Zhang J G, Chen G, Zheng D S, Chen J H, Zhang C L, Wei S T, Zeng H C, Lin H L
Department of Epidemiology, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.
Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, Guilin Medical University, Guilin 541199, China.
Zhonghua Liu Xing Bing Xue Za Zhi. 2024 Oct 10;45(10):1362-1370. doi: 10.3760/cma.j.cn112338-20240522-00292.
To analyze the association between air pollution, genetic susceptibility, and the risk of all-cause mortality and cardiovascular outcomes in patients with atrial fibrillation (AF). AF patients aged between 40-69 years old registered in the United Kingdom Biobank from 2006 to 2010 were included. After excluding those lost to follow-up or with incomplete data during follow-up, 5 814 subjects were analyzed. Long-term exposure to air pollution was estimated at the geocoded residential address of each participant. Genetic risk scores for all-cause mortality, cardiovascular disease, heart failure, myocardial infarction, and stroke were constructed separately for each object to assess the corresponding genetic susceptibility. The Cox proportional hazards model was used to analyze the association between air pollution, genetic susceptibility, and the risk of all-cause mortality and cardiovascular outcomes in AF patients. During a median follow-up of 12.4 years, there were 929 of all-cause mortality (15.98%) and 1 772 of cardiovascular events (30.48%). Multivariable-adjusted analyses revealed that higher exposure to PM, PM, NO, and NO was associated with an increased risk of cardiovascular disease mortality, heart failure, myocardial infarction, and stroke, with hazard ratios (s) ranging from 1.26 to 1.48. Specifically, for each interquartile range () increase in PM exposure, the s for the outcomes mentioned above were 1.33 (95%: 1.14-1.54), 1.42 (95%: 1.31-1.54), 1.46 (95%: 1.30-1.64), and 1.43 (95%: 1.27-1.61), respectively. Both NO and NO exposures were associated with a 9% increased risk of all-cause mortality per increment, with corresponding s of 1.09 (95%: 1.02-1.17) and 1.09 (95%: 1.01-1.17), respectively. Individuals with high genetic susceptibility to AF had a higher risk of myocardial infarction and stroke compared to those with low genetic susceptibility, with corresponding s of 1.39 (95%: 1.04-1.87) and 1.46 (95%: 1.09-1.95), respectively. Compared to AF patients with low air pollution exposure, those with high air pollution exposure have adjusted population attributable fractions of up to 33.57% (95%: 17.87%-46.26%) for cardiovascular mortality, 28.61% (95%: 20.67%-35.75%) for heart failure, 33.35% (95%: 20.97%-43.79%) for myocardial infarction, and 42.29% (95%: 30.05%-52.71%) for stroke. Furthermore, there was an additive interaction between PM, NO, and NO exposure and high genetic susceptibility on the incidence of myocardial infarction. An additive interaction was also observed between NO, NO exposure, and high genetic susceptibility on the incidence of heart failure (all <0.05). Both air pollution and genetic susceptibility increase the risk of all-cause mortality and cardiovascular outcomes in AF patients.
分析空气污染、遗传易感性与心房颤动（AF）患者全因死亡率和心血管疾病结局风险之间的关联。纳入2006年至2010年在英国生物银行登记的40 - 69岁的AF患者。在排除随访期间失访或数据不完整的患者后，对5814名受试者进行分析。根据每位参与者地理编码的居住地址估算长期空气污染暴露情况。为每个对象分别构建全因死亡率、心血管疾病、心力衰竭、心肌梗死和中风的遗传风险评分，以评估相应的遗传易感性。采用Cox比例风险模型分析空气污染、遗传易感性与AF患者全因死亡率和心血管疾病结局风险之间的关联。在中位随访12.4年期间，有929例全因死亡（15.98%）和1772例心血管事件（30.48%）。多变量调整分析显示，较高的PM、PM、NO和NO暴露与心血管疾病死亡率、心力衰竭、心肌梗死和中风风险增加相关，风险比在1.26至1.48之间。具体而言，PM暴露每增加一个四分位数间距（），上述结局的风险比分别为1.33（95%：1.14 - 1.54）、1.42（95%：1.31 - 1.54）、1.46（95%：1.30 - 1.64）和1.43（95%：1.27 - 1.61）。NO和NO暴露每增加 ，全因死亡率风险均增加9%，相应的风险比分别为1.09（95%：1.02 - 1.17）和1.09（95%：1.01 - 1.17）。与遗传易感性低的个体相比，AF遗传易感性高的个体发生心肌梗死和中风的风险更高，相应的风险比分别为1.39（95%：1.04 - 1.87）和1.46（95%：1.09 - 1.95）。与空气污染暴露低的AF患者相比，空气污染暴露高的患者心血管死亡率的调整人群归因分数高达33.57%（95%：17.87% - 46.26%），心力衰竭为28.61%（95%：20.67% - 35.75%），心肌梗死为33.35%（95%：20.97% - 43.79%），中风为42.29%（95%：30.05% - 52.71%）。此外，PM、NO和NO暴露与高遗传易感性之间在心肌梗死发生率上存在相加交互作用。在心力衰竭发生率上，NO、NO暴露与高遗传易感性之间也观察到相加交互作用（均P<0.05）。空气污染和遗传易感性均增加AF患者的全因死亡率和心血管疾病结局风险。
