Curr Atheroscler Rep. 2008 Aug;10(4):309-17. doi: 10.1007/s11883-008-0048-5.
Identification of high-risk patients presenting with chest pain remains challenging. The use of a single biomarker or a panel of biomarkers to detect occult plaque destabilization or rupture without frank infarction would allow for appropriate triage of such patients. Current data suggest that plaque vulnerability is determined by the relationship between forces that increase the size of the lipid core and destabilize the overlying thin fibrous cap. A variety of interrelated pathways are imputed to play important roles in this process of plaque evolution, destabilization, and rupture. These mechanisms include increased systemic and local inflammation, increased oxidative stress, matrix metalloproteinase modulation, and hemodynamic variables related to altered shear stress. Select candidate biomarkers that either reflect or influence these underlying processes and may ultimately have clinical application are highlighted in this review, which focuses on emerging biomarkers to define and predict the risks associated with the complex nature of vulnerable plaque biology.
识别表现为胸痛的高危患者仍然具有挑战性。使用单一生物标志物或一组生物标志物来检测隐匿性斑块不稳定或破裂而没有明显的梗死，将允许对这些患者进行适当的分诊。目前的数据表明，斑块脆弱性取决于增加脂质核心大小并破坏覆盖的薄纤维帽的力之间的关系。多种相互关联的途径被认为在斑块演化、不稳定和破裂的过程中发挥重要作用。这些机制包括全身性和局部炎症增加、氧化应激增加、基质金属蛋白酶调节以及与剪切应力改变相关的血液动力学变量。在本综述中强调了选择候选生物标志物，这些标志物反映或影响这些潜在过程，并且最终可能具有临床应用，该综述重点介绍了新兴的生物标志物，以定义和预测与易损斑块生物学的复杂性相关的风险。
