Key result
Air pollution acts as a modifiable driver of heart failure progression and compounds exposomic vulnerability.
Why the study?
Does air pollution exposure increase the risk of heart failure progression?
Does air pollution exposure increase the risk of heart failure progression?
Air pollution is a critical, modifiable driver in the pathogenesis and progression of heart failure, necessitating targeted risk stratification and mitigation strategies.
Air pollution is a major global environmental health threat and the leading environmental risk factor contributing to cardiovascular morbidity and mortality. Emerging evidence increasingly implicates air pollution as a critical, modifiable driver in the pathogenesis, progression, and prognosis of heart failure. Air pollution is increasingly recognized as part of the exposome—a complex interplay of environmental, social, and behavioral exposures accumulated across the life course. In this review, we synthesize experimental data demonstrating mechanistic links between air pollution and heart failure, along with growing experimental, clinical, and epidemiological evidence connecting both short- and long-term air pollution exposure with increased risk of heart failure progression across heart failure stages. We further examine how air pollution interacts with other exposomic risk domains—such as the social exposome, built environment, and access to greenery—compounding vulnerability in marginalized and underserved populations. The review will also summarize current approaches to communicate air pollution risk and propose practical strategies for both individuals and healthcare systems to mitigate its cardiovascular impact. Finally, we present a clinical framework for assessing and managing air pollution exposure in patients with heart failure, emphasizing the need for targeted risk stratification and the development of context-specific mitigation interventions.
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Al‐Kindi et al. (2025) conducted a review in Heart failure. Air pollution was evaluated. Air pollution is a critical, modifiable driver in the pathogenesis, progression, and prognosis of heart failure, interacting with other exposomic risk domains to compound vulnerability.
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