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Published on: January 13, 2012
Carotid Endarterectomy Reduces Systemic Inflammatory Burden: A Prospective Analysis of Preoperative and Postoperative
Metin Onur Beyaz1, Sefer Kaya1, Gizem Kaynar Beyaz2
1Department of Cardiovascular Surgery, Hatay Mustafa Kemal University, Faculty of Medicine, Hatay, Turkey.
Insights
Carotid endarterectomy (CEA) significantly reduces inflammatory biomarkers like IL-6 and CRP, particularly in high-risk patients. This suggests CEA offers anti-inflammatory benefits beyond plaque removal, aiding in personalized treatment selection.
Area of Science:
- Vascular Surgery
- Immunology
- Biomarker Research
Background:
- Carotid atherosclerosis is a chronic inflammatory condition linked to cytokines like IL-6, IL-1β, and TNF-α.
- These cytokines contribute to endothelial dysfunction, plaque instability, and thromboembolic events.
- Carotid endarterectomy (CEA) reduces stroke risk, but its impact on systemic inflammation needs further characterization.
Purpose of the Study:
- To comprehensively evaluate changes in inflammatory biomarker profiles after CEA.
- To identify patient subgroups with distinct inflammatory responses post-CEA.
- To explore the anti-inflammatory effects of carotid revascularization.
Main Methods:
- Prospective observational study of 87 patients undergoing CEA.
- Measurement of 10 inflammatory biomarkers (CRP, IL-6, TNF-α, IL-10, IL-1β, TGF-β, fibrinogen, NLR, WBC, procalcitonin) pre- and post-operatively.
- Statistical analysis included Wilcoxon signed-rank tests, Mann-Whitney U tests, and Spearman correlations.
Main Results:
- All 10 measured biomarkers significantly decreased post-CEA (p < 0.001).
- Greatest reductions observed in IL-6, NLR, IL-1β, procalcitonin, and CRP with large effect sizes.
- Symptomatic patients and those with unstable plaques showed greater inflammatory marker reduction compared to asymptomatic/stable plaque patients.
Conclusions:
- CEA significantly reduces systemic inflammatory biomarkers, demonstrating an anti-inflammatory effect.
- Higher-risk inflammatory phenotypes experience greater benefits from CEA.
- Findings support inflammatory biomarker-guided patient selection for carotid revascularization.
Background:
Carotid atherosclerosis is a chronic inflammatory disease in which cytokines, particularly interleukin (IL)-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α), lead to endothelial dysfunction, plaque destabilization, and thromboembolic events. While carotid endarterectomy (CEA) effectively reduces the risk of stroke, its effect on systemic inflammatory biomarkers has not been fully characterized. In this study, we aimed to comprehensively evaluate the changes in inflammatory biomarker profiles after CEA and identify patient subgroups showing different inflammatory responses.
Methods:
This prospective observational study included 87 consecutive patients who underwent CEA between January 2024 and June 2025 at Hatay Mustafa Kemal University Hospital. Ten inflammatory biomarkers (C-reactive protein [CRP], IL-6, TNF-α, IL-10, IL-1β, tumor necrosis growth factor [TGF]-β, fibrinogen, neutrophil-lymphocyte ratio [NLR], white blood cell count [WBC], and procalcitonin)] were measured from peripheral venous blood samples collected preoperatively (24 h before surgery) and postoperatively (48-72 h after surgery). Serum was obtained after centrifugation for cytokine analysis. Wilcoxon signed-rank tests were used for preoperative and postoperative comparisons; Mann-Whitney U-tests were used for subgroup analyses; and Spearman coefficients were used for correlations.
Results:
All 10 biomarkers were significantly reduced in the postoperative period (all P < 0.001). The greatest reductions occurred in IL-6 (-29.3%), NLR (-28.6%), IL-1β (-28.1%), procalcitonin (-27.5%), and CRP (-26.2%), with high effect sizes (Cohen's d > 2.0). Symptomatic patients and those with unstable plaques showed significantly greater reductions in inflammation compared to asymptomatic patients and those with stable plaques (P < 0.05 for CRP, IL-6, fibrinogen, NLR, and IL-1β). IL-6 showed a strong correlation with stenosis severity (ρ = 0.602, P < 0.001). Interestingly, baseline CRP (P = 0.024), IL-6 (P = 0.049), and fibrinogen (P = 0.004) levels were lower in patients who developed restenosis.
Conclusion:
CEA delivers significant and consistent reductions in systemic inflammatory biomarkers and shows greater effects in high-risk inflammatory phenotypes. These findings support the anti-inflammatory benefit of carotid revascularization beyond mechanical plaque clearance and suggest potential for inflammatory biomarker-guided patient selection.
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