Air Pollution &Increase in Ventricular Tachyarrhythmias
Epidemiologic studies have demonstrated a consistent link between sudden cardiac deaths and particulate air pollution. We used implanted cardioverter defibrillator (ICD) records of ventricular tachyarrhythmias to assess the role of air pollution as a trigger of these potentially life-threatening events. The study cohort consisted of 203 cardiac patients with ICD devices in the Boston metropolitan area who were followed for an average of 3.1 years between 1995 and 2002. Fine particle mass and gaseous air pollution plus temperature and relative humidity were measured on almost all days, and black carbon, sulfate, and particle number on a subset of days. Date, time, and intracardiac electrograms of ICD-detected arrhythmias were downloaded at the patients' regular follow-up visits (about every 3 months). Ventricular tachyarrhythmias were identified by electrophysiologist review. Risk of ventricular arrhythmias associated with air pollution was estimated with logistic regression, adjusting for season, temperature, relative humidity, day of the week, patient, and a recent prior arrhythmia. We found increased risks of ventricular arrhythmias associated with 2-day mean exposure for all air pollutants considered, although these associations were not statistically significant. We found statistically significant associations between air pollution and ventricular arrhythmias for episodes within 3 days of a previous arrhythmia. The associations of ventricular tachyarrhythmias with fine particle mass, carbon monoxide, nitrogen dioxide, and black carbon suggest a link with motor vehicle pollutants. The associations with sulfate suggest a link with stationary fossil fuel combustion sources.

A large number of epidemiologic studies have found an association between short-term episodes of increased particulate air pollution and cardiovascular morbidity and mortality (Brook et al. 2004). Respirable particulate matter has been specifically implicated in the triggering of myocardial infarction (D'Ippoliti et al. 2003; Peters et al. 2001), arrhythmias (Peters et al. 2000), decompensation of heart failure patients (Morris and Naumova 1998; Schwartz and Morris 1995; Wellenius et al., in press), and the exacerbation of myocardial ischemia (Pekkanen et al. 2002; Wellenius et al. 2003). Particulate-related changes in autonomic nervous system activity, as assessed by heart rate variability, have been observed in both experimental animal studies (Godleski et al. 2000) and human panel studies (Creason et al. 2001; Gold et al. 2000; Liao et al. 1999, 2004; Pope et al. 1999), suggesting sympathetic activation or vagal suppression after particulate air pollution exposure. Such changes in autonomic tone may increase the risk of ventricular arrhythmias in vulnerable patients (Huikuri et al. 2001). Ventricular tachyarrhythmias, primarily ventricular tachycardia and ventricular fibrillation, are common precursors to sudden cardiac death (Bayes de Luna et al. 1989; Myerburg et al. 1992).

Implanted cardioverter defibrillators (ICDs) passively monitor for ventricular tachyarrhythmias that, if not terminated, could be life threatening. On detecting such an arrhythmia, the ICD can apply cardiac pacing or cardioverter shock to restore normal rhythms. The ICD also records the date and time of arrhythmias plus intracardiac electrograms immediately before and during these events. In a pilot study of 100 Boston area ICD patients with follow-up for up to 3 years, we found increased risk of an ICD therapeutic discharge on days after elevated air pollution concentrations (Peters et al. 2000). In this pilot study, we did not collect data on patient characteristics or medication. However, we did find stronger air pollution associations among patients with frequent ICD discharges.

This study was designed to confirm the pilot study observations. In a larger sample of ICD patients in Boston with longer follow-up, we identified ventricular tachyarrhythmias by review of ICD-recorded electrograms. We assessed the association between community air pollution and ventricular tachyarrhythmias using time-series methods. We also evaluated modification of the air pollution association by patient medical conditions, antiarrhythmic medications, and recent arrhythmias.