[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 PM _2.5 , PM ₁₀ , NO _x , and NO ₂ was associated with an increased risk of cardiovascular disease mortality, heart failure, myocardial infarction, and stroke, with hazard ratios ( HR s) ranging from 1.26 to 1.48. Specifically, for each interquartile range ( IQR ) increase in PM _2.5 exposure, the HR s 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 NO _x and NO ₂ exposures were associated with a 9% increased risk of all-cause mortality per IQR increment, with corresponding HR s 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 HR s 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 PM _2.5 , NO _x , and NO ₂ exposure and high genetic susceptibility on the incidence of myocardial infarction. An additive interaction was also observed between NO _x , NO ₂ 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.