Huang H, Virmani R, Younis H, Burke A P, Kamm R D, Lee R T
MassachusettsInstitute of Technology, Cambridge, MA, USA.
Circulation. 2001 Feb 27;103(8):1051-6. doi: 10.1161/01.cir.103.8.1051.
Increased biomechanical stresses in the fibrous cap of atherosclerotic plaques contribute to plaque rupture and, consequently, to thrombosis and myocardial infarction. Thin fibrous caps and large lipid pools are important determinants of increased plaque stresses. Although coronary calcification is associated with worse cardiovascular prognosis, the relationship between atheroma calcification and stresses is incompletely described.
To test the hypothesis that calcification impacts biomechanical stresses in human atherosclerotic lesions, we studied 20 human coronary lesions with techniques that have previously been shown to predict plaque rupture locations accurately. Ten ruptured and 10 stable lesions derived from post mortem coronary arteries were studied using large-strain finite element analysis. Maximum stress was not correlated with percentage of calcification, but it was positively correlated with the percentage of lipid (P:=0.024). When calcification was eliminated and replaced with fibrous plaque, stress changed insignificantly; the median increase in stress for all specimens was 0.1% (range, 0% to 8%; P:=0.85). In contrast, stress decreased by a median of 26% (range, 1% to 78%; P:=0.02) when lipid was replaced with fibrous plaque.
Calcification does not increase fibrous cap stress in typical ruptured or stable human coronary atherosclerotic lesions. In contrast to lipid pools, which dramatically increase stresses, calcification does not seem to decrease the mechanical stability of the coronary atheroma.
动脉粥样硬化斑块纤维帽中生物力学应力的增加会导致斑块破裂，进而引发血栓形成和心肌梗死。薄纤维帽和大脂质池是斑块应力增加的重要决定因素。尽管冠状动脉钙化与更差的心血管预后相关，但动脉粥样硬化钙化与应力之间的关系尚未完全阐明。
为了验证钙化会影响人类动脉粥样硬化病变中生物力学应力这一假设，我们使用先前已被证明能准确预测斑块破裂位置的技术，研究了20例人类冠状动脉病变。使用大应变有限元分析研究了来自尸检冠状动脉的10个破裂病变和10个稳定病变。最大应力与钙化百分比无关，但与脂质百分比呈正相关（P = 0.024）。当消除钙化并用纤维斑块替代时，应力变化不显著；所有标本应力的中位数增加为0.1%（范围为0%至8%；P = 0.85）。相比之下，当用纤维斑块替代脂质时，应力中位数下降了26%（范围为1%至78%；P = 0.02）。
在典型的破裂或稳定人类冠状动脉粥样硬化病变中，钙化不会增加纤维帽应力。与显著增加应力的脂质池不同，钙化似乎不会降低冠状动脉粥样硬化的机械稳定性。
