Key result
Higher non-classical monocyte percentage is linked to ~13% lower odds of significant carotid stenosis.
Why the study?
The association between circulating monocyte subset profiles and carotid artery stenosis severity, as well as their relationship with inflammatory and atherosclerosis-related parameters, was not well understood.
Cross-Sectional (n=73)
No
Odds Ratio: 0.872 (95% CI 0.765–0.994)
p-value: p=0.040
While non-classical monocyte percentages are inversely associated with carotid artery stenosis severity, this relationship is heavily attenuated by systemic inflammatory markers like fibrinogen, suggesting monocyte distribution must be interpreted within the broader inflammatory context of atherosclerosis.
Non-classical monocyte assessment should not yet guide carotid stenosis evaluation; leaves open whether subsets add value beyond inflammatory markers like fibrinogen.
Background and Objectives: This study aimed to investigate the association between circulating monocyte subset profiles and carotid artery stenosis (CAS) severity and to examine their relationships with inflammatory and atherosclerosis-related parameters. Materials and Methods: This cross-sectional study included 73 adult patients who underwent carotid Doppler ultrasonography. Participants were classified according to internal CAS severity as <50% (n = 44) or ≥50% (n = 29). Monocyte subsets were analyzed using flow cytometry and categorized as classical (CD14++CD16−), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) monocytes. Serum MCP-1 concentrations were measured using an enzyme-linked immunosorbent assay. Clinical characteristics, biochemical parameters, inflammatory indices, and carotid intima–media thickness (cIMT) were compared between the groups. Multivariate logistic regression analyses were performed to identify independent associations with significant stenosis. Results: Patients with CAS ≥50% exhibited significantly higher classical monocyte percentages and lower non-classical monocyte percentages than those with CAS < 50% (p = 0.044 and p = 0.027, respectively). Intermediate monocyte percentages did not differ significantly between the groups. Significant stenosis was also associated with a higher white blood cell count, neutrophil count, systemic inflammatory response index, fibrinogen, and HbA1c levels. Non-classical monocyte percentages showed a significant inverse correlation with cIMT (r = −0.320, p = 0.006). In a multivariable model adjusted for age, sex, and systolic blood pressure, lower non-classical monocyte percentage was associated with significant CAS (OR 0.872, 95% CI 0.765–0.994; p = 0.040). However, this association was no longer statistically significant after further adjustment for fibrinogen, neutrophil count, and HbA1c, whereas fibrinogen remained independently associated with significant CAS. Conclusions: Lower circulating non-classical monocyte percentages were associated with significant CAS and inversely correlated with cIMT and inflammatory markers. However, the attenuation of this association after adjusting for inflammatory parameters suggests that monocyte subset distribution should be interpreted within the broader inflammatory context that accompanies advanced carotid atherosclerosis.
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Deniz et al. (2026) conducted a cross-sectional in Carotid artery stenosis (n=73). Non-classical monocyte percentage was evaluated on Significant carotid artery stenosis (≥50%) (OR 0.872, 95% CI 0.765-0.994, p=0.040). Lower non-classical monocyte percentage was associated with significant carotid artery stenosis (OR 0.872) after adjusting for demographic factors, though this was attenuated by inflammatory markers.
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