Key result
Chronic PM2.5 exposure linked to higher synthetic-ECV in structurally normal hearts, suggesting early fibrosis.
Why the study?
The impact of particulate matter exposure on early myocardial remodeling remains incompletely understood.
Does long-term exposure to PM2.5 and PM10 air pollution increase CMR markers of subclinical myocardial fibrosis in patients with structurally normal hearts?
Observational (n=231)
Does long-term exposure to PM2.5 and PM10 air pollution increase CMR markers of subclinical myocardial fibrosis in patients with structurally normal hearts?
Chronic exposure to particulate matter air pollution is associated with CMR markers of early diffuse myocardial fibrosis in individuals with structurally normal hearts.
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Supports clean air efforts for CV protection; extends evidence to subclinical myocardial fibrosis but should not yet change practice.
Background The impact of particulate matter (PM) exposure on early myocardial remodeling remains incompletely understood. Cardiac magnetic resonance (CMR) mapping provides sensitive markers of diffuse myocardial fibrosis and inflammation that may reveal subclinical injury. Methods Patients with structurally normal hearts and no late-gadolinium-enhancement on CMR from May 2020 to November 2024 were included. Long-term exposure to PM2.5 and PM10 was derived from the nearest European-Environment-Agency monitoring stations. Associations between PM and CMR parameters were tested with multivariable linear and logistic regression adjusted for demographic, clinical, socioeconomic factors, and inflammatory markers. Results Two-hundred-thirty-one patients (45±21 years; 53% males; mean annual PM2.5 and PM10 exposure of 28.6±14.8 µg/m3 and 56.0±35.3 µg/m3) were included. After adjustment, exposure to PM2.5 (β = 0.034%; 95% CI 0.005–0.063; p = 0.023) and PM10 (β = 0.021 per 1 µg/m3; 95% CI 0.009–0.032; p = 0.001) were associated with higher synthetic-extracellular volume (ECV), whereas only PM2.5 was associated with higher native T1 (β = 0.317 ms per 1 µg/m3; 95% CI 0.07–0.564; p = 0.012). No associations were observed with other CMR parameters, including T2 mapping. By multivariable logistic regression, PM2.5, but not PM10, was associated with increased native T1 and synthetic-ECV. The association between PM and mapping was most pronounced in males and patients ≥50 years, and no mediation effect of inflammatory markers was found. Conclusions In individuals with structurally normal hearts, chronic exposure to PM2.5 and PM10 was associated with higher synthetic-ECV values, suggesting early diffuse myocardial fibrosis related to air pollution.
Figliozzi et al. (2026) conducted an observational in Structurally normal hearts (n=231). Particulate matter (PM2.5 and PM10) exposure was evaluated on Synthetic-extracellular volume (ECV) associated with PM2.5 exposure (β 0.034%, 95% CI 0.005-0.063, p=0.023). Chronic exposure to PM2.5 was associated with higher synthetic-extracellular volume (β 0.034%; 95% CI 0.005-0.063; p=0.023) in patients with structurally normal hearts, suggesting early fibrosis.
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