European Heart Journal Advance Access published online on May 2, 2009
European Heart Journal, doi:10.1093/eurheartj/ehp136
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Individual exposure to particulate matter and the short-term arrhythmic and autonomic profiles in patients with myocardial infarction
1 Department of Cardiology, University of Padua, Via Giustiniani, 2, Padova 35128, Italy
2 Department of Environmental Medicine, Public Health of the University of Padua, Padova, Italy
3 Department of Clinical Medicine, Nephrology and Health Science, University of Parma, Italy
Received 5 February 2009; revised 5 March 2009; accepted 12 March 2009 * Corresponding author. Tel: +39 049 821 1844, Fax: +39 049 876 1764, Email: franco.folino{at}unipd.it
Aims: Epidemiological studies show that peak exposure to air pollution is associated with increased morbidity and mortality from cardiovascular events. Panel and controlled exposure studies show that particulate matter (PM) may influence the parasympathetic regulation of the heart. The aim of this study was to concurrently measure individual exposure to PM of various sizes, heart rate variability (HRV), and electrical instability in patients with myocardial infarction.
Methods and results: Personal exposures to PM10, PM2.5, and PM0.25 was measured over 24 h in 39 patients (36 males, 3 females; mean age 60.3 years) with prior myocardial infarction (>6 months). Simultaneously, a 24 h ECG was recorded and then analysed for HRV and ventricular arrhythmias. Breath condensate and blood samples also were collected at the end of monitoring to measure several indexes of inflammation. Negative correlation was found between HRV and exposure to PM0.25 in a group of patients not taking β-blockers. More severe ventricular arrhythmias were observed at the highest concentrations of PM10 and PM2.5. Indexes of inflammation in either breath condensate or blood did not correlate with PM exposures.
Conclusion: Our study shows that exposure to ultrafine particles is associated with autonomic dysregulation in selected patients with myocardial infarction. More severe arrhythmias occur at the highest exposures to larger particles. Nevertheless, the underlying mechanisms remain hypothetical because inflammation may be evoked by PM or be related to the disease itself.
Key Words: Air pollution Myocardial infarction Autonomic nervous system Arrhythmias Inflammation