Changing views of the biomechanics of vulnerable plaque rupture: a review.

Changing views of the biomechanics of vulnerable plaque rupture: a review.
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DOI:
10.1007/s10439-013-0855-x
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发表时间:
2014-02
影响因子:
3.8
通讯作者:
Weinbaum, Sheldon
Weinbaum, Sheldon
中科院分区:
工程技术2区
文献类型:
--
作者:
Cardoso, Luis;Weinbaum, Sheldon

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本文回顾了过去25年来易损斑块破裂生物力学的变化,从第一个FEA显示脂质池的存在显着增加了动脉粥样硬化帽中的局部组织应力,到最新的成像和3D FEA研究揭示了帽中大量的微钙化和帽破裂的新范例。综述的第一部分总结了描述纤维帽厚度、组织特性和病变几何形状作为破裂风险主要决定因素的研究。目前的成像技术的优点和局限性评估易损斑块进行了讨论。然而,关于为什么破裂经常与PCS的位置不一致以及为什么厚度> 65 μm的帽在组织应力显著低于300 kPa临界阈值时会破裂的基本矛盾仍然没有解决。综述的第二部分介绍了最近的研究中的作用的微钙化,其起源,形状和集群在解释这些悬而未决的问题,包括实际的机制,由于爆炸性增长的微小空隙(空化)的高应力集中的局部地区之间的紧密间隔的微夹杂物定向沿着其拉伸轴破裂。
This review examines changing perspectives on the biomechanics of vulnerable plaque rupture over the past 25 years from the first FEA showing that the presence of a lipid pool significantly increases the local tissue stress in the atheroma cap to the latest imaging and 3D FEA studies revealing numerous microcalcifications in the cap proper and a new paradigm for cap rupture. The first part of the review summarizes studies describing the role of the fibrous cap thickness, tissue properties and lesion geometry as main determinants of the risk of rupture. Advantages and limitations of current imaging technologies for assessment of vulnerable plaques are also discussed. However, the basic paradoxes as to why ruptures frequently did not coincide with location of PCS and why caps > 65 μm thickness could rupture at tissue stresses significantly below the 300 kPa critical threshold still remained unresolved. The second part of the review describes recent studies in the role of microcalcifications, their origin, shape and clustering in explaining these unresolved issues including the actual mechanism of rupture due to the explosive growth of tiny voids (cavitation) in locals regions of high stress concentration between closely spaced microinclusions oriented along their tensile axis.
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