2021, Vol. 3, Issue 1, Part I

Methods: A prospective observational study was conducted on 140 patients undergoing carotid ultrasonography. Participants were categorized into control, mild (<60%), and severe (≥60%) stenosis groups. Plaque morphology was classified as echolucent (soft) or echogenic (hard). Inflammatory markers (CRP, UA), hematological indices (neutrophil-to-lymphocyte ratio [NLR], platelet-to-lymphocyte ratio [PLR], monocyte-to-HDL ratio [MHR]), and metabolic parameters were analyzed. Multivariate regression and correlation analyses were performed to identify associations and predictors.

Results: Patients with carotid stenosis exhibited progressively higher levels of CRP, UA, NLR, and PLR compared to controls. CRP increased from 0.27 mg/dL in controls to 0.49 mg/dL in mild and 0.66 mg/dL in severe stenosis. Uric acid and triglycerides were also elevated in stenotic groups. Soft plaques demonstrated significantly higher CRP (0.55 mg/dL vs. 0.53 mg/dL), MPV (11.39 fL vs. 10.46 fL), PDW (14.44% vs. 11.71%), WBC, and monocyte counts than hard plaques, indicating greater inflammatory and thrombotic potential. Multivariate analysis identified age, CRP, and UA as independent predictors of carotid stenosis severity. CRP correlated positively with MHR (r = 0.231, P < 0.01) and GGT (r = 0.219, p< 0.05), and negatively with HDL-C (r = -0.172, p< 0.05).

Conclusion: Inflammation plays a pivotal role in the progression of carotid stenosis and plaque vulnerability. Elevated CRP and UA are valuable predictive markers for stenosis severity and soft plaque formation. The findings highlight the clinical relevance of incorporating inflammatory biomarkers in risk assessment to improve prediction of plaque instability and cerebrovascular events.