Intimomedial interface damage is increased beneath disrupted and adventitial inflammation atherosclerosis in the aorta - Implications for plaque vulnerability
Intimomedial interface damage is increased beneath disrupted and adventitial inflammation atherosclerosis in the aorta - Implications for plaque vulnerability
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DOI：
10.1161/01.cir.0000017265.52501.37
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发表时间：
2002-05-28
期刊：
影响因子：
37.8
通讯作者：
O'Connor, WN
中科院分区：
文献类型：
--
作者：
Moreno, PR;Purushothaman, KR;O'Connor, WN
背景-动脉粥样硬化斑块的进展经常伴随着代偿性增大以保护管腔。然而，这些扩大的斑块发展出脆弱的特征，导致破裂和管腔阻塞。这种从代偿性扩张到斑块破裂的复杂转变可能不仅仅源于进行性内膜疾病。内膜-中膜界面以及图尼卡膜和外膜内的并发变化可能在斑块不稳定性中发挥作用。我们通过调查是否界面变化，包括内弹性膜（IEL）破裂，以及中膜和外膜变化，包括炎症，纤维化和萎缩，更频繁地伴随破裂而不是非破裂的动脉粥样硬化斑块来验证这一假设。根据AHA分类，对598例人主动脉斑块的血管外膜组织病理学特征进行分析。破裂斑块表现出更大的斑块和脂质池面积（P=0.0001）和更高的发生率4-破裂的IEL（P=0.0001）。破裂斑块的中膜和外膜炎症（P=0.01）、中膜纤维化（P=0.0001）和中膜萎缩（P=0.0001）也较高。此外，破裂斑块的中膜厚度减少（P=0.0001）。Logistic回归分析确定IEL破裂为纤维帽破裂的独立预测因子（P=0.0001）。结论与非破裂斑块相比，破裂斑块的IEL破裂、中膜和外膜炎症、中膜纤维化和中膜萎缩的发生率增加。这些内膜-中层界面和外膜变化可能在复杂动脉粥样硬化病变的自然病程中发挥作用。中膜和外膜病理与内膜动脉粥样硬化过程之间的相互作用值得进一步研究。
Background-Atherosclerotic plaque progression is frequently accompanied by compensatory enlargement to preserve the lumen. These enlarging plaques develop features of vulnerability, however, leading to disruption and lumen obstruction. This complex transition from compensatory expansion to plaque disruption may not derive solely from progressive intimal disease. Concurrent changes at the intimomedial interface and within the tunica media and adventitia may play a role in plaque instability. We tested this hypothesis by investigating whether interface changes, including internal elastic lamina (IEL) rupture, and medial and adventitial changes, including inflammation, fibrosis, and atrophy, more frequently accompany disrupted than nondisrupted atherosclerotic plaques.Methods and Results-Computerized planimetry and ocular micrometry were used for systematic quantification of intimal, medial, and adventitial histopathological features in 598 human aortic plaques according to the AHA classification. Disrupted plaques exhibited larger plaque and lipid pool areas (P=0.0001) and a higher incidence of 4-rupture of the IEL (P=0.0001). Medial and adventitial inflammation (P=0.01), medial fibrosis (P=0.0001), and medial atrophy (P=0.0001) were also higher in disrupted plaques. Furthermore, medial thickness was reduced in disrupted plaques (P=0.0001). Logistic regression analysis identified rupture of the IEL as an independent predictor for fibrous cap disruption (P=0.0001).Conclusions-Compared with nondisrupted plaques, disrupted plaques have an increased incidence of IEL rupture, medial and adventitial inflammation, medial fibrosis, and medial atrophy. These intimomedial interface and adventitial changes may play a role in the natural history of complex atherosclerotic lesions. The interaction between medial and adventitial pathology and the intimal atherosclerotic process deserves further investigation.