Segmental heterogeneity of vasa vasorum neovascularization in human coronary atherosclerosis.
Segmental heterogeneity of vasa vasorum neovascularization in human coronary atherosclerosis.
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DOI：
10.1016/j.jcmg.2009.10.009
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发表时间：
2010-01
期刊：
影响因子：
--
通讯作者：
Lerman A
中科院分区：
文献类型：
--
作者：
Gössl M;Versari D;Hildebrandt HA;Bajanowski T;Sangiorgi G;Erbel R;Ritman EL;Lerman LO;Lerman A
探讨冠状动脉血管新生在冠状动脉粥样硬化斑块形成和并发症中的作用。越来越多的证据支持VV新生血管在冠状动脉疾病的动脉粥样硬化形成和病变位置确定中的重要作用。VV新生血管可导致斑块内出血，这已被确定为斑块进展和并发症（如斑块破裂）的促进因素。我们假设在人类冠状动脉粥样硬化的不同阶段可以发现VV新生血管和相关斑块并发症的独特模式。在尸检时获得来自15名患者（年龄52±5岁，平均值±SEM）的心脏，用Microfil™灌注，随后用微型计算机断层扫描（micro-CT）扫描。2 cm节段（n=50）在组织学上分为正常（n=12）、非狭窄斑块（狭窄<50%，n=18）、钙化（n=10）或非钙化（n=10）狭窄斑块。分析Micro-CT图像的VV密度（#/mm 2）、VV血管面积分数（mm 2/mm 2）和VV内皮表面分数（mm 2/mm 3）。对组织切片进行马洛里（铁）、von Kossa（钙）和血型糖蛋白-A（红细胞碎片）以及内皮型一氧化氮合酶（eNOS）、血管内皮生长因子（VEGF）和肿瘤坏死因子-α（TNF-α）染色。非狭窄段和非钙化段的VV密度均高于正常段（3.36±0.45，3.72± 1.03vs.1.16 ±0.21，P<0.01）。钙化狭窄斑块VV空间密度最低（0.95±0.21，P<0.05）。非狭窄斑块和狭窄斑块中铁和血型糖蛋白A含量均显著高于正常斑块，并与VV密度相关（Kendall-Tau相关系数分别为0.65和0.58，P<0.01）。此外，在钙化斑块中发现了相对大量的铁和血型糖蛋白A。免疫组化结果显示，VV中eNOS和TNF-α表达阳性，而VEGF表达阴性。我们的研究结果支持VV新生血管形成，VV破裂和斑块内出血在人类冠状动脉粥样硬化的进展和并发症中的可能作用。
To investigate the role of coronary vasa vasorum (VV) neovascularization in the progression and complications of human coronary atherosclerotic plaques. Accumulating evidence supports an important role of VV neovascularization in atherogenesis and lesion location determination in coronary artery disease. VV neovascularization can lead to intraplaque hemorrhage, which has been identified as a promoter of plaque progression and complications like plaque rupture. We hypothesized that distinctive patterns of VV neovascularization and associated plaque complications can be found in different stages of human coronary atherosclerosis. Hearts from 15 patients (age 52±5, mean±SEM) were obtained at autopsy, perfused with Microfil™ and subsequently scanned with micro-computed tomography (micro-CT). Two-cm-segments (n=50) were histologically classified as either normal (n=12), nonstenotic plaque (<50% stenosis, n=18), or calcified (n=10) or non-calcified (n=10) stenotic plaque. Micro-CT images were analyzed for VV density (#/mm2), VV vascular area fraction (mm2/mm2) and VV endothelial surface fraction (mm2/mm3). Histological sections were stained for Mallory’s (iron), von Kossa (calcium) and glycophorin-A (erythrocyte fragments) as well as endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-α). VV density was higher in segments with non-stenotic and non-calcified stenotic plaques as compared to normals (3.36±0.45, 3.72±1.03 vs. 1.16±0.21, P<0.01). In calcified stenotic plaques VV spatial density was lowest (0.95±0.21, P<0.05 vs. non-stenotic and non-calcified stenotic plaque). The amount of iron and glycophorin A was significantly higher in non-stenotic and stenotic plaques as compared to normals, and correlated with VV density (Kendall-Tau correlation-coefficient 0.65 and 0.58 respectively, P<0.01). Moreover, relatively high amounts of iron and glycophorin A were found in calcified plaques. Further immunohistochemical characterization of VV revealed positive staining for eNOS and TNF-α but not VEGF. Our results support a possible role of VV neovascularization, VV rupture and intraplaque hemorrhage in the progression and complications of human coronary atherosclerosis.
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影响因子：
24
作者：
Goessl, Mario;Moedder, Ulrike I.;Atkinson, Elizabeth J.;Lerman, Amir;Khosla, Sundeep
通讯作者：
Khosla, Sundeep
影响因子：
24
作者：
Virmani, R;Burke, AP;Kolodgie, FD
通讯作者：
Kolodgie, FD
影响因子：
37.8
作者：
EGGEN, DA;STRONG, JP;MCGILL, HC
通讯作者：
MCGILL, HC
DOI：
10.1016/0735-1097(90)90282-t
发表时间：
1990-03-15
影响因子：
24
作者：
AGATSTON, AS;JANOWITZ, WR;DETRANO, R
通讯作者：
DETRANO, R
影响因子：
10.8
作者：
Herrmann, J;Lerman, LO;Lerman, A
通讯作者：
Lerman, A