Association Between Long-Term Exposure to Ambient Air Pollution and Lesion Ischemia in Atherosclerotic Patients

Abstract

BACKGROUND AND AIM: Air pollution has been associated with coronary artery diseases (CAD) worldwide. The underlying mechanisms are understudied, especially through the coronary stenosis pathway to induce myocardial ischemia. The advances of computed tomography (CT) allows novel quantifications on lesion ischemia. We aim to investigate associations between long-term exposure to air pollution and fractional flow reserve on CT (CT-FFR), a subclinical measure of blood flow limitation to gain insight into potential mechanism. METHODS: CT-FFR, which defines a ratio of maximal myocardial blood flow compared to its normal value (range: 0-100%), was characterized in 1897 patients with atherosclerosis between 2015-2017 from a cohort study. Annual average exposure to air pollutants, including ozone (O3), nitrogen dioxide (NO2), and fine particulate matter (PM2.5), was estimated by high-resolution spatiotemporal exposure model for individual participants. Linear regression models, controlling for potential confounders, were used to assess the association of each air pollutant with CT-FFR. Adjusted logistic regression models were used to estimate associations with prevalence of myocardial ischemia CT-FFR 80%). RESULTS:Participants were on average 60 years old with 62% males. Annual average O3, NO2, PM2.5 were 61, 47 and 60 µg/m3, respectively. Mean CT-FFR value was 77%. In the main analysis, higher level of O3 exposure is associated with smaller CT-FFR value (-1.28%, 95% CI: -2.36, -0.19 per 8 µg/m3), adjusting for risk factors and plaque phenotypes, independent from the effects of exposure to NO2 and PM2.5. No associations were observed for PM2.5 nor for NO2 with CT-FFR or for any exposure metrics with prevalence of myocardial ischemia. CONCLUSIONS:Long-term exposure to O3 is associated with lower CT-FFR value in atherosclerotic patient, indicating higher risk of lesion ischemia. The novel finding needs to be examined broadly among larger population at risk of CAD. KEYWORDS: Air pollution, Cardiovascular diseases, Environmental epidemiology, Outcomes