Long-term air pollution damage observed in cardiac MRI of cardiomyopathy patients: Study

A new study published in the journal of Radiology showed that in both dilated cardiomyopathy (DCM) patients and healthy controls, increased diffuse myocardial fibrosis at cardiac MRI native T1 mapping is linked to longer-term exposure to ambient fine particle air pollution.

Hazardous pollutants are released into the atmosphere by burning fossil fuels, wildfire smoke, and other human activities. Because air pollutants and greenhouse gases are often co-emitted, there is a connection between climate change and air pollution. Cardiovascular morbidity is linked to poor air quality. Uncertainty surrounds the underlying pathophysiologic processes, though. Therefore, this investigation looked in to the link between the degree of diffuse myocardial fibrosis as measured by cardiac MRI and long-term exposure to ambient fine particulate matter having an aerodynamic diameter of 2.5 µm or less (PM2.5).

Individuals with dilated cardiomyopathy or controls with normal cardiac MRI results were included in this single-center retrospective study (January 2018 to December 2022). Using cardiac MRI native T1 mapping z scores, diffuse myocardial fibrosis was measured. Using direct data from the closest monitoring station, the mean of daily exposure concentrations in the year before to cardiac MRI was used to calculate the residence-specific ambient PM2.5 concentration. Clinically significant factors were taken into account while adjusting multivariable models.

There were 443 men, 493 patients with DCM, and 201 controls among the 694 patients (mean age, 47 years ± 16 [SD]). In multivariable models, patients with DCM had a 0.30 higher native T1 z score (adjusted β coefficient: 0.30; 95% CI: 0.13, 0.47; P <.001) and controls had a 0.27 higher native T1 z score (adjusted β coefficient: 0.27; 95% CI: 0.04, 0.51; P =.02) for every 1-µg/m3 increase in 1-year mean PM2.5 exposure.

For absolute values, there was a 9.1 msec increase in native T1 at 1.5 T (β coefficient: 9.1; 95% CI: 2.04, 15.97; P =.01) and a 12.1 msec increase at 3 T (β coefficient: 12.1; 95% CI: 5.74, 18.52; P <.001) for every 1-µg/m3 increase in 1-year mean PM2.5 exposure.

Women (β coefficient: 0.49; 95% CI: 0.23, 0.76; P <.001), smokers (β coefficient: 0.43; 95% CI: 0.02, 0.84; P =.04), and hypertensive patients (β coefficient: 0.48; 95% CI: 0.16, 0.80; P =.004) had the largest effect sizes for the relationship between PM2.5 exposure and native T1 z scores, according to stratified models.

Overall, increased long-term exposure to ambient fine particulate air pollution is linked to greater diffuse myocardial fibrosis at cardiac MRI native T1 mapping in patients with dilated cardiomyopathy and healthy controls. This suggests that myocardial fibrosis may be an underlying pathophysiologic mechanism through which air pollution causes detrimental cardiovascular health outcomes.

Source:

Du Plessis, J., DesRoche, C., Delaney, S., Nethery, R. C., Hong, R., Thavendiranathan, P., Ross, H., Castillo, F., & Hanneman, K. (2025). Association between long-term exposure to ambient air pollution and myocardial fibrosis assessed with cardiac MRI. Radiology, 316(1). https://doi.org/10.1148/radiol.250331