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
Keywords: Atherosclerosis, Biomarkers, Vulnerable Plaque, Inflammattion, Chemokines, Cytokines, Oxidative Stress, macrophage accumulation, inflammatory reaction, cytokines
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