Human epicardial adipose tissue: A review
Human epicardial adipose tissue: A review
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DOI：
10.1016/j.ahj.2007.03.019
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发表时间：
2007-06-01
影响因子：
4.8
通讯作者：
Fain, John N.
中科院分区：
文献类型：
--
作者：
Sacks, Harold S.;Fain, John N.
我们讨论心外膜脂肪组织的解剖学、生理学和病理生理学及其与冠状动脉粥样硬化的关系。心外膜脂肪储存甘油三酯，为心肌能量产生提供游离脂肪酸，并产生脂肪因子。它与肠系膜和网膜脂肪有着共同的胚胎起源。像腹部内脏脂肪一样，心外膜脂肪厚度，通过超声心动图测量，在肥胖中增加。心外膜脂肪可能影响冠状动脉粥样硬化形成和心肌功能，因为没有纤维筋膜层来阻止游离脂肪酸和脂肪因子在其与下方血管壁以及心肌之间的扩散。缺乏心外膜脂肪或通过心肌组织桥与心外膜脂肪分离的冠状动脉节段可防止这些节段发生动脉粥样硬化。然而，当先天性全身性脂肪营养不良的心外膜脂肪完全缺失时，冠状动脉粥样硬化仍然可能发生。与纤维钙化或非动脉粥样硬化冠状动脉相比，具有脂质核心的人动脉粥样硬化冠状动脉的外膜周围脂肪中的巨噬细胞数量更多且密集。在有多种心血管危险因素的肥胖患者中，动脉粥样硬化冠状动脉周围的心外膜脂肪分泌几种促炎细胞因子，并被巨噬细胞、淋巴细胞和嗜碱性粒细胞浸润。没有冠状动脉粥样硬化的肥胖患者心外膜脂肪因子的表达尚未确定。在非肥胖患者中，动脉粥样硬化冠状动脉周围的心外膜脂肪表达促炎细胞因子，但产生的脂联素（一种血管保护性脂肪因子）比非动脉粥样硬化冠状动脉周围的脂肪少，或与胸部皮下脂肪相似。心外膜脂肪组织产生和释放的脂肪因子可能在局部参与冠状动脉粥样硬化的发病机制，这一假说有待进一步研究。
We discuss the anatomy, physiology, and pathophysiology of epicardial adipose tissue and its relationship to coronary atherosclerosis. Epicardial fat stores triglyceride to supply free fatty acids for myocardial energy production and produces adipokines. It shares a common embryological origin with mesenteric and omental fat. Like visceral abdominal fat, epicardial fat thickness, measured by echocardiography, is increased in obesity. Epicardial fat could influence coronary atherogenesis and myocardial function because there is no fibrous fascial layer to impede diffusion of free fatty acids and adipokines between it and the underlying vessel wall as well as the myocardium. Segments of coronary arteries lacking epicardial fat or separated from it by a bridge of myocardial tissue are protected against the development of atherosclerosis in those segments. However, when epicardial fat is totally absent in congenital generalized lipodystrophy, coronary atherosclerosis can still occur. Macrophages are more numerous and densely packed in the periadventitial fat of human atherosclerotic coronary arteries with lipid cores than in that of fibrocalcific or nonatherosclerotic coronary arteries. In obese patients with multiple cardiovascular risk factors, epicardial fat around atheromatous coronaries secretes several proinflarnmatory cytokines and is infiltrated by macrophages, lymphocytes, and basophils. Epicardial adipokine expression in obesity without coronary atherosclerosis has not been determined. In nonobese patients, epicardial fat around atheromatous coronary arteries expresses proinflarnmatory cytokines but produces either less adiponectin, a vasoprotective adipokine, than fat around nonatheromatous coronaries or a similar amount compared with thoracic subcutaneous fat. Further studies should be done to test the hypothesis that adipokines produced by and released from human epicardial adipose tissue might contribute locally to the pathogenesis of coronary atherosclerosis.