Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Abstract

The association between short-term increases in particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Recent studies suggest an association between particulate matter with aerodynamic diameter < 2.5 μm (PM2.5) and supraventricular arrhythmias (SVA), but the results have been inconsistent. We evaluated this hypothesis in a rat model of acute myocardial infarction (AMI). Diazepam-sedated Sprague-Dawley rats with AMI were exposed (1 h) to either filtered air (n = 16), concentrated ambient fine particles (CAPS; mean = 645.7 μg/m3; n = 23), carbon monoxide (CO; 35 ppm; n = 19), or CAPs and CO (n = 24). Each exposure was immediately preceded and followed by a 1-h exposure to filtered air (baseline and postexposure periods, respectively). Surface electrocardiograms were recorded and the frequency of supraventricular premature beats was quantified. Among rats in the CAPS group, the probability of observing any SVA decreased from baseline to the exposure and postexposure periods. This patterm was significantly different than that observed for the filtered air group during the exposure period (p = .048) only. In the subset of rats with one or more SVA during the baseline period, the change in SVA rate from baseline to exposure period was significantly lower in the CAPS (p = .04) and CO (p = .007) groups only, as compared to the filtered air group. No significant effects were observed in the group simultaneously exposed to CAPS and CO. Thus, the results of this study do not support the hypothesis that exposure to ambient air pollution increases the risk or frequency of supraventricular arrhythmias.