of the right coronary artery and subcutaneous adipose was taken from the leg before cardiopulmonary bypassing, adiponectin and CD68 + were detected by using RT-PCR and immunohistochemistry. Our results showed that plasma adiponectin level was significantly lower in the group II as compared with group I (P<0.05). There were no differences in plasma concentration (IL-10, TNF-α, tatal-chol, HDL-chol, LDL-chol) between group I and group II. The number of CD68+ cells in epicardial adipose tissue of group II was significantly higher than that in subcutaneous adipose tissue. Adiponectin mRNA expression was 6 fold higher in subcutaneous adipose tissue than in epicardial adipose tissue of group II (P<0.01). Furthermore, the level of adiponectin mRNA in the epicardial adipose tissue in group II was also significantly lower than in group I (P<0.05). We are led to conclude that inflammation that occurs locally in epicardial adipose tissue of CAD contributes to the pathogenesis of coronary artery disease.
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