Association of air pollution and 1-year clinical outcomes of patients with acute myocardial infarction

by Se Yeon Choi, Seung-Woon Rha, Jinah Cha, Jae Kyeong Byun, Byoung Geol Choi, Myung ho Jeong, on behalf of The Korea Acute Myocardial Infraction Registry study group

Background

Exposure to air pollution (AP) is an important environmental risk factor for increased risk of cardiovascular morbidity and triggering acute myocardial infarction (AMI). However, there are limited data regarding the clinical impact of AP on long-term major clinical outcomes of AMI patients. This study aimed to evaluate the clinical effects of ambient AP concentration on short-term and 1-year clinical outcomes of AMI patients.

Methods

A total of 46,263 eligible patients were enrolled in the Korea Acute Myocardial Infarction (KAMIR) and KAMIR-National Institutes of Health (NIH) registry from January 2006 to December 2015. We performed Cox proportional hazard regression to assess the risk of all-cause death and any-revascularization according to the annual average concentration of AP during one-year follow-up period.

Results

The assessment of the annual average of air pollutants before symptom date and all-cause death up to 30 days showed the hazard ratio (HR) of SO₂ per 1 part per billion (ppb) increase was 1.084 (95% confidence interval [CI]: 1.016–1.157), and particulate matter with diameter of 10 microns or less (PM₁₀) per 1 μg/m³ increase was 1.011 (95% CI: 1.002–1.021). The results of the 30-day and one-year all-cause death showed a similar trend. For SO₂, the HR per 1 ppb increase was 1.084 (95% CI: 1.003–1.172), and the HR of PM₁₀ was 1.021 (95% CI: 1.009–1.033) per 1 μg/m³ increase. We observed that SO₂, CO, and PM₁₀ were associated with an increased risk of incidence for any-revascularization up to one-year.

Conclusion

In some air pollutants, a higher AP concentration was an environmental risk factor for poor prognosis in AMI patients up to 1 year. AMI patients and high-risk individuals need a strategy to reduce or prevent exposure to high AP concentrations.