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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Kinin B1 receptor as a novel, prognostic progression biomarker for carotid atherosclerotic plaques
Tiantian Liu1, Hengfang Liu2, Li Feng1
1Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Insights
Inflammatory biomarkers like interleukin-6, interleukin-10, and kinin B1 receptor (B1R) were studied in stroke patients. Serum B1R levels showed a significant correlation with carotid plaque characteristics, suggesting its potential as a prognostic indicator for atherosclerosis progression.
Area of Science:
- Cardiovascular Science
- Immunology
- Biomarker Research
Background:
- Atherosclerosis-induced stroke is a major global health concern, linked to carotid plaque rupture and inflammation.
- Predictive inflammatory biomarkers for carotid plaque progression remain incompletely understood.
Purpose of the Study:
- To investigate the association between carotid plaque vulnerability and specific inflammatory biomarkers (IL-6, IL-10, B1R) in patients with atherosclerosis.
- To evaluate the potential of these biomarkers as indicators of plaque progression and stability post-stroke.
Main Methods:
- Carotid plaque specimens and serum samples were collected from 111 patients (80 stroke, 14 TIA, 17 asymptomatic).
- Plaque histological characteristics were analyzed based on the time elapsed since the last ischemic stroke.
- Serum levels of IL-6, IL-10, and B1R were quantified using ELISA; immunohistochemistry was also performed on plaque tissues.
Main Results:
- Plaques exhibited an unstable phenotype within 30-90 days post-stroke, transitioning to more stable forms at later time points (90-180 and >180 days).
- Serum levels of IL-6 and B1R decreased over time post-stroke, while IL-10 levels increased.
- Only serum B1R levels demonstrated a significant correlation with histological plaque characteristics.
Conclusions:
- Serum B1R levels may offer prognostic value for patients with carotid atherosclerosis.
- B1R is identified as a potential indicator for monitoring atherosclerosis progression.
Abstract:
Stroke caused by atherosclerosis remains a leading cause of morbidity and mortality worldwide, associated with carotid plaque rupture and inflammation progression. However, the inflammatory biomarkers which aid in predicting the future course of plaques are less detailed. The present study investigated the association between plaque vulnerable and inflammatory biomarkers using blood and plaque specimens. Carotid plaque specimens were obtained from 80 patients following stroke, 14 patients suffering from transient ischaemic attack and 17 asymptomatic patients that underwent carotid endarterectomy. To assess changes in plaque characteristics at histological levels, plaques were categorized by the time between the latest ischemic stroke and surgical intervention within 30, 30‑90, 90‑180 and over 180 days following stroke. Serum levels of inflammatory biomarkers interleukin (IL)‑6, IL‑10 and kinin B1 receptor (B1R) were measured by ELISA. Histological assessment of plaque was used to evaluate the plaque stability, progression and the inflammatory biomarker levels. Comparisons of histological characteristics demonstrated that plaques revealed an unstable phenotype following stroke within 30, 30‑90 days and then remodeled into more stable plaques following stroke at 90‑180 and over 180 days. By comparing the serum levels of inflammatory biomarkers, it was observed that IL‑6 and B1R levels tended to decline whereas IL‑10 levels increased in stroke patients from <30 days to over 180 days. Immunohistochemical analysis of IL‑6, IL‑10 and B1R demonstrated similar alterations in serum levels. Correlation analyses revealed that only B1R serum level was significantly correlated with histological level in patients with carotid atherosclerosis. The findings revealed that serum B1R levels may provide prognostic information and currently act as potential indicators for progression in atherosclerosis.
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