TY - JOUR
T1 - Association between particulate matter air pollution and subclinical myocardial fibrosis in structurally normal hearts
T2 - a CMR-based study
AU - Figliozzi, Stefano
AU - Filiberti, Gaia
AU - Catapano, Federica
AU - Donia, Dario
AU - Lisi, Costanza
AU - Cambini, Lorenzo
AU - Locatelli, Elena
AU - Di Maio, Silvana
AU - Bellada, Laura
AU - Kallikourdis, Marinos
AU - Stranges, Saverio
AU - Imbriaco, Massimo
AU - Slipczuk, Leandro
AU - Masci, Pier Giorgio
AU - Francone, Marco
AU - Stefanini, Giulio
AU - Georgiopoulos, Georgios
AU - Laghi, Andrea
AU - Condorelli, Gianluigi
N1 - Publisher Copyright:
© The Author(s) 2026. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact [email protected].
PY - 2026/7
Y1 - 2026/7
N2 - Aims: The impact of particulate matter (PM) exposure on early myocardial remodelling remains incompletely understood. Cardiac magnetic resonance (CMR) mapping provides sensitive markers of diffuse myocardial fibrosis and inflammation that may reveal subclinical injury. Methods and results: 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. 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. Conclusion: 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.
AB - Aims: The impact of particulate matter (PM) exposure on early myocardial remodelling remains incompletely understood. Cardiac magnetic resonance (CMR) mapping provides sensitive markers of diffuse myocardial fibrosis and inflammation that may reveal subclinical injury. Methods and results: 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. 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. Conclusion: 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.
KW - air pollution
KW - cardiac magnetic resonance imaging (CMR)
KW - global health
KW - myocardial fibrosis
KW - particulate matter (PM2.5, PM10)
KW - subclinical myocardial damage
UR - https://www.scopus.com/pages/publications/105043450867
U2 - 10.1093/ehjci/jeag075
DO - 10.1093/ehjci/jeag075
M3 - Article
C2 - 41843748
AN - SCOPUS:105043450867
SN - 2047-2404
VL - 27
SP - 1382
EP - 1393
JO - European Heart Journal Cardiovascular Imaging
JF - European Heart Journal Cardiovascular Imaging
IS - 7
ER -