Abstract 672: Histopathological Comparison of Ascending Aortic Aneurysm: Bicuspid versus Tricuspid Aortic Valve Patients
Introduction: The pathogenic mechanisms of ascending aortic aneurysm are not fully understood. The aim of this study was to identify the beginning of aortic wall dilatation based on histopathological evaluation by comparison of patients with bicuspid versus tricuspid aortic valves.
Methods: Twenty-one patients (9 males, 12 females; mean age, 69±8.9 years) who underwent ascending aortic repair from 2008 to 2014 were divided into bicuspid aortic valve (n=8, Group B) and tricuspid aortic valve (n=13, Group T) subgroups. We compared the histopathological characteristics of the ascending aortic wall in these patients.
Results: There were no significant differences between the two groups in age, sex, history of hypertension, and maximum diameter of the ascending aorta (Group B: 51.4±5.1 mm; Group T: 55.5±8.8 mm; p=0.247) at the time of operation. While all Group B cases exhibited aortic stenosis, there was only one case in Group T. Sclerosis or hypertrophy of the vasa vasorum was evident in both groups (Group B: 7 patients, 87.5%; Group T: 10 patients, 76.9%; p=1.000). Group B patients exhibited a much thinner aortic wall, resulting from frail smooth muscle cells of media, which induced a fragile thinner elastic lamina. The histopathological pattern of Group T was variable and included atheroma, inflammatory granulation tissue and a Marfan-like acid mucopolysaccharide pool, which produce severe fragmentation of elastic lamina.
Conclusions: Degeneration of the vasa vasorum, which induces chronic ischemia or malnutrition of the aortic wall, is an important emerging substrate for the development of ascending aortic aneurysm. Bicuspid aortic valve patients exhibited congenital maldevelopment of the medial smooth muscle cells and elastic lamina. Tricuspid aortic valve patients exhibited severe fragmentation of elastic lamina, which induced by pathological changes including atheroma, inflammatory granuloma, and a Marfan-like acid mucopolysaccharide pool.
Author Disclosures: H. Osada: None. K. Meshii: None. M. Ohnaka: None. N. Kanemitsu: None. H. Nakajima: None. M. Kyogoku: None.
- © 2015 by American Heart Association, Inc.