Iwayama Tadateru, Nitobe Joji, Watanabe Tetsu, Ishino Mitsunori, Tamura Harutoshi, Nishiyama Satoshi, Takahashi Hiroki, Arimoto Takanori, Shishido Tetsuro, Miyashita Takehiko, Miyamoto Takuya, Toyama Shuji, Sadahiro Mitsuaki, Kubota Isao
Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
J Cardiol. 2014 May;63(5):344-9. doi: 10.1016/j.jjcc.2013.10.002. Epub 2013 Nov 11.
Epicardial adipose tissue (EAT) surrounding the heart may contribute to the development of coronary artery disease (CAD) through its local secretion of adipocytokines. Although the quantity of EAT is associated with obesity and metabolic syndrome, the role of EAT in the development of CAD in non-obese patients remains to be determined.
This study included 41 patients with CAD who underwent coronary artery bypass graft surgery and 28 patients without CAD who underwent other cardiac surgery. EAT volume was measured by 64-slice multi-detector computed tomography before the surgery. We obtained pericardial fluid and epicardial and subcutaneous adipose tissue samples at the surgery. We investigated the relationship between EAT volume and adiponectin levels in pericardial fluid and incident CAD in patients with and without obesity (body mass index>25 kg/m(2)).
There was no significant difference in EAT volume between obese patients with and without CAD (55.5 ± 40.2 mL vs. 40.1 ± 19.7 mL, p=0.323). However, EAT volume was significantly greater in non-obese patients with CAD compared to those without CAD (35.0 ± 18.8 mL vs. 15.7 ± 11.0 mL, p<0.001). Adiponectin concentrations in pericardial fluid were significantly lower in non-obese patients with CAD compared to those without CAD (2.7 ± 2.0 μg/mL vs. 4.3 ± 3.7 μg/mL, p=0.049), whereas the adiponectin levels were decreased in obese patients regardless of the presence of CAD. Non-obese patients with CAD had significantly larger size adipocytes in EAT but not subcutaneous adipose tissue compared to those without CAD. Multiple logistic regression analysis showed that increased EAT volume was independently associated with incident CAD in non-obese patients.
Increased EAT may play a crucial role in development of CAD through impairment of adiponectin secretion in non-obese patients.
心脏周围的心外膜脂肪组织（EAT）可能通过其局部分泌的脂肪细胞因子促进冠状动脉疾病（CAD）的发展。尽管EAT的数量与肥胖和代谢综合征相关，但EAT在非肥胖患者CAD发展中的作用仍有待确定。
本研究纳入了41例行冠状动脉旁路移植术的CAD患者和28例行其他心脏手术的非CAD患者。术前通过64层多探测器计算机断层扫描测量EAT体积。术中获取心包液以及心外膜和皮下脂肪组织样本。我们研究了肥胖和非肥胖患者（体重指数>25kg/m²）的EAT体积与心包液中脂联素水平以及CAD发生率之间的关系。
肥胖的CAD患者与非CAD患者的EAT体积无显著差异（55.5±40.2mL对40.1±19.7mL，p=0.323）。然而，与非CAD的非肥胖患者相比，CAD的非肥胖患者的EAT体积显著更大（35.0±18.8mL对15.7±11.0mL，p<0.001）。与非CAD的非肥胖患者相比，CAD的非肥胖患者心包液中的脂联素浓度显著降低（2.7±2.0μg/mL对4.3±3.7μg/mL，p= .049），而无论是否患有CAD，肥胖患者的脂联素水平均降低。与非CAD的患者相比，CAD的非肥胖患者的心外膜脂肪组织而非皮下脂肪组织中的脂肪细胞显著更大。多因素逻辑回归分析显示，EAT体积增加与非肥胖患者发生CAD独立相关。
在非肥胖患者中，EAT增加可能通过损害脂联素分泌在CAD发展中起关键作用。
