Pisano Calogera, Maresi Emiliano, Merlo Daniele, Balistreri Carmela Rita, Candore Giuseppina, Caruso Marco, Codispoti Massimiliano, Ruvolo Giovanni
Unit of Cardiac Surgery, Department of Surgery and Oncology, University of Palermo, Palermo, Italy.
Interact Cardiovasc Thorac Surg. 2012 Nov;15(5):840-6. doi: 10.1093/icvts/ivs347. Epub 2012 Aug 14.
We aimed to identify a phenotype of ascending thoracic aortic aneurysm (TAA), which, more than others, evolves into type A dissection (TAD).
Aortic specimens were obtained from patients undergoing surgical repair of TAA and TAD (108 and 26, respectively). Histopathological and immunohistochemical analyses were performed by using adequate tissue specimens, appropriate techniques and criteria.
We identified the three following TAA phenotypes: phenotype I (cystic medial degeneration balanced by a substitutive fibrosis, in absence of medial apoptosis and with a faint collagenase concentration), phenotype II (cystic medial degeneration of higher grade, respectively, than substitutive fibrosis, with focal medial apoptosis and moderate collagenase concentration), and phenotype III (elevated cystic medial degeneration without substitutive fibrosis, with plurifocal medial apoptosis and severe collagenase concentration). The same medial degenerative lesions of TAA phenotype III were observed in TAD tissue samples.
The morphological identity of medial lesions observed in both the TAA phenotype III and in TAD aortas might be assumed to be the precursor-and consequently the optimal biomarker- of dissection, independently of aneurysm diameter or valvular disorder. Identification of genetic risk factors, useful both in diagnostics and in developing more targeted treatment for individual patients, might also be needed.
我们旨在确定一种升主动脉瘤(TAA)的表型,该表型比其他表型更容易发展为A型主动脉夹层(TAD)。
从接受TAA和TAD手术修复的患者中获取主动脉标本(分别为108例和26例)。使用适当的组织标本、合适的技术和标准进行组织病理学和免疫组织化学分析。
我们确定了以下三种TAA表型:表型I(囊性中层退变由替代性纤维化平衡,无中层凋亡且胶原酶浓度低),表型II(囊性中层退变程度分别高于替代性纤维化,有局灶性中层凋亡且胶原酶浓度中等),以及表型III(囊性中层退变加重且无替代性纤维化,有多灶性中层凋亡且胶原酶浓度高)。在TAD组织样本中观察到与TAA表型III相同的中层退行性病变。
TAA表型III和TAD主动脉中观察到的中层病变的形态学特征可能被认为是夹层的前驱病变,因此也是最佳生物标志物,与动脉瘤直径或瓣膜疾病无关。可能还需要确定遗传风险因素,这在诊断和为个体患者制定更有针对性的治疗中都很有用。