Even in places where the air seems clean, invisible particles may be quietly reshaping the heart.
Long-term exposure to ambient fine particulate matter (PM2.5) was linked to increased diffuse myocardial fibrosis in both patients with dilated cardiomyopathy (DCM) and in individuals with no cardiac abnormalitites on imaging, according to a retrospective cardiac magnetic resonance imaging (MRI) study of 694 adults in Ontario, Canada.
Researchers measured myocardial fibrosis using native T1 mapping on cardiac MRI and estimated air pollution exposure using the 1-year mean daily PM2.5 concentrations from the nearest air monitoring station. Of the 694 participants, 493 had DCM and 201 served as controls with no cardiac abnormalities on imaging.
Each 1 microgram per cubic meter (µg/m³ )increase in annual PM2.5 exposure was associated with a 0.30-point higher native T1 z score in patients with DCM (adjusted β coefficient: 0.30; 95% confidence interval [CI] = 0.13, 0.47; P < .001) and a 0.27-point higher T1 z score in control participants (adjusted β coefficient: 0.27; 95% CI = 0.04, 0.51; P = .02).
For absolute T1 values, each 1-µg/m³ increase in PM2.5 was associated with a 9.1-millisecond rise at 1.5 Tesla (β coefficient: 9.1; 95% CI = 2.04, 15.97; P = .01) and a 12.1-millisecond rise at 3 Tesla (β coefficient: 12.1; 95% CI: 5.74, 18.52; P < .001).
The median PM2.5 exposure was 7.7 µg/m³ (IQR: 7.2, 8.0), and 97.3% of participants were exposed to levels below the Canadian Ambient Air Quality Standard of 8.8 µg/m³. Despite this, changes in myocardial tissue characteristics were still observed.
In stratified analysis, larger effect sizes were seen in women (β coefficient: 0.49; 95% CI = 0.23, 0.76; P < .001), people with hypertension (β coefficient: 0.48; 95% CI = 0.16, 0.80; P = .004), and those with a history of smoking (β coefficient: 0.43; 95% CI =: 0.02, 0.84; P = .04).
“Nearly 70% of the 4.2 million deaths attributed to ambient air pollution in 2019 were caused by cardiovascular conditions. However, the underlying pathophysiologic mechanisms by which exposure to PM 2.5 leads to adverse cardiovascular outcomes are unclear,” wrote Jacques Du Plessis, MD, from the Department of Medical Imaging at the University of Toronto.
Additional cardiac remodeling markers were also associated with higher PM2.5 exposure. Each 1-µg/m³ increase was linked to a 3.6 mL/m² increase in left ventricular end-diastolic volume (95% CI = 0.10, 7.2; P = .047), a 2.2% decrease in ejection fraction (95% CI = –3.5, –0.80; P = .002), and 40% increase in the odds of late gadolinium enhancement (adjusted OR: 1.4; 95% CI = 1.1, 1.7; P = .005).
The study controlled for a wide range of confounding variables, including age, sex, comorbidities, socioeconomic indicators, MRI field strength, and ambient temperature. Sensitivity analyses confirmed the associations across subgroups, including participants living within 10 km of monitoring stations and those scanned before the COVID-19 pandemic.
These results offer imaging-based evidence that environmental exposure may affect on myocardial tissue and suggest that myocardial fibrosis could serve as a subclinical marker for pollution-related cardiovascular risk.
Full disclosures can be found in the study.
Source: Radiology