Key result
Acute amiodarone fails to prevent right atrial arrhythmias in rats with pulmonary hypertension.
Why the study?
Atrial arrhythmias are common in PH and tied to poor outcomes, but little is known about right atrium function and arrhythmogenic propensity in the monocrotaline-induced PH model.
Does amiodarone prevent the occurrence of atrial arrhythmias in the right atrium of a rat model of monocrotaline-induced pulmonary hypertension?
Does amiodarone prevent the occurrence of atrial arrhythmias in the right atrium of a rat model of monocrotaline-induced pulmonary hypertension?
In a rat model of monocrotaline-induced pulmonary hypertension, acute ex vivo exposure to amiodarone failed to attenuate the onset of right atrial arrhythmias.
Does not support amiodarone for right atrial arrhythmias in pulmonary hypertension; leaves open identification of effective antiarrhythmics in this population.
Atrial arrhythmias (AA) are common in pulmonary hypertension (PH) and are closely associated with poor clinical outcomes. One of the most studied models to investigate PH is the rat model of monocrotaline (MCT) induced PH (MCT-PH). To date, little is known about right atrium (RA) function in the MCT-PH model and the propensity of RA to develop arrhythmias. Therefore, the aim of the study was to evaluate the function of the RA of control (CTRL) and MCT treated rats, and the ability of amiodarone, a classical antiarrhythmic, to prevent the occurrence of AA in the RA in MCT-PH rats. RA function was studied in MCT-PH rats 20 days after a single subcutaneous injection of MCT 50 mg/kg. The histological results indicated the presence of RA and right ventricular hypertrophy. Surface electrocardiogram demonstrated increased P wave duration, PR wave duration and QT interval in MCT rats. RA from MCT rats were more susceptible to develop ex vivo burst pacing arrhythmias when compared to CTRL. Intriguingly, amiodarone in clinical relevant concentration was not able to prevent the occurrence arrhythmias in RA from MCT-PH animals. Hence, we conclude that the rat model of MCT-PH impairs RA structure and function, and acute exposure of RA to amiodarone in clinical relevant concentration is not able to attenuate the onset of arrhythmias in the ex vivo RA preparation.
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Teixeira‐Fonseca et al. (2023) studied Pulmonary hypertension (monocrotaline-induced rat model). Amiodarone vs. Control (CTRL) rats was evaluated on Occurrence of arrhythmias in the right atrium (ex vivo burst pacing). Acute exposure to amiodarone in clinically relevant concentrations did not prevent the occurrence of ex vivo burst pacing arrhythmias in the right atrium of rats with monocrotaline-induced pulmonary hypertension.
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