Effect of a course of fabomotizole on atrial depolarization in rats with post-infarction chronic heart failure

Relevance. Post-infarction chronic heart failure contributes to the development of atrial fibrillation, the most common form of arrhythmia. The search for new drugs with pronounced antiarrhythmic activity is currently relevant. Purpose of the study. To study the sequence of atrial epicardial depolarization in rats with post-infarction chronic heart failure after long-term administration of fabomotizole. Methods. The sequence of atrial epicardial depolarization in rats with post-infarction chronic heart failure caused by anterior transmural myocardial infarction and sham-operated animals was studied using synchronous multichannel cardiac electrochronotopography after a course of fabomotizole administration. Results. Post-infarction chronic heart failure provokes the appearance of an additional excitatory focus in the pulmonary vein lacunae of the left atrium, which is a predictor of atrial arrhythmogenicity. Fabomotizole suppresses an additional arrhythmogenic focus of excitation in the area where the pulmonary veins enter the left atrium, minimizing the risk of developing atrial tachyarrhythmias, including atrial fibrillation.