Inhalation of diluted diesel engine emission impacts heart rate variability and arrhythmia occurrence in a rat model of chronic ischemic heart failure |
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Authors: | Frédéric Anselme Stéphane Loriot Jean-Paul Henry Frédéric Dionnet Jean-Gérard Napoleoni Christian Thuillez Jean-Paul Morin |
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Institution: | (1) Service de Cardiologie, Rouen University Hospital, Rouen, France;(2) INSERM U644, School of Medicine-Pharmacy, University of Rouen France, 22 bd Gambetta, Rouen, Cedex, 76 183, France;(3) Centre d’Etudes et de Recherches Technologiques en Aérothermique et Moteurs, Saint Etienne du Rouvray, France;(4) EMKA Technologies, Paris, France |
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Abstract: | Both increase in cardiac arrhythmia incidence and decrease in heart rate variability (HRV) have been described following human
and experimental animal exposures to air pollutants. However, the potential causal relationship between these two factors
remains unclear. Incidence of ventricular arrhythmia and HRV were evaluated during and after a 3 h period of Diesel engine
exhaust exposure in ten healthy and ten chronic ischemic heart failure (CHF, 3 months after coronary ligation) Wistar rats
using implantable ECG telemetry. Air pollutants were delivered to specifically designed whole body individual exposure chambers
at particulate matter concentrations similar to those measured inside cabins of cars inserted in congested urban traffic.
Recordings were obtained from unrestraint and unsedated vigil rats. Immediate decrease in RMSSD was observed in both healthy
(6.64 ± 2.62 vs. 4.89 ± 1.67 ms, P < 0.05) and CHF rats (8.01 ± 0.89 vs. 6.6 ± 1.37 ms, P < 0.05) following exposure. An immediate 200–500% increase in ventricular premature beats was observed in CHF rats only.
Whereas HRV progressively returned to baseline values within 2.5 h after exposure start, the proarrhythmic effect persisted
as late as 5 h after exposure termination in CHF rats. Persistence of ventricular proarrhythmic effects after HRV normalization
suggests that HRV reduction is not the mechanism of cardiac arrhythmias in this model. Our methodological approach, closely
reflecting the real clinical situations, appeared to be a unique tool to provide further insight into the pathophysiological
mechanisms of traffic related airborne pollution health impact. |
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Keywords: | Chronic heart failure Heart rate variability Arrhythmia ECG telemetry Diesel engine emissions Inhalation toxicology |
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