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- Title
Neovascularization with chronic inflammation characterizes ascending aortic dissection.
- Authors
Nünimäki, Eetu; Pynnönen, Ville; Kholova, Ivana; Paavonen, Timo; Mennander, Ari
- Abstract
Objective: Neovascularization of the aortic wall may be associated with aortic dissection (AD). Aortic wall endothelial CD31 deposition together with chronic inflammation indicates angiogenesis that may lead to tissue disruption. We studied the presence of neovascularization of the ascending aortic wall by characterizing CD31 positive endothelial cells. Methods: Aortic wall routine histology and immunohistochemistry for CD31, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, and cell proliferation were performed on 35 selected patients who underwent surgery for the ascending aorta, and the samples were grouped according to the presence of AD. Results: Three subjects with Marfan syndrome were excluded from the study. A total of 14 out of 32 patients had AD. A total of 18 patients were operated on due to dilatation only. Chronic inflammation of the adventitia (p=0.003), media (p=0.001), and intima (p=0.005) was increased in AD. Neovascularization was predominant in the outer third medial layer in AD (p=0.037), corresponding to the site of aortic wall disruption. A receiver operating characteristic curve analysis showed that neovascularization was associated with AD (AUC 0.750; SE 0.092; p=0.022; 95% CI 0.570-0.930). Conclusion: Endothelial immunohistochemistry confirms neovascularization of the outer third medial layer during AD. Aortic wall remodeling including neovascularization characterizes AD. Chronic inflammation and neovascularization of the dilated ascending aorta suggest susceptibility for AD.
- Subjects
NEOVASCULARIZATION; BLOOD-vessel development; CARDIOVASCULAR diseases; IMMUNOHISTOCHEMISTRY; MACROPHAGES
- Publication
Anatolian Journal of Cardiology / Anadolu Kardiyoloji Dergisi, 2018, Vol 20, Issue 5, p289
- ISSN
2149-2263
- Publication type
Article
- DOI
10.14744/AnatolJCardiol.2018.42223