Key result
Elevated PM2.5 exposure is linked to ~10% higher odds of NSTEMI versus STEMI presentation.
Why the study?
Air pollution is recognized as a modifiable cardiovascular risk factor, prompting evaluation of its differential impact on STEMI versus NSTEMI presentation to explore potential pathophysiological mechanisms of pollution-related ischemic events.
Does prolonged exposure to air pollutants (PM2.5, PM10, NO₂) influence the clinical presentation of acute myocardial infarction (STEMI versus NSTEMI) in patients admitted for AMI?
Observational (n=3,974)
Yes
Does prolonged exposure to air pollutants (PM2.5, PM10, NO₂) influence the clinical presentation of acute myocardial infarction (STEMI versus NSTEMI) in patients admitted for AMI?
Prolonged bimonthly exposure to particulate matter (PM2.5 and PM10) is independently associated with presenting with NSTEMI rather than STEMI among patients with acute myocardial infarction.
Higher bimonthly PM2.5 exposure was associated with NSTEMI versus STEMI; leaves open causal links and should not alter practice yet.
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
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Manaresi et al. (2026) conducted an observational in Acute myocardial infarction (AMI) (n=3,974). Environmental air pollution exposure (PM2.5, PM10, and NO2 per 10 µg/m³ increase) vs. Lower pollutant exposure / STEMI vs NSTEMI presentation was evaluated on NSTEMI versus STEMI clinical presentation (OR 1.10, 95% CI 1.02-1.22, p=0.022). Elevated bimonthly PM2.5 (OR 1.10; 95% CI 1.02-1.22; p=0.022) and PM10 (OR 1.008; 95% CI 1.001-1.016; p=0.028) exposures independently predicted NSTEMI over STEMI presentation.
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