Key result
Elevated systemic immune inflammation index (OR 1.031 per 10-unit increase) and plaque thickness (OR 1.897) were independent risk factors for carotid intraplaque neovascularization.
Why the study?
This study aimed to investigate the correlation between carotid intraplaque neovascularization scores and immune-inflammatory indicators in patients with different degrees of coronary artery stenosis.
Observational (n=107)
Elevated systemic immune inflammation index and increased carotid plaque thickness are associated with intraplaque neovascularization and may indicate more severe coronary artery stenosis.
Answers are grounded in this paper and cite their sources.
May aid carotid plaque risk stratification; leaves open prospective validation and therapeutic targeting of SII.
Background: Intraplaque neovascularization (IPN) correlates significantly with plaque vulnerability and can be detected using Angio PLanewave UltraSensitive imaging technology (Angio PL.U.S.; AP). Several immune–inflammatory biomarkers that reflect the state of inflammation and immune homeostasis in the body are currently used to assess cardiovascular and cerebrovascular diseases. This study aimed to investigate the correlation between carotid IPN scores and several immune–inflammatory indicators in patients with different degrees of coronary artery stenosis. Methods: This study prospectively enrolled 107 patients with coronary artery stenosis confirmed by coronary angiography (CAG). Preoperative ultrasonography was performed to screen for carotid plaques, and AP was conducted to determine whether IPN was present and correctly scored. The levels of immune–inflammatory indicators, plaques, and coronary artery lesions between groups with and without IPN and different IPN scores were analyzed. We utilized logistic regression models to determine the independent predictors of IPN and constructed receiver operating characteristic (ROC) curves. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Results: Differences in systemic immune inflammation index (SII) levels and plaque thicknesses were found between the groups with and without IPN and between different IPN scores (p < 0.05). The IPN scores were positively correlated with SII levels (r = 0.268, p = 0.005), plaque thickness (r = 0.273, p = 0.005), and Gensini score (r = 0.446, p < 0.001). SII levels (per 10-unit increase) (OR = 1.031) and plaque thickness (OR = 1.897) were independent risk factors for IPN. When the SII was 541 × 109/L and the thickness of the plaque was 2.25 mm, the area under the curve (AUC) was 0.653 and 0.656, respectively. The AUC of the combined diagnosis was 0.711. Conclusion: Elevated SII levels and increased plaque thickness were associated with the vulnerability of carotid plaques in patients with coronary artery stenosis and may signal increased coronary artery stenosis. The Clinical Trial Registration: ChiCTR2400094458, https://www.chictr.org.cn/hvshowprojectEN.html?id=266292&v=1.0.
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A 2025 study conducted an observational in Coronary artery stenosis (n=107). Systemic immune inflammation index (SII) and plaque thickness vs. Lower SII and plaque thickness was evaluated on Intraplaque neovascularization (IPN) (OR 1.031). Elevated systemic immune inflammation index (OR 1.031 per 10-unit increase) and plaque thickness (OR 1.897) were independent risk factors for carotid intraplaque neovascularization.
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