Guo Xinru, Mi Shiting, Zhao Lin, Chen Tielong
Department of Cardiology, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Mediators Inflamm. 2025 Aug 21;2025:3250786. doi: 10.1155/mi/3250786. eCollection 2025.
Inflammation plays a central role in the occurrence and progression of cardiovascular disease (CVD). However, the intricate relationships between sleep patterns, inflammatory markers, and CVD risk remain insufficiently understood. This study aims to explore these associations, with a specific focus on the mediating role of inflammatory markers and their nonlinear effects. This study used a multiethnic adult population ( = 8752) from the National Health and Nutrition Examination Survey (NHANES) database (four data cycles from 2005-2006, 2007-2008, 2015-2016, and March 2017-2020). Multivariate logistic regression assessed the effects of sleep patterns and inflammatory markers on CVD risk. Furthermore, the mediating effects of the neutrophil-platelet ratio (NPR) and the systemic immune-inflammation index (SII) were assessed. Binary logistic regression was utilized to analyze the correlations between quartile groupings of inflammatory markers (SII and NPR) and CVD, as well as its specific types. The nonlinear relationship between inflammatory markers and CVD risk was explored using a generalized additive model (GAM). Trouble sleep pattern significantly increased the risk of CVD (odds ratio [OR] = 2.7558, 95% confidence interval [CI]: 1.9019, 3.9931, < 0.0001). Mediation analyses showed NPR mediated 17.38% and SII mediated 3.27% of the association. GAM showed that NPR (-trend < 0.0001) and SII (-trend = 0.001) had a significant inverted "U" shaped relationship with CVD risk, with higher inflammation increasing CVD risk up to a point, after which the risk decreased. Trouble sleep pattern significantly increased CVD risk, NPR and SII partially mediated the relationship between sleep patterns and CVD risk, and the nonlinear relationship with CVD risk suggests a bi-directional mechanism for the regulation of inflammatory markers. These findings offer new insights for inflammatory interventions and sleep health management in CVD prevention.
炎症在心血管疾病（CVD）的发生和发展中起着核心作用。然而，睡眠模式、炎症标志物和CVD风险之间的复杂关系仍未得到充分理解。本研究旨在探讨这些关联，特别关注炎症标志物的中介作用及其非线性效应。本研究使用了来自美国国家健康与营养检查调查（NHANES）数据库的多民族成年人群（n = 8752）（2005 - 2006年、2007 - 2008年、2015 - 2016年以及2017年3月至2020年的四个数据周期）。多变量逻辑回归评估了睡眠模式和炎症标志物对CVD风险的影响。此外，评估了中性粒细胞与血小板比值（NPR）和全身免疫炎症指数（SII）的中介作用。采用二元逻辑回归分析炎症标志物（SII和NPR）的四分位数分组与CVD及其特定类型之间的相关性。使用广义相加模型（GAM）探索炎症标志物与CVD风险之间的非线性关系。睡眠问题模式显著增加了CVD风险（优势比[OR] = 2.7558，95%置信区间[CI]：1.9019，3.9931，P < 0.0001）。中介分析表明，NPR介导了17.38%的关联，SII介导了3.27%的关联。GAM显示，NPR（-趋势 < 0.0001）和SII（-趋势 = 0.001）与CVD风险呈显著的倒“U”形关系，炎症水平升高在一定程度上增加CVD风险，之后风险降低。睡眠问题模式显著增加CVD风险，NPR和SII部分介导了睡眠模式与CVD风险之间的关系，且与CVD风险的非线性关系提示了炎症标志物调节的双向机制。这些发现为CVD预防中的炎症干预和睡眠健康管理提供了新的见解。
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