Association of short-term exposure to air pollution with myocardial infarction with and without obstructive coronary artery disease.

BACKGROUND

Air pollution including particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) increases the risk of acute myocardial infarction. However, whether short-term exposure to PM2.5 triggers the onset of myocardial infarction with nonobstructive coronary arteries, compared with myocardial infarction with coronary artery disease, has not been elucidated. This study aimed to estimate the association between short-term exposure to PM2.5 and admission for acute myocardial infarction, myocardial infarction with coronary artery disease, and myocardial infarction with nonobstructive coronary arteries.

DESIGN

This was a time-stratified case-crossover study and multicenter validation study.

METHODS

This study used a nationwide administrative database in Japan between April 2012-March 2016. Of 137,678 acute myocardial infarction cases, 123,633 myocardial infarction with coronary artery disease and 14,045 myocardial infarction with nonobstructive coronary arteries were identified by a validated algorithm combined with International Classification of Disease (10th revision), diagnostic, and procedure codes. Air pollutants and meteorological data were obtained from the monitoring station nearest to the admitting hospital.

RESULTS

In spring (March-May), the short-term increase of 10 µg/m3 in PM2.5 2 days before admission was significantly associated with admission for acute myocardial infarction, myocardial infarction with nonobstructive coronary arteries, and myocardial infarction with coronary artery disease after adjustment for meteorological variables (odds ratio 1.060, 95% confidence interval 1.038-1.082; odds ratio 1.151, 1.079-1.227; odds ratio 1.049, 1.026-1.073, respectively), while the association was not significant in other variables. These associations were also observed after adjustment for other co-pollutants. The risk for myocardial infarction with nonobstructive coronary arteries (vs myocardial infarction with coronary artery disease) was associated with an even lower concentration of PM2.5 under the current environmental standards.

CONCLUSIONS

This study showed the seasonal difference of acute myocardial infarction risk attributable to PM2.5 and the difference in the threshold of triggering the onset of acute myocardial infarction subtype.