Differentiating the Impact of Hourly Particulate Air Pollution on the Onset of Myocardial Infarction with or Without Obstructive Coronary Arteries: A Nationwide, Case-Crossover Study. | AMiner
Differentiating the Impact of Hourly Particulate Air Pollution on the Onset of Myocardial Infarction with or Without Obstructive Coronary Arteries: A Nationwide, Case-Crossover Study.
Division of Health Risk Factor Monitoring and Control
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摘要
BACKGROUND:Acute myocardial infarction comprises two distinct entities, myocardial infarction with obstructive coronary artery disease (MI-CAD) and myocardial infarction with nonobstructive coronary arteries (MINOCA), characterized by divergent pathogenesis and potential links to particulate air pollution. This study aimed to investigate the differential impacts of such pollution on the onset of MI-CAD and MINOCA to inform precise prevention and control of myocardial infarction. METHODS:Based on the Chinese Cardiovascular Association Database-Chest Pain Center Registry, we performed a nationwide, time-stratified, case-crossover study from 2015 to 2021. Hourly concentrations of fine particulate matter (PM2.5) and inhalable particulate matter (PM10) were acquired through nearby fixed-site monitoring. We combined a conditional logistic regression model with polynomial distributed lag nonlinear models to differentiate the exposure-response relationships of the hourly concentrations of PM2.5 and PM10 with the onset of MI-CAD and MINOCA over 72 hours. We further calculated the attributable fractions (AFs) due to particulate air pollution accordingly. RESULTS:A total of 918,730 patients with MI-CAD and 83,802 patients with MINOCA were included. The risks of MINOCA and MI-CAD onset were highest at the concurrent exposure hour and diminished within 30 hours. Exposure to PM2.5 and PM10 was associated with a 1-2-fold higher risk of MINOCA compared with MI-CAD. Each interquartile range increase in the concentrations of PM2.5 and PM10 resulted in a 2.17% (95% CI: 0.82-3.53%) and 1.57% (95% CI: 0.23-2.94%) increased risk of MINOCA onset, respectively. The corresponding effect estimates for MI-CAD were 1.14% (95% CI: 0.74-1.55%) and 0.47% (95% CI: 0.13-0.81%), respectively. There were no apparent thresholds for these associations. The AFs of MINOCA attributable to PM2.5 and PM10 were 2.43% and 1.72%, respectively, which were almost one to two times greater than those of MI-CAD (1.27% and 0.54%, respectively). CONCLUSIONS:This nationwide study provides robust evidence that, compared with MI-CAD, MINOCA is more sensitive to particulate air pollution. This effect could occur during concurrent hours and under health-based air quality guidelines.