Journals / The Anatolian Journal of Cardiology / 2018 / Cilt: 20 - Sayı: 5

Neovascularization with chronic inflammation characterizes ascending aortic dissection

Pages
289–295
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Chronic inflammation and neovascularization of the dilated ascending aorta suggest susceptibility for AD. (Anatol J Cardiol 2018; 20: 289-95)

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Neovascularization of the aortic wall may be associated with aortic dissection (AD).
📊
Key Findings & Data:Aortic wall endothelial CD31 deposition together with chronic inflammation indicates angiogenesis that may lead to tissue disruption.
💡
Conclusion & Impact:Chronic inflammation and neovascularization of the dilated ascending aorta suggest susceptibility for AD. (Anatol J Cardiol 2018; 20: 289-95)
🔬Design:Modeling & Simulation
📍Scope:2018 Verileri
⚙️Variables:Domain Parameters

Özet

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. (Anatol J Cardiol 2018; 20: 289-95)

🔖

Cite This Article

NİİNİMAKİ, E., PYNNÖNEN, V., KHOLOVA, I., PAAVONEN, T., MENNANDER, A. (2018). Neovascularization with chronic inflammation characterizes ascending aortic dissection. The Anatolian Journal of Cardiology, Cilt: 20 - Sayı: 5, 289–295. https://ajindex.com/articles/365338

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Narayan P, Rogers CA, Davies I, Angelini GD, Bryan AJ. Type A aortic dissection: has surgical outcome improved with time? J Thorac Cardiovasc Surg 2008; 136: 1172-7
  2. Elefteriades JA. Thoracic aortic aneurysm: reading the enemy’s playbook. World J Surg 2008; 32: 366-74
  3. Trimarchi S, Jonker FHW, Hutchison S, Isselbacher EM, Pape LA, Patel HJ, et al. Descending aortic diameter of 5.5 cm or greater is not accurate predictor of acute type B aortic dissection. J Thorac Cardiovasc Surg 2011; 142: e101-7
  4. Osada H, Kyogoku M, Ishidou M, Morishima M, Nakajima H. Aortic dissection in the outer third of the media: what is the role of the vasa vasorum in the triggering process? Eur J Cardiothorac Surg 2013; 43: e82-8
  5. Thompson MM, Jones L, Nasim A, Sayers RD, Bell PR. Angiogenesis in abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 1996; 11: 464-9
  6. Kaiser M, Younge B, Björnsson J, Goronzy JJ, Weyand CM. Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells. Am J Pathol 1999; 155: 765-74
  7. Moraes F, Paye J, Mac Gabhann F, Zhuang ZW, Zhang J, Lanahan AA, et al. Endothelial cell-dependent regulation of arteriogenesis. Circ Res 2013; 113: 1076-86
  8. Levula M, Paavonen T, Valo T, Pelto-Huikko M, Laaksonen R, Kahonen M, et al. A disintegrin and metalloprotease-8 and -15 and susceptibility for ascending aortic dissection. Scand J Clin Lab Invest 2011; 71: 515-22
  9. Feng D, Nagy JA, Pyne K, Dvorak HF, Dvorak AM. Ultrastructural localization of platelet endothelial cell adhesion molecule (PECAM-1, CD31) in vascular endothelium. J Histochem Cytochem 2004; 52: 87- 101
  10. Woodfin A, Voisin MB, Nourshargh S. PECAM-1: a multi-functional molecule in inflammation and vascular biology. Arterioscler Thromb Vasc Biol 2007; 27: 2514-23
  11. Peterss S, Mansour AM, Ross JA, Vaitkeviciute I, Charilaou P, Dumfarth J, et al. Changing pathology of the thoracic aorta from acute to chronic dissection: literature review and insights. J Am Coll Cardiol 2016; 68: 1054-65
  12. Spittell PC, Spittell Jr JA, Joyce JW, Tajik AJ, Edwards WD, Schaff HV, et al. Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990). Mayo Clin Proc 1993; 68: 642-51
  13. Golestani R, Sadeghi MM. Emergence of molecular imaging of aortic aneurysm; implications for risk stratification and management. J Nucl Cardiol 2014; 21: 251-67
  14. Kirsch EW, Radu NC, Gervais M, Allaire E, Loisance DY