Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison (M.C.T., A.D.G., M.M.K., M.H.H., J.H.S.).
Department of Biostatistics, University of Washington, Seattle (A.S.D., R.L.M.).
Circ Arrhythm Electrophysiol. 2020 Feb;13(2):e007685. doi: 10.1161/CIRCEP.119.007685. Epub 2020 Feb 4.
Asthma and atrial fibrillation (AF) share an underlying inflammatory pathophysiology. We hypothesized that persistent asthmatics are at higher risk for developing AF and that this association would be attenuated by adjustment for baseline markers of systemic inflammation.
The MESA (Multi-Ethnic Study of Atherosclerosis) is a prospective longitudinal study of adults free of cardiovascular disease at baseline. Presence of asthma was determined at exam 1. Persistent asthma was defined as asthma requiring use of controller medications. Intermittent asthma was defined as asthma without use of controller medications. Participants were followed for a median of 12.9 (interquartile range, 10-13.6) years for incident AF. Multivariable Cox regression models were used to assess associations of asthma subtype and AF.
The 6615 participants were a mean (SD) 62.0 (10.2) years old (47% male, 27% black, 12% Chinese, and 22% Hispanic). AF incidence rates were 0.11 (95% CI, 0.01-0.12) events/10 person-years for nonasthmatics, 0.11 (95% CI, 0.08-0.14) events/10 person-years for intermittent asthmatics, and 0.19 (95% CI, 0.120.49) events/10 person-years for persistent asthmatics (log-rank =0.008). In risk-factor adjusted models, persistent asthmatics had a greater risk of incident AF (hazard ratio, 1.49 [95% CI, 1.03-2.14], =0.03). IL (Interleukin)-6 (hazard ratio, 1.26 [95% CI, 1.13-1.42]), TNF (tumor necrosis factor)-α receptor 1 (hazard ratio, 1.09 [95% CI, 1.08-1.11]) and D-dimer (hazard ratio, 1.10 [95% CI, 1.02-1.20]) predicted incident AF, but the relationship between asthma and incident AF was not attenuated by adjustment for any inflammation marker (IL-6, CRP [C-reactive protein], TNF-α R1, D-dimer, and fibrinogen).
In a large multiethnic cohort with nearly 13 years follow-up, persistent asthma was associated with increased risk for incident AF. This association was not attenuated by adjustment for baseline inflammatory biomarkers.
哮喘和心房颤动（AF）具有共同的潜在炎症发病机制。我们假设持续性哮喘患者发生 AF 的风险更高，并且这种关联可以通过调整基线全身炎症标志物来减弱。
MESA（动脉粥样硬化多民族研究）是一项在基线时无心血管疾病的成年人的前瞻性纵向研究。在检查 1 时确定哮喘的存在。持续性哮喘定义为需要使用控制器药物的哮喘。间歇性哮喘定义为不使用控制器药物的哮喘。参与者中位随访 12.9（四分位距，10-13.6）年发生 AF。使用多变量 Cox 回归模型评估哮喘亚型和 AF 的关联。
6615 名参与者的平均（SD）年龄为 62.0（10.2）岁（47%为男性，27%为黑人，12%为中国人，22%为西班牙裔）。非哮喘患者的 AF 发生率为 0.11（95%CI，0.01-0.12）/10 人年，间歇性哮喘患者为 0.11（95%CI，0.08-0.14）/10 人年，持续性哮喘患者为 0.19（95%CI，0.12-0.49）/10 人年（对数秩=0.008）。在风险因素调整模型中，持续性哮喘患者发生 AF 的风险更高（风险比，1.49[95%CI，1.03-2.14]，=0.03）。白细胞介素（IL）-6（风险比，1.26[95%CI，1.13-1.42]）、肿瘤坏死因子（TNF）-α受体 1（风险比，1.09[95%CI，1.08-1.11]）和 D-二聚体（风险比，1.10[95%CI，1.02-1.20]）预测 AF 事件，但调整任何炎症标志物（IL-6、C 反应蛋白（CRP）、TNF-α R1、D-二聚体和纤维蛋白原）后，哮喘与 AF 事件之间的关系并未减弱。
在一项随访近 13 年的大型多民族队列中，持续性哮喘与 AF 事件风险增加相关。这种关联在调整基线炎症生物标志物后并未减弱。
