[空气污染、遗传易感性对心房颤动患者全因死亡风险和心血管后果的影响]。

J G Zhang, G Chen, D S Zheng, J H Chen, C L Zhang, S T Wei, H C Zeng, H L Lin
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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. <b>Results:</b> 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<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>x</sub>, and NO<sub>2</sub> was associated with an increased risk of cardiovascular disease mortality, heart failure, myocardial infarction, and stroke, with hazard ratios (<i>HR</i>s) ranging from 1.26 to 1.48. Specifically, for each interquartile range (<i>IQR</i>) increase in PM<sub>2.5</sub> exposure, the <i>HR</i>s for the outcomes mentioned above were 1.33 (95%<i>CI</i>: 1.14-1.54), 1.42 (95%<i>CI</i>: 1.31-1.54), 1.46 (95%<i>CI</i>: 1.30-1.64), and 1.43 (95%<i>CI</i>: 1.27-1.61), respectively. Both NO<sub>x</sub> and NO<sub>2</sub> exposures were associated with a 9% increased risk of all-cause mortality per <i>IQR</i> increment, with corresponding <i>HR</i>s of 1.09 (95%<i>CI</i>: 1.02-1.17) and 1.09 (95%<i>CI</i>: 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 <i>HR</i>s of 1.39 (95%<i>CI</i>: 1.04-1.87) and 1.46 (95%<i>CI</i>: 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%<i>CI</i>: 17.87%-46.26%) for cardiovascular mortality, 28.61% (95%<i>CI</i>: 20.67%-35.75%) for heart failure, 33.35% (95%<i>CI</i>: 20.97%-43.79%) for myocardial infarction, and 42.29% (95%<i>CI</i>: 30.05%-52.71%) for stroke. 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引用次数: 0

摘要

目的分析空气污染、遗传易感性与心房颤动(房颤)患者全因死亡风险和心血管后果之间的关联。方法:对年龄在 40-69 岁之间的心房颤动患者进行调查:纳入 2006 年至 2010 年期间在英国生物数据库登记的 40-69 岁心房颤动患者。在排除了失去随访或随访期间数据不完整的患者后,对 5 814 名受试者进行了分析。根据每位受试者的地理编码居住地址估算其长期暴露于空气污染的程度。针对每个对象分别构建了全因死亡率、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 比例危险模型分析空气污染、遗传易感性与房颤患者全因死亡和心血管疾病风险之间的关系。结果显示在中位随访 12.4 年期间,全因死亡率为 929 例(15.98%),心血管事件为 1 772 例(30.48%)。多变量调整分析显示,PM2.5、PM10、氮氧化物和二氧化氮暴露量越高,心血管疾病死亡率、心力衰竭、心肌梗死和中风的风险越高,危险比(HRs)从1.26到1.48不等。具体来说,PM2.5暴露量每增加一个四分位数间距(IQR),上述结果的危险比分别为1.33(95%CI:1.14-1.54)、1.42(95%CI:1.31-1.54)、1.46(95%CI:1.30-1.64)和1.43(95%CI:1.27-1.61)。暴露于氮氧化物和二氧化氮时,每增加一个 IQR 值,全因死亡风险就会增加 9%,相应的 HR 值分别为 1.09(95%CI:1.02-1.17)和 1.09(95%CI:1.01-1.17)。与遗传易感性低的人群相比,房颤遗传易感性高的人群发生心肌梗死和中风的风险更高,相应的HR值分别为1.39(95%CI:1.04-1.87)和1.46(95%CI:1.09-1.95)。与空气污染暴露程度低的房颤患者相比,空气污染暴露程度高的房颤患者心血管死亡率的调整后人群归因分数高达 33.57%(95%CI:17.87%-46.26%),心力衰竭死亡率为 28.61%(95%CI:20.67%-35.75%),心肌梗死死亡率为 33.35%(95%CI:20.97%-43.79%),中风死亡率为 42.29%(95%CI:30.05%-52.71%)。此外,PM2.5、氮氧化物和二氧化氮暴露与高遗传易感性对心肌梗死发病率之间存在相加相互作用。在氮氧化物、二氧化氮暴露和高遗传易感性之间也观察到相加的相互作用,从而影响心力衰竭的发病率(所有 PConclusions):空气污染和遗传易感性都会增加房颤患者的全因死亡风险和心血管后果。
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[Effect of air pollution, genetic susceptibility on the risk of all-cause mortality and cardiovascular outcomes among atrial fibrillation patients].

Objective: 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). Methods: 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. Results: 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 PM2.5, PM10, NOx, and NO2 was associated with an increased risk of cardiovascular disease mortality, heart failure, myocardial infarction, and stroke, with hazard ratios (HRs) ranging from 1.26 to 1.48. Specifically, for each interquartile range (IQR) increase in PM2.5 exposure, the HRs for the outcomes mentioned above were 1.33 (95%CI: 1.14-1.54), 1.42 (95%CI: 1.31-1.54), 1.46 (95%CI: 1.30-1.64), and 1.43 (95%CI: 1.27-1.61), respectively. Both NOx and NO2 exposures were associated with a 9% increased risk of all-cause mortality per IQR increment, with corresponding HRs of 1.09 (95%CI: 1.02-1.17) and 1.09 (95%CI: 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 HRs of 1.39 (95%CI: 1.04-1.87) and 1.46 (95%CI: 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%CI: 17.87%-46.26%) for cardiovascular mortality, 28.61% (95%CI: 20.67%-35.75%) for heart failure, 33.35% (95%CI: 20.97%-43.79%) for myocardial infarction, and 42.29% (95%CI: 30.05%-52.71%) for stroke. Furthermore, there was an additive interaction between PM2.5, NOx, and NO2 exposure and high genetic susceptibility on the incidence of myocardial infarction. An additive interaction was also observed between NOx, NO2 exposure, and high genetic susceptibility on the incidence of heart failure (all P<0.05). Conclusions: Both air pollution and genetic susceptibility increase the risk of all-cause mortality and cardiovascular outcomes in AF patients.

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来源期刊
中华流行病学杂志
中华流行病学杂志 Medicine-Medicine (all)
CiteScore
5.60
自引率
0.00%
发文量
8981
期刊介绍: Chinese Journal of Epidemiology, established in 1981, is an advanced academic periodical in epidemiology and related disciplines in China, which, according to the principle of integrating theory with practice, mainly reports the major progress in epidemiological research. The columns of the journal include commentary, expert forum, original article, field investigation, disease surveillance, laboratory research, clinical epidemiology, basic theory or method and review, etc.  The journal is included by more than ten major biomedical databases and index systems worldwide, such as been indexed in Scopus, PubMed/MEDLINE, PubMed Central (PMC), Europe PubMed Central, Embase, Chemical Abstract, Chinese Science and Technology Paper and Citation Database (CSTPCD), Chinese core journal essentials overview, Chinese Science Citation Database (CSCD) core database, Chinese Biological Medical Disc (CBMdisc), and Chinese Medical Citation Index (CMCI), etc. It is one of the core academic journals and carefully selected core journals in preventive and basic medicine in China.
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