Relationship Between Air Pollutants And Atrial Arrhythmia Recorded By Cieds And Its Mechanism

Objective:Explore the exposure-effect relationship between the levels of atmospheric pollutants(PM_2.5,PM₁₀,CO,NO₂,SO₂,O₃)and atrial arrhythmias recorded by CIEDs in Shanghai area,and explore the possible mechanism of atmospheric pollutants triggering arrhythmias using the method of ion channels.Methods:402 patients with CIEDs implanted in the arrhythmia center of Shanghai Jiaotong University were selected as the research objects,and the inclusion and exclusion criteria of the research objects were strictly implemented,and 116 patients were finally included.The age,sex,residence address,smoking,drug use,whether suffering from ischemic heart disease,diabetes,etc.of the subjects were investigated through questionnaires.All subjects were followed up for 2 years and once a month in outpatient clinic.The moment,frequency and degree of atrial high frequency events（AHRE）in the months before the subjects were recorded through CIEDs connection network platform.The control groups were the moment the events happened and 1,2 and 3 days after the onset,and the exposure groups were 2,4,6,12 hours and1,2,3,4,5and 6 days before the onset.The conditional Logistic regression modelwas used to analyze the exposure-effect relationship between atmospheric pollutant concentration and atrial arrhythmia onset,and the generalized linear model was used to analyze the relationship between atmospheric pollutant concentration and atrial arrhythmia onset degree.The effect of100ug/ml of PM_2.5.5 suspension on ion channel current of myocardial cells was recorded by patch clamp method of animal myocardial cells,so as to explore the possible mechanism of arrhythmia caused by air pollutants.Results:1210 effective AHRE events were selected from 116patients implanted with CIEDs.The results showed that PM2.5,PM10,SO2,O3,and CO exposure were positively correlated with theoccurrence of AHRE,and the results were statistically significant.Among them,PM2.5（lag4h OR 1.024,95%CI 1.010-1.038,p=0.001、lag12h OR 0.977,95%CI 0.963-0.990,p=0.001、lag4d OR 1.013,95%CI1.001-1.025,p=0.029、lag6d OR 1.019,95%CI 1.006-1.033,p=0.005）、PM10（lag12h OR 1.010,95%CI 1.004-1.016,p=0.001）、SO2（lag4h OR 1.046,95%CI 1.006-1.089,lag1d OR 1.075,95%CI 1.006-1.148,p=0.033、lag3d OR 1.074,95%CI 1.007-1.146,p=0.029、lag4d OR1.085,95%CI 1.018-1.157,p=0.012、lag5d OR 1.070,95%CI1.005-1.139,p=0.035）、O3（lag4h OR 1.006,95%CI 1.002-1.010,p=0.001）,CO（lag2h OR 4.051,95%CI 1.695-9.682,p=0.002）.With delay effect,the most obvious time delay effects of PM2.5,PM10,SO2,O3,PM10 and CO were 4 hours,12 hours,4 days,4 hours and 2 hours before the onset.There was no significant correlation between NO2concentration and AHRE.CO concentration was negatively correlated with AHRE episodes 5d and 6d before onset.The O3 exposure level and the AHRE load（1h,6h,12h）have a positive linear correlation,and the CO exposure level has a negative correlation with the AHRE load.The other pollutants have no significant correlation with the AHRE load.100ug/ml of PM_2.5.5 suspension has inhibitory effect on Cav1.2 channel,Kir2.1 potassium channel and Nav1.5 sodium channel ion current on the surface of animal atrial cells,while 100μg/ml of pm_2.5.5 has no obvious inhibitory effect on NaHS,aconitine and isoproterenol pretreated Nav1.5sodium channel current（p>0.05）.Conclusion:Exposure to PM2.5,PM10,SO2,O3,and CO areindependent risk factors for atrial tachyarrhythmia.Delay effect time are respectively 4 hours,12 hours,4 days,4 hours and 2 hours Exposure to There was no significant correlation between NO2 exposure and AHRE.The CO concentration at 5d and 6d before the event was negativelycorrelated with AHRE.CO concentration has negative correlation with AHRE,and O₃exposure level has positive correlation with AHRE load（1h,6h,12h）.PM_2.5.5 suspension has inhibitory effect on ion current of Cav1.2 channel,Kir2.1 potassium channel and Nav1.5 sodium channel,which may be the mechanism of arrhythmia.