早晨高血压（MHT）对老年人发生新发房颤（AF）的风险以及机制尚未明确。 本研究旨在调查MHT与新发AF之间的关联，并探讨亚临床炎症在这一关联中的中介效应。2008年至2010年，在中国山东地区招募了1789名年龄≥60岁的老年人。使用24小时动态血压监测来评估早晨血压（BP）。定义MHT为在清晨至上午9点期间BP≥135/85mm Hg。使用高敏C-反应蛋白（hsCRP）、肿瘤坏死因子-α（TNF-α）、全身免疫炎症指数（SII）、中性粒细胞与淋巴细胞比值（NLR）、血小板与淋巴细胞比值（PLR）和galectin-3评估亚临床炎症。在随访期间记录新发AF情况。平均随访时间为129.0个月（标准差：21.58个月），与非MHT参与者相比，MHT患者新发AF的风险比为1.39（95%置信区间：1.01至1.91），P调整=0.027。早晨收缩压每增加一个标准差，新发AF的风险增加1.17倍。亚临床炎症与新发AF显著相关。hsCRP、TNF-α、SII、NLR、PLR和galectin-3每增加一个标准差，新发AF的风险比分别为2.29、2.04、2.08、2.08、2.03和3.25（P调整 < 0.001）。分析显示，hsCRP、TNF-α、SII、NLR、PLR和galectin-3分别在MHT引起新发AF的过程中起到中介作用（P调整 < 0.05）。早晨高血压与新发AF的风险增加有关。亚临床炎症可能在这种关联中起到中介作用。

The impacts and mechanisms of morning hypertension (MHT) on the risk of new-onset atrial fibrillation (AF) in the elderly have not been clarified. We aimed to investigate an association between MHT and new-onset AF and explore a mediating effect of subclinical inflammation on this association.From 2008 to 2010, 1789 older adults aged ≥60 years were recruited in Shandong area, China. Morning blood pressure (BP) was assessed using 24-hour ambulatory BP monitoring. MHT was defined as BP ≥ 135/85 mm Hg during the period from wake time to 0900 a.m. Subclinical inflammation was assessed by hypersensitive C-reactive protein (hsCRP), tumor necrosis factor-alpha (TNF-α), systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and galectin-3. New-onset AF was rated during the follow-up period.Over an average 129.0 [standard deviation (SD): 21.58] months of follow-up, the hazard ratio of new-onset AF in MHT patients was 1.39 (95% confidence interval: 1.01 to 1.91) compared with non-MHT participants (Padjusted = 0.027). The risk of new-onset AF was 1.17-fold with one-SD increment of morning systolic BP. Subclinical inflammation was significantly associated with new-onset AF. The hazard ratios of new-onset AF were 2.29, 2.04, 2.08, 2.08, 2.03, and 3.25 for one-SD increment in hsCRP, TNF-α, SII, NLR, PLR, and galectin-3, respectively (Padjusted < 0.001). The analysis showed that hsCRP, TNF-α, SII, NLR, PLR, and galectin-3 separately mediated the process of MHT inducing new-onset AF (Padjusted < 0.05).MHT is associated with an increased risk of new-onset AF. The subclinical inflammation might play a mediating role in this association.