Morphometric and Mechanical Analyses of Calcifications and Fibrous Plaque Tissue in Carotid Arteries for Plaque Rupture Risk Assessment
Morphometric and Mechanical Analyses of Calcifications and Fibrous Plaque Tissue in Carotid Arteries for Plaque Rupture Risk Assessment
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DOI：
10.1109/tbme.2020.3038038
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发表时间：
2021-04-01
影响因子：
4.6
通讯作者：
Akyildiz, Ali C.
中科院分区：
文献类型：
--
作者：
Gijsen, Frank J. H.;Vis, Bas;Akyildiz, Ali C.
目的：颈动脉粥样硬化斑块破裂是脑血管事件的主要来源。钙化在颈动脉斑块中非常普遍，但其在斑块破裂中的作用仍知之甚少。这项工作研究了颈动脉斑块中钙化的形态特征及其对钙化界面处纤维斑块组织中应力分布的影响，作为斑块破裂和临床事件的潜在来源。研究方法：对16个颈动脉斑块的65个组织学横截面进行了全面的形态测量分析，以识别斑块钙化的形态（大小和形状）和位置，以及它们周围的纤维组织纤维组织。建立钙化特异性有限元模型，以检查钙化界面处的纤维斑块组织应力。统计相关性分析，以阐明钙化形态和纤维组织结构对界面应力的影响。结果：171个钙化灶在组织学切片上被识别，其形态变化很大。在钙化周围的斑块组织中观察到四种不同的纤维组织模式。它们被称为附着型、推开型、环绕型和随机型。应力分析表明，钙化与高界面应力相关，其可能与斑块强度相当或甚至高于斑块强度。应力水平取决于钙化形态和纤维组织。较厚的钙化与周围细长的形状，靠近管腔，最显着相关的高界面应力。结论：根据其形态和周围的纤维组织，动脉粥样硬化斑块中的钙化可以作为应力集中器并引起高界面应力。重要性：本研究证明了动脉粥样硬化斑块中钙化导致斑块组织应力升高的可能性，并为钙化相关斑块破裂的组织病理学结果提供了生物力学解释。
Objective: Atherosclerotic plaque rupture in carotid arteries is a major source of cerebrovascular events. Calcifications are highly prevalent in carotid plaques, but their role in plaque rupture remains poorly understood. This work studied the morphometric features of calcifications in carotid plaques and their effect on the stress distribution in the fibrous plaque tissue at the calcification interface, as a potential source of plaque rupture and clinical events. Methods: A comprehensive morphometric analysis of 65 histology cross-sections from 16 carotid plaques was performed to identify the morphology (size and shape) and location of plaque calcifications, and the fibrous tissue fiber organization around them. Calcification-specific finite element models were constructed to examine the fibrous plaque tissue stresses at the calcification interface. Statistical correlation analysis was performed to elucidate the impact of calcification morphology and fibrous tissue organization on interface stresses. Results: Hundred-seventy-one calcifications were identified on the histology cross-sections, which showed great variation in morphology. Four distinct patterns of fiber organization in the plaque tissue were observed around the calcification. They were termed as attached, pushed-aside, encircling and random patterns. The stress analyses showed that calcifications are correlated with high interface stresses, which might be comparable to or even above the plaque strength. The stress levels depended on the calcification morphology and fiber organization. Thicker calcification with a circumferential slender shape, located close to the lumen were correlated most prominently to high interface stresses. Conclusion: Depending on its morphology and the fiber organization around it, a calcification in an atherosclerotic plaque can act as a stress riser and cause high interface stresses. Significance: This study demonstrated the potential of calcifications in atherosclerotic plaques to cause elevated stresses in plaque tissue and provided a biomechanical explanation for the histopathological findings of calcification-associated plaque rupture.