Cardoso Luis, Weinbaum Sheldon
Department of Biomedical Engineering, The City College of New York, Steinman Hall, 160 Convent Ave, New York, NY, 10031, USA.
Ann Biomed Eng. 2014 Feb;42(2):415-31. doi: 10.1007/s10439-013-0855-x. Epub 2013 Jul 11.
This review examines changing perspectives on the biomechanics of vulnerable plaque rupture over the past 25 years from the first finite element analyses (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 local regions of high stress concentration between closely spaced microinclusions oriented along their tensile axis.
本综述探讨了过去25年中对易损斑块破裂生物力学的观点变化,从首次有限元分析(FEA)显示脂质池的存在显著增加动脉粥样硬化帽中的局部组织应力,到最新的成像和三维有限元分析研究揭示帽本身存在大量微钙化以及帽破裂的新范式。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。还讨论了当前用于评估易损斑块的成像技术的优缺点。然而,关于破裂为何常常与斑块破裂综合征(PCS)的位置不一致,以及为何厚度>65μm的帽在组织应力显著低于300kPa临界阈值时仍会破裂等基本矛盾问题仍未得到解决。综述的第二部分描述了近期关于微钙化的作用、其起源、形状和聚集的研究,这些研究解释了这些未解决的问题,包括由于沿其拉伸轴排列的紧密间隔微内含物之间高应力集中局部区域微小空隙(空化)的爆发性生长导致破裂的实际机制。