Atherosclerotic Coronary Plaque Is Associated With Adventitial Vasa Vasorum and Local Inflammation in Adjacent Epicardial Adipose Tissue in Fresh Cadavers.
Atherosclerotic Coronary Plaque Is Associated With Adventitial Vasa Vasorum and Local Inflammation in Adjacent Epicardial Adipose Tissue in Fresh Cadavers.
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DOI：
10.1253/circj.cj-19-0914
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发表时间：
2020-04
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通讯作者：
Hiroyuki Ito;T. Wakatsuki;K. Yamaguchi;D. Fukuda;Y. Kawabata;T. Matsuura;K. Kusunose;T. Ise;T. Tobiume;S. Yagi;H. Yamada;T. Soeki;Yoshihiro Tsuruo;M. Sata
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作者：
Hiroyuki Ito;T. Wakatsuki;K. Yamaguchi;D. Fukuda;Y. Kawabata;T. Matsuura;K. Kusunose;T. Ise;T. Tobiume;S. Yagi;H. Yamada;T. Soeki;Yoshihiro Tsuruo;M. Sata
冠状动脉外膜作为炎症的来源最近引起了人们的注意，因为它含有营养血管，称为血管（VV）。本研究评估了在相邻的心外膜脂肪组织（EAT）和冠状动脉粥样硬化在新鲜cavers.Methods和结果：病变特征在左前降支冠状动脉的10个新鲜尸体心脏进行了评价，使用背向散射血管内超声（IB-IVUS），和密度的VV和炎症分子水平的相邻EAT的测量每个评估病变。根据IB-IVUS评估的脂质体积百分比，将病变分为富脂组、中等脂质组和贫脂组。炎症分子的更高表达（即，在相邻的富含脂质的EAT（n = 11）中观察到血管内皮生长因子A [VEGFA]和VEGFB（分别为7.99±3.37和0.45±0.85任意单位[Au]; VEGFB分别为0.27±0.15和0.11±0.07 Au; P<0.05）。高脂组血管外膜VV密度明显高于低脂组（1.50±0.58% vs.0.88 ±0.23%; P<0.05）。结论：新鲜尸体中富含脂质的冠状动脉斑块与外膜VV和邻近EAT的局部炎症有关。这项研究表明，EAT的局部炎症与冠状动脉斑块通过VV进展相关。
BACKGROUND The coronary adventitia has recently attracted attention as a source of inflammation because it harbors nutrient blood vessels, termed the vasa vasorum (VV). This study assessed the link between local inflammation in adjacent epicardial adipose tissue (EAT) and coronary arterial atherosclerosis in fresh cadavers.Methods and Results:Lesion characteristics in the left anterior descending coronary artery of 10 fresh cadaveric hearts were evaluated using integrated backscatter intravascular ultrasound (IB-IVUS), and the density of the VV and levels of inflammatory molecules from the adjacent EAT were measured for each of the assessed lesions. The lesions were divided into lipid-rich, lipid-moderate, and lipid-poor groups according to percentage lipid volume assessed by IB-IVUS. Higher expression of inflammatory molecules (i.e., vascular endothelial growth factor A [VEGFA] andVEGFB) was observed in adjacent EAT of lipid-rich (n=11) than in lipid-poor (n=11) lesions (7.99±3.37 vs. 0.45±0.85 arbitrary units [AU], respectively, forVEGFA; 0.27±0.15 vs. 0.11±0.07 AU, respectively, forVEGFB; P<0.05). The density of adventitial VV was greater in lipid-rich than lipid-poor lesions (1.50±0.58% vs. 0.88±0.23%; P<0.05). CONCLUSIONS Lipid-rich coronary plaques are associated with adventitial VV and local inflammation in adjacent EAT in fresh cadavers. This study suggests that local inflammation of EAT is associated with coronary plaque progression via the VV.