Abstract 15973: Ambient Air Pollution is Associated With Coronary Artery Disease and Adverse Outcomes in Patients With Stable Chest Pain Across the U.S.: Insights From the PROMISE Trial

Abstract

Introduction: Air pollution is associated with coronary artery disease (CAD) and cardiovascular (CV) outcomes. Hypothesis: The relationships of air pollutants to CAD and outcomes are independent of traditional CV risk factors and socioeconomic determinants of health (SDoH) and vary by pollutant type. Methods: Clinical and CT data from stable chest pain patients without known CAD in the PROMISE trial, were linked by home zip code to U.S. EPA-derived PM 2.5 and PM 10 (Figure 1a) . CT metrics included any plaque, obstructive CAD (≥50%), and high-risk plaque (HRP); major adverse CV events were defined as death (all cause or CV), myocardial infarction, or unstable angina. Logistic and Cox regressions were adjusted for age, sex, obesity, ASCVD risk, statins, and US Census-based SDoH by zip code. We conducted a mediation analysis for the effect of pollutants on events using obstructive CAD as mediator. Results: In 4,343 individuals (48% men; age: 61±8 years), 46.9% were exposed to PM 2.5 above the standard cut point of 9.5 μg/m 3 and 62.1% to PM 10 ≥15 μg/m 3 . Participants exposed to PM 2.5 ≥9.5 μg/m 3 had 27% higher odds of obstructive CAD (aOR=1.27, 95%CI: 1.03-1.56, p=0.026), not significant for PM 10 . No associations existed between pollutants and any plaque or HRP. PM 2.5 and PM 10 were independently associated with CV events in fully adjusted models (Figure 1b) . In mediation analysis, the effects of PM 2.5 on events were significant (direct effect: OR=1.66, 95%CI: 1.11-2.50, p=0.014; indirect effect: OR=1.06, 95%CI: 1.01-1,12, p=0.022) with comparable results for PM 10 . Conclusions: Air pollution relates independently to adverse events in stable chest pain patients, only partly driven by CAD phenotypes, specifically an association between small particular matter and obstructive CAD. Further studies investigating the pathogenesis of atherosclerotic disease in people exposed to pollution may help form strategies to reduce exposure.