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A型夹层与慢性扩张:腱生蛋白-C作为主动脉壁失稳的关键因素

Type A dissection and chronic dilatation: tenascin-C as a key factor in destabilization of the aortic wall.

作者信息

Trescher Karola, Thometich Barbara, Demyanets Svitlana, Kassal Hermann, Sedivy Roland, Bittner Reginald, Holzinger Christoph, Podesser Bruno K

机构信息

Department of Cardiac Surgery, LK St. Pölten, St. Poelten, Austria.

出版信息

Interact Cardiovasc Thorac Surg. 2013 Aug;17(2):365-70. doi: 10.1093/icvts/ivt204. Epub 2013 May 8.

DOI:10.1093/icvts/ivt204
PMID:23656926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3715195/
Abstract

OBJECTIVES

Tenascin-C plays an important role in myocardial and vascular remodelling. We hypothesized that tenascin-C is a key factor in the development of degenerative disease of the ascending aorta, leading to chronic dilatation and acute aortic dissection.

METHODS

Ascending aortic wall specimens were obtained during surgery for chronic dilatation (n=52) and acute Type A dissection (n=30). Patients (n=12) undergoing aortic valve replacement served as controls. Tenascin-C expression was evaluated by immunostaining and semi-quantitatively assessed using the ImageJ software. TN-C levels in peripheral blood were determined by enzyme-linked immunosorbent assay.

RESULTS

Histological examination showed a clear difference between chronic dilatation and acute dissection. In chronic dilatation, tenascin-C staining was homogenously distributed throughout the media parallel to vascular smooth muscle cells. In acute dissection, a strong staining with a heterogenous and spotty distribution was detected. Control aortas showed no tenascin-C staining. Tenascin-C expression was significantly higher in Type-A dissection compared with chronic dilatation. This was accompanied by a significant elevation of tenascin-C levels in peripheral blood in acute dissection. There was no statistical correlation between the tenascin-C level in peripheral blood and the aortic diameter either in dissection or in dilatation.

CONCLUSIONS

Tenascin-C is a marker of progressive destabilization of the aortic wall independent of size in chronic dilatation and acute dissection. Therefore, it might be a valuable tool in guiding intervention strategies in patients with disease of the ascending aorta.

摘要

目的

肌腱蛋白-C在心肌和血管重塑中起重要作用。我们推测肌腱蛋白-C是升主动脉退行性疾病发展的关键因素,可导致慢性扩张和急性主动脉夹层。

方法

在慢性扩张手术(n=52)和急性A型夹层手术(n=30)期间获取升主动脉壁标本。接受主动脉瓣置换术的患者(n=12)作为对照。通过免疫染色评估肌腱蛋白-C的表达,并使用ImageJ软件进行半定量评估。采用酶联免疫吸附测定法测定外周血中的TN-C水平。

结果

组织学检查显示慢性扩张和急性夹层之间存在明显差异。在慢性扩张中,肌腱蛋白-C染色均匀分布于整个中膜,与血管平滑肌细胞平行。在急性夹层中,检测到染色强烈且分布不均、呈斑点状。对照主动脉未显示肌腱蛋白-C染色。与慢性扩张相比,急性A型夹层中肌腱蛋白-C的表达明显更高。这伴随着急性夹层外周血中肌腱蛋白-C水平的显著升高。无论是在夹层还是扩张中,外周血中的肌腱蛋白-C水平与主动脉直径之间均无统计学相关性。

结论

肌腱蛋白-C是主动脉壁进行性失稳的标志物,在慢性扩张和急性夹层中与大小无关。因此,它可能是指导升主动脉疾病患者干预策略的有价值工具。

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