A single exposure to acrolein causes arrhythmogenesis, cardiac electrical dysfunction and decreased heart rate variability in hypertensive rats

Abstract

Epidemiological studies demonstrate an association between cardiovascular morbidity, arrhythmias, and exposure to air toxicants such as acrolein. We hypothesized that a single exposure to acrolein would increase arrhythmias and cause changes in the electrocardiogram (ECG) of hypertensive rats. Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats implanted with radiotelemeters were exposed to either air or 3ppm acrolein for 3 hours, while heart rate (HR) and ECG were continuously monitored. When compared to WKY rats, SH rats had higher baseline HR, prolonged PR interval (PRi), QRS complex duration, and QTc. During acrolein exposure both WKY and SH rats had significantly increased HR, PRi, QTc, and JTc; only PRi returned to baseline levels in both strains after exposure. SH rats had a significant increase in non‐conducted P‐waves and atrial premature beats during exposure to acrolein, which were further augmented after exposure. Although increased, fewer arrhythmias were seen in WKY rats during the same period. Heart rate variability was significantly decreased in SH rats only after exposure, but remained unchanged in WKY rats. Air exposure did not affect any parameters in the WKY or SH rats. These findings suggest that a single exposure to acrolein can increase the sensitivity of the cardiac electrical conduction system and trigger arrhythmias, which may pose a particular health risk to people with cardiovascular disease. Funded by USEPA. (This abstract does not reflect EPA policy.)