慢性PM2.5暴露与侵入性评估的冠状动脉内皮功能障碍相关
该观察性研究纳入2000至2023年在Mayo Clinic因心绞痛及非阻塞性冠心病行冠状动脉反应性测试的1485例患者，基于居住地址估算测试前2年平均PM2.5暴露，以乙酰胆碱激发后冠状动脉直径变化小于-20%定义心外膜内皮功能障碍。加权多因素logistic回归显示，PM2.5每升高1 μg/m3与内皮功能障碍风险增加相关（OR: 1.078; 95% CI: 1.021-1.139; P = 0.007）。
要点
- 慢性PM2.5暴露与侵入性评估的心外膜冠状动脉内皮功能障碍独立相关。
- PM2.5每升高1 μg/m3，内皮功能障碍风险增加（OR: 1.078; 95% CI: 1.021-1.139; P = 0.007）。
- 提示PM2.5可能与冠心病早期血管损伤存在生物学联系。
核心结论
- 慢性PM2.5暴露与心外膜冠状动脉内皮功能障碍相关，提示PM2.5与冠心病之间可能存在生物学联系。
研究设计与样本
- 观察性研究，前瞻性纳入2000至2023年在Mayo Clinic因心绞痛及非阻塞性冠心病行冠状动脉反应性测试的患者，共1485例，中位年龄51.7岁（Q1-Q3: 42.7-60.1岁）。
- 基于测试时居住地址地理编码，以0.01°×0.01°空间分辨率估算测试前2年平均PM2.5暴露。
- 采用广义倾向评分伽马分布模型生成稳定逆概率权重，并应用于多因素logistic回归。
主要发现
- PM2.5暴露高于美国环境保护署标准（9 μg/m3）的个体更年轻、心血管合并症更少，但血脂谱更差。
- 加权多因素logistic回归中，PM2.5每升高1 μg/m3与内皮功能障碍风险增加相关（OR: 1.078; 95% CI: 1.021-1.139; P = 0.007），校正年龄、性别、体重指数及心血管合并症。
关键数值与推荐
- 心外膜内皮功能障碍定义为乙酰胆碱输注后冠状动脉直径变化百分比小于-20%。
- 美国环境保护署PM2.5标准为9 μg/m3。
临床怎么用
- 对心绞痛及非阻塞性冠心病患者，评估长期PM2.5暴露可能有助于识别冠状动脉内皮功能障碍高危个体。
- PM2.5暴露可作为冠心病早期血管损伤的非传统心血管风险因素纳入临床考量。
以上解读依据论文摘要（全文未开放获取或许可不允许翻译转载）。
原文
BACKGROUND: Coronary endothelial dysfunction (ED) represents an early stage of coronary artery disease (CAD). Several factors may induce ED. Air pollution, more specifically particulate matter <2.5 μm (PM2.5), has emerged as a major nontraditional cardiovascular risk factor contributing to early vascular injury, but its impact on coronary ED remains poorly defined. OBJECTIVES: In this study, we sought to identify an association between chronic PM2.5 exposure and epicardial endothelial dysfunction (EED) determined by means of invasive coronary vasoreactivity testing, the criterion standard technique to assess EED. METHODS: This observational study included prospectively enrolled patients with angina and nonobstructive CAD who underwent coronary reactivity testing at Mayo Clinic from 2000 to 2023. Residential addresses at the time of testing were geocoded to derive monthly PM2.5 exposure at a 0.01° × 0.01° spatial resolution, averaged over the 2 years preceding testing. EED was defined as percentage change of less than -20% in coronary artery diameter in response to acetylcholine infusion. Associations between continuous PM2.5 and EED were assessed according to a generalized propensity score with a gamma-distributed model to derive stabilized inverse probability weights, applied in multivariable logistic regression. RESULTS: A total of 1,485 patients with a median age of 51.7 years (Q1-Q3: 42.7-60.1 years) were included in the analysis. Individuals exposed to PM2.5 above environmental protection agency standards (9 μg/m3) were younger and had less cardiovascular comorbidities, although they had worse lipid profiles. In weighted multivariable logistic regression, each 1 μg/m3 increase in PM2.5 was associated with increased odds of EED (OR: 1.078; 95% CI: 1.021-1.139; P = 0.007), adjusted for age, sex, body mass index, and cardiovascular comorbidities. CONCLUSIONS: Chronic PM2.5 exposure is associated with epicardial coronary ED, suggesting a potential biological link between PM2.5 and CAD.
引用
- Manzato M, Kalhor P, Nogami K, et al. Chronic PM2.5 Exposure Is Associated With Invasively Assessed Coronary Endothelial Dysfunction. J Am Coll Cardiol. 2026. PMID: 42159534. doi:10.1016/j.jacc.2026.03.155
供执业医师工作参考，不替代临床判断；数值与分级以指南原文为准。