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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Candidate biomarkers for the detection of coronary plaque destabilization and rupture
Insights
Identifying high-risk patients with chest pain is difficult. Emerging biomarkers may help detect vulnerable plaque rupture, improving patient triage and guiding treatment for cardiovascular disease.
Area of Science:
- Cardiology
- Biomarker Discovery
- Vascular Biology
Background:
- Chest pain evaluation requires better risk stratification tools.
- Current methods struggle to identify patients with vulnerable plaque before infarction.
- Understanding plaque destabilization mechanisms is crucial for early detection.
Purpose of the Study:
- To review emerging biomarkers for vulnerable plaque.
- To explore biomarkers reflecting plaque evolution and rupture.
- To assess clinical applications for risk prediction in chest pain patients.
Main Methods:
- Literature review of current research on vulnerable plaque biomarkers.
- Analysis of pathways involved in plaque destabilization (inflammation, oxidative stress, MMPs, hemodynamics).
- Identification of candidate biomarkers reflecting these processes.
Main Results:
- Vulnerable plaque is driven by lipid core expansion and cap thinning.
- Inflammation, oxidative stress, matrix metalloproteinases, and shear stress are key pathways.
- Several candidate biomarkers show potential for detecting occult plaque instability.
Conclusions:
- Emerging biomarkers offer promise for identifying high-risk patients with chest pain.
- These biomarkers could enable earlier detection of plaque rupture and improve triage.
- Further research is needed to validate these biomarkers for clinical use.
Abstract:
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.
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