Biomarkers Associated with Vulnerable Atheromatous Plaque

Atherogenesis progresses through lipid core expansion and macrophage accumulation at the plaque, leading to fibrous cap rupture. Plaque rupture occurs in the plaque fissuring at one point, which ultimately brings the platelets into contact with the content of the lipid core, and the blood coagulation factors together with tissue factor. The transition from stable atherosclerotic plaques to vulnerable plaques finally resulting in the plaque rupture is the consequence of an inflammatory reaction. This process involves complex cellular interactions engaging many mediators, chemokines, and cytokines which can be measured in serum and plasma and thus serve as biomarkers that differentiate the pathophysiologic phases of disease progression. Pathological studies support the risk of inflammation in high-risk patients to a greater extent than the degree of vessel stenosis. It is therefore important to identify reliable biomarkers allowing us to monitor vascular inflammatory state.In clinical investigations, several new biomarkers have been identified that provide increasing diagnostic and prognostic significance. However, more confirmatory studies are required to clinical use. Furthermore, assays for automated use need to be developed, and cut-off levels need to be defined. Further technological advances will likely facilitate the use of multimarker profiling to identify with coronary vulnerable plaque.

动脉粥样硬化的形成是通过脂质核心扩大以及斑块处巨噬细胞聚集，导致纤维帽破裂。斑块破裂是指斑块在某一点出现裂隙，最终使血小板与脂质核心内容物以及凝血因子和组织因子接触。从稳定的动脉粥样硬化斑块转变为易损斑块并最终导致斑块破裂是炎症反应的结果。这一过程涉及复杂的细胞相互作用，涉及许多介质、趋化因子和细胞因子，它们可以在血清和血浆中检测到，因此可作为区分疾病进展病理生理阶段的生物标志物。病理学研究表明，高危患者炎症的风险在更大程度上取决于炎症而非血管狭窄程度。因此，确定可靠的生物标志物以便我们监测血管炎症状态非常重要。在临床研究中，已经确定了几种新的生物标志物，它们具有越来越重要的诊断和预后意义。然而，要应用于临床还需要更多的验证性研究。此外，需要开发自动检测方法，并确定临界值。进一步的技术进步可能会促进多标志物分析用于识别冠状动脉易损斑块。