Albini Paul T, Segura Ana Maria, Liu Guanghui, Minard Charles G, Coselli Joseph S, Milewicz Dianna M, Shen Ying H, LeMaire Scott A
Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Adult Cardiothoracic Surgery, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA.
Department of Cardiovascular Pathology, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA.
Atherosclerosis. 2014 Feb;232(2):361-8. doi: 10.1016/j.atherosclerosis.2013.10.035. Epub 2013 Nov 18.
The pathogenesis of non-familial, sporadic ascending aortic aneurysms (SAAA) is poorly understood, and the relationship between ascending aortic atherosclerosis and medial degeneration is unclear. We evaluated the prevalence and severity of aortic atherosclerosis and its association with medial degeneration in SAAA.
Atherosclerosis was characterized in ascending aortic tissues collected from 68 SAAA patients (mean age, 62.9 ± 12.0 years) and 15 controls (mean age, 56.6 ± 11.4 years [P = 0.07]) by using a modified American Heart Association classification system. Upon histologic examination, 97% of SAAA patients and 73% of controls showed atherosclerotic changes. Most SAAA samples had intermediate (types 2 and 3, 35%) or advanced atherosclerosis (types ≥ 4; 40%), whereas most control samples showed minimal atherosclerosis (none or type 1, 80%; P < 0.001 after adjusting for age). In a separate analysis, we examined the total incidence and grade distribution of medial degenerative changes among SAAA samples according to atherosclerosis grade. Advanced atherosclerosis was associated with higher grades of smooth muscle cell depletion (P < 0.001), elastic fiber depletion (P = 0.02), elastic fiber fragmentation (P < 0.001), and mucopolysaccharide accumulation (P = 0.04). Aortic diameter was larger in SAAA patients with advanced atherosclerosis than in patients with minimal (P = 0.04) or intermediate atherosclerosis (P = 0.04). Immunostaining showed marked CD3+ T-cell and CD68+ macrophage infiltration, MMP-2 and MMP-9 production, and cryopyrin expression in the medial layer adjacent to atherosclerotic plaque.
SAAA tissues exhibited advanced atherosclerosis that was associated with severe medial degeneration and increased aortic diameter. Our findings suggest a role for atherosclerosis in the progression of sporadic ascending aortic aneurysms.
非家族性、散发性升主动脉瘤（SAAA）的发病机制尚不清楚，升主动脉动脉粥样硬化与中膜退变之间的关系也不明确。我们评估了SAAA中主动脉动脉粥样硬化的患病率和严重程度及其与中膜退变的关联。
采用改良的美国心脏协会分类系统，对68例SAAA患者（平均年龄62.9±12.0岁）和15例对照者（平均年龄56.6±11.4岁[P = 0.07]）的升主动脉组织中的动脉粥样硬化进行特征分析。组织学检查显示，97%的SAAA患者和73%的对照者有动脉粥样硬化改变。大多数SAAA样本有中度（2型和3型，35%）或重度动脉粥样硬化（≥4型；40%），而大多数对照样本显示轻度动脉粥样硬化（无或1型，80%；校正年龄后P < 0.001）。在另一项分析中，我们根据动脉粥样硬化分级检查了SAAA样本中膜退变改变的总发生率和分级分布。重度动脉粥样硬化与更高程度的平滑肌细胞减少（P < 0.001）、弹性纤维减少（P = 0.02）、弹性纤维断裂（P < 0.001）和粘多糖积聚（P = 0.04）相关。重度动脉粥样硬化的SAAA患者的主动脉直径大于轻度（P = 0.04）或中度动脉粥样硬化患者（P = 0.04）。免疫染色显示，在动脉粥样硬化斑块相邻的中膜层有明显的CD3 + T细胞和CD68 +巨噬细胞浸润、MMP - 2和MMP - 9产生以及cryopyrin表达。
SAAA组织表现出重度动脉粥样硬化，其与严重的中膜退变和主动脉直径增加相关。我们的研究结果提示动脉粥样硬化在散发性升主动脉瘤进展中起作用。
