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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine