It is well established that exposure to particulate air pollution increases mortality and risk of age-related conditions. The primary mechanism is thought to be increased chronic inflammation resulting from the interactions of inhaled particles with the cells of epithelial and other tissues. One of the consequences of chronic inflammation is increased fibrosis, a dysfunction in normal tissue maintenance in which excessive extracellular matrix is created, forming scar-like structures that impair tissue function. Here, researchers correlate increased fibrosis in heart tissue with long-term exposure to particulate matter, an outcome that isn't all that surprising given the established epidemiological data linking cardiovascular disease to particulate exposure.
Fine particulate matter with 2.5-µm or smaller aerodynamic diameter (PM2.5) is the most thoroughly studied component of air pollution. PM2.5 is associated with an increased risk of cardiovascular diseases - including myocardial infarction, heart failure, and stroke - and promotes the development of cardiovascular risk factors such as hypertension and diabetes. The World Health Organization estimates that 31% of cardiovascular disease is attributable to environmental factors.
However, the underlying pathophysiologic mechanisms by which exposure to PM2.5 leads to adverse cardiovascular outcomes are unclear. Hypothesized mechanisms include oxidative stress, inflammation, and autonomic stimulation, potentially leading to activation of cardiac fibroblasts and increased extracellular matrix protein deposition. Given its role in maladaptive left ventricular remodeling, myocardial fibrosis could potentially mediate the adverse cardiovascular effects of particulate air pollution and help explain some of the variability in heart failure progression and other adverse cardiac events that are not explained by traditional cardiovascular risk factors.
This retrospective study aimed to determine the relationship between long-term exposure to ambient PM2.5 air pollution and the extent of diffuse myocardial fibrosis quantified with cardiac MRI. Patients with dilated cardiomyopathy (DCM) or controls with normal cardiac MRI findings were included. Diffuse myocardial fibrosis was quantified using cardiac MRI native T1 mapping z scores. A total of 694 patients (mean age, 47 years) were included. In multivariable models, each 1-µg/m3 increase in 1-year mean PM2.5 exposure was associated with a 0.30 higher native T1 z score in patients with DCM and 0.27 higher native T1 z score in controls. In conclusion, higher long-term exposure to ambient fine particulate air pollution is associated with greater diffuse myocardial fibrosis.
Link: https://doi.org/10.1148/radiol.250331
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