Long term air pollution and myocardial infarction: differences between STEMI and NSTEMI
T Manaresi, A Maida, M Basile, N Vasumini, M Di Leo, M Casuso Alvarez, M Moretti, P Stradaioli, L Toni, S Amicone, M Armillotta, L Bergamaschi, D Fedele, F Angeli, C PizziAbstract
Background
Air pollution is increasingly recognized as a modifiable cardiovascular risk factor, given the growing body of evidence supporting its role in cardiovascular disease and its substantial socio-economic and public health implications.
Purpose
This study aimed to evaluate the impact of air pollution on the clinical presentation of acute myocardial infarction (AMI)—STEMI versus NSTEMI—in order to explore potential pathophysiological mechanisms underlying pollution-related ischemic events.
Methods
We analyzed data from the AMIPE registry, including patients admitted for AMI to the STEMI Hub hospitals in the province of Bologna (Ospedale Maggiore and Ospedale Sant’Orsola Malpighi) between January 2018 and December 2023.
Environmental exposure was assessed using daily mean concentrations of PM2.5, PM10, and NO₂ recorded by the monitoring station closest to each patient’s residence. Average pollutant levels were calculated over multiple time windows (daily, weekly, monthly, bimonthly, and yearly) preceding the index event and scaled per 10 µg/m³ increase. Comparisons were performed between STEMI and NSTEMI presentations.
Results
The study population included 3974 AMI cases (mean age 69.7 ± 13 years; 68.5% male; NSTEMI 60%; STEMI 40%). Patients presenting with NSTEMI showed significantly higher mean exposure to PM2.5 and PM10 in the two months preceding the acute event compared with STEMI patients (PM2.5: p = 0.007; PM10: p = 0.016). No significant differences were observed for monthly or annual exposure (p > 0.05). In multivariable analysis adjusted for age, sex, smoking status, and chronic obstructive pulmonary disease (COPD), elevated bimonthly exposure to PM2.5 and PM10 emerged as an independent predictor of NSTEMI presentation (PM2.5 [10 µg/m³]: OR 1.10; 95% CI 1.02–1.22; p = 0.022; PM10 [10 µg/m³]: OR 1.008; 95% CI 1.001–1.016; p = 0.028).
Conclusions
Prolonged exposure to PM2.5 and PM10 is independently associated with NSTEMI rather than STEMI. The exact pathophysiology remains partly unclear, but type II mechanisms (supply–demand mismatch, endothelial dysfunction, microvascular impairment) and diffuse coronary artery disease may act as triggers. Further studies and environmental prevention strategies are warranted.OR PM2.5/PM10