Reduction in heart rate variability with traffic and air pollution in patients with coronary artery disease

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Abstract

INTRODUCTION: Ambient particulate pollution and traffic have been linked to myocardial infarction and cardiac death risk. Possible mechanisms include autonomic cardiac dysfunction. METHODS: In a repeated-measures study of 46 patients 43-75 years of age, we investigated associations of central-site ambient particulate pollution, including black carbon (BC) (a marker for regional and local traffic), and report of traffic exposure with changes in half-hourly averaged heart rate variability (HRV), a marker of autonomic function measured by 24-hr Holter electrocardiogram monitoring. Each patient was observed up to four times within 1 year after a percutaneous intervention for myocardial infarction, acute coronary syndrome without infarction, or stable coronary artery disease (4,955 half-hour observations). For each half-hour period, diary data defined whether the patient was home or not home, or in traffic. RESULTS: A decrease in high frequency (HF; an HRV marker of vagal tone) of -16.4% [95% confidence interval (CI), -20.7 to -11.8%] was associated with an interquartile range of 0.3-μ g/m3 increase in prior 5-day averaged ambient BC. Decreases in HF were independently associated both with the previous 2-hr averaged BC (-10.4%; 95% CI, -15.4 to -5.2%) and with being in traffic in the previous 2 hr (-38.5%; 95% CI, -57.4 to -11.1%). We also observed independent responses for particulate air matter with aerodynamic diameter ≤ 2.5 μm and for gases (ozone or nitrogen dioxide). CONCLUSION: After hospitalization for coronary artery disease, both particulate pollution and being in traffic, a marker of stress and pollution, were associated with decreased HRV.

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Zanobetti, A., Gold, D. R., Stone, P. H., Suh, H. H., Schwartz, J., Coull, B. A., & Speizer, F. E. (2010). Reduction in heart rate variability with traffic and air pollution in patients with coronary artery disease. Environmental Health Perspectives, 118(3), 324–330. https://doi.org/10.1289/ehp.0901003

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