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Research Article

Lack of C4d deposition may reveal susceptibility for ascending aortic dissection

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Pages 177-182 | Received 22 Dec 2011, Accepted 30 Jan 2012, Published online: 18 May 2012
 

Abstract

Objectives. Complement activation as evidenced by C4d deposition indicates immunological tissue reactivity. We sought to study the vascular reactivity of the aortic wall by characterizing C4d deposits. Design. Aortic wall histology and immunohistochemistry for C4d, leukocytes, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastase, and Van–Gieson-staining were performed to 91 consecutive patients that underwent surgery for ascending aorta, and the samples were grouped according to presence of C4d deposits. Results. Fifty-three out of 91 patients had C4d deposits mainly within the adventitia (C4d +), whereas 38 patients lacked C4d deposits (C4d−) including decreased staining of intra-aortic vessels (p < 0.005). Intimal thickness and cellularity, together with inflammation consisting of plasma cells were increased in C4d‐ as compared with C4d + (p < 0.05). Receiver operating characteristic curve (ROC) analysis showed that C4d was associated with stabile nondissecting ascending aorta (AUC 0.792; SE 0.053; p = 0.000; 95% CI 0.688–0.895), but not with presence of aortitis per se (AUC 0.523; SE 0.069; p = 0.752; 95 % CI 0.388–0.658). Conclusions. Lack of C4d may indicate active remodeling of the aortic wall leading to aortic dissection (AD). Immunologic complement factors may be amenable to diagnosis of instability after aortic surgery.

Acknowledgements

This study was supported by research funding from The Competitive Research Foundation of Tampere University Hospital (Grant 9L058), Tuberculosis Foundation, The Finnish Heart Association and The Finnish Cultural Foundation. Dr A Mennander is the recipient of the Ingegeerd and Viking O Bjork award for Scandinavian Cardiovascular Research.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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