Journal of the American College of Cardiology · 2013
Acute exposure to air pollution triggers atrial fibrillation.
СтатьяПоддержка NIH: внешняя программаПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Link Mark S, Luttmann-Gibson Heike, Schwartz Joel, Mittleman Murray A, Wessler Benjamin, Gold Diane R, Dockery Douglas W, Laden Francine
Аннотация
OBJECTIVES: This study sought to evaluate the association of air pollution with the onset of atrial fibrillation (AF).
BACKGROUND: Air pollution in general and more specifically particulate matter has been associated with cardiovascular events. Although ventricular arrhythmias are traditionally thought to convey the increased cardiovascular risk, AF may also contribute.
METHODS: Patients with dual chamber implantable cardioverter-defibrillators (ICDs) were enrolled and followed prospectively. The association of AF onset with air quality including ambient particulate matter <2.5 μm aerodynamic diameter (PM2.5), black carbon, sulfate, particle number, NO2, SO2, and O3 in the 24 h prior to the arrhythmia was examined utilizing a case-crossover analysis. In sensitivity analyses, associations with air pollution between 2 and 48 h prior to the AF were examined.
RESULTS: Of 176 patients followed for an average of 1.9 years, 49 patients had 328 episodes of AF lasting ≥ 30 s. Positive but nonsignificant associations were found for PM2.5 in the prior 24 h, but stronger associations were found with shorter exposure windows. The odds of AF increased by 26% (95% confidence interval: 8% to 47%) for each 6.0 μg/m(3) increase in PM2.5 in the 2 h prior to the event (p = 0.004). The odds of AF were highest at the upper quartile of mean PM2.5.
CONCLUSIONS: PM was associated with increased odds of AF onset within hours following exposure in patients with known cardiac disease. Air pollution is an acute trigger of AF, likely contributing to the pollution-associated adverse cardiac outcomes observed in epidemiological studies.
BACKGROUND: Air pollution in general and more specifically particulate matter has been associated with cardiovascular events. Although ventricular arrhythmias are traditionally thought to convey the increased cardiovascular risk, AF may also contribute.
METHODS: Patients with dual chamber implantable cardioverter-defibrillators (ICDs) were enrolled and followed prospectively. The association of AF onset with air quality including ambient particulate matter <2.5 μm aerodynamic diameter (PM2.5), black carbon, sulfate, particle number, NO2, SO2, and O3 in the 24 h prior to the arrhythmia was examined utilizing a case-crossover analysis. In sensitivity analyses, associations with air pollution between 2 and 48 h prior to the AF were examined.
RESULTS: Of 176 patients followed for an average of 1.9 years, 49 patients had 328 episodes of AF lasting ≥ 30 s. Positive but nonsignificant associations were found for PM2.5 in the prior 24 h, but stronger associations were found with shorter exposure windows. The odds of AF increased by 26% (95% confidence interval: 8% to 47%) for each 6.0 μg/m(3) increase in PM2.5 in the 2 h prior to the event (p = 0.004). The odds of AF were highest at the upper quartile of mean PM2.5.
CONCLUSIONS: PM was associated with increased odds of AF onset within hours following exposure in patients with known cardiac disease. Air pollution is an acute trigger of AF, likely contributing to the pollution-associated adverse cardiac outcomes observed in epidemiological studies.