Air pollution exposure can be a key contributing factor to increasingly diffuse myocardial fibrosis, according to cardiac magnetic resonance imaging (MRI) findings from a new study.
For the retrospective study, recently published in Radiology, researchers reviewed cardiac MRI data for 694 patients (mean age of 47), including 493 people with dilated cardiomyopathy (DCM) and 201 people with normal cardiac MRI.
In a multivariable analysis, the study authors found that for patients with DCM, each 1 µg/m3 increase in one-year mean exposure to ambient fine particulate matter with 2.5-µm or smaller aerodynamic diameter (PM2.5) corresponded to a 30 percent higher native T1 z score.
The researchers also noted that each 1 µg/m3 increase in one-year mean exposure to PM2.5 was associated with a 27 percent higher native T1 z score in people with normal cardiac MRI findings.
“In line with other studies, our results indicate that adverse effects of fine particulate air pollution on the heart are observed at exposures below current air quality guidelines, reinforcing that there are no safe exposure limits. Our results bolster evidence that air pollution is a modifiable risk factor for cardiovascular disease,” noted study co-author Kate Hanneman, M.D., MPH, FRCPC, an associate professor and vice chair of research with the Department of Medical Imaging at the University of Toronto, and colleagues.
Late gadolinium enhancement (LGE) was 25 percent more likely for each 1 µg/m3 increase in one-year mean exposure to PM2. in patients with DCM, according to the study authors.
The researchers also found that the association between ambient PM2.5 exposure and native T1 z scores was particularly prevalent among women (β coefficient of 49 percent), people with hypertension (β coefficient of 48 percent) and smokers (β coefficient of 43 percent).
“Myocardial fibrosis is irreversible; therefore, it is imperative to implement measures to reduce exposure to long-term air pollution, especially in the most vulnerable patients,” emphasized Hanneman and colleagues.
Three Key Takeaways
- Air pollution correlates with myocardial fibrosis. Each 1 µg/m³ increase in PM2.5 exposure over one year was linked to a 30 percent higher native T1 z score in patients with dilated cardiomyopathy (DCM) and a 27 percent increase in individuals with normal cardiac MRI findings, indicating diffuse myocardial fibrosis.
- Risk is heightened in vulnerable subgroups. Stronger associations between PM2.5 exposure and elevated native T1 z scores were observed in women (49 percent), individuals with hypertension (48 percent), and smokers (43 percent).
- Pollution exposure linked to structural heart changes. Among patients with DCM, each 1 µg/m³ increase in PM2.5 exposure was associated with a 25 percent higher likelihood of late gadolinium enhancement (LGE), further indicating structural myocardial injury.
In an accompanying editorial, Davis M. Vigneault, M.D., D.Phil, said the study builds upon previous biochemical and epidemiological studies demonstrating elevated cardiovascular risks with air pollution exposure.
“… This study provides new and compelling evidence for a potential pathologic mechanism by which fine particulate matter pollution increases cardiovascular risk, tying together biochemical evidence implicating PM2.5 in the induction of myocardial fibrosis with epidemiologic evidence associating PM2.5 with morphologic changes and increased cardiovascular morbidity and mortality,” wrote Dr. Vigneault, who is affiliated with the Department of Radiology at the Stanford University School of Medicine in Stanford, Ca.
(Editor’s note: For related content, see “Could Cardiac MRI Improve Risk Stratification in Patients with Dilated Cardiomyopathy?,” “Stress Cardiovascular MRI: What a New Meta-Analysis Reveals” and “Multimodal AI with CCTA and MRI Data Shows Promise in Predicting MACE in Patients with Obstructive CAD.”)
Beyond the inherent limitations of a single-center retrospective study, the study authors conceded possible differences with respect to the timing of exposure to PM2.5, and potentially unknown confounding factors that may have affected the results. The researchers acknowledged that indoor PM2.5, ozone and nitrogen dioxide exposures were not assessed. They also noted that the COVID-19 pandemic occurred within the study period.
