EN
To determine changes in physiological parameters of the myocardium in experimentally induced hyperthyreosis in an animal model, the occurrence and type of arrhythmias triggered during programmed electrical stimulation and changes in electrophysiological parameters of ventricular cardiomyocytes with hypertrophy due to hyperthyreosis were investigated. Hyperthyreosis was induced experimentally in five pigs, which were orally administered L-thyroxine at a dose of 20 µg/kg. Five untreated pigs served as the control. Programmed electrical stimulation was performed before administration of L-thyroxine (EPS 1), four (EPS 2) and eight (EPS 3) weeks after the onset of thyroxine administration, and four weeks after drug withdrawal (EPS 4). After the last stimulation, the animals were sacrificed and necropsied, with particular regard to heart autopsy. During the EPS 2, VERP was decreased in the group treated with the hormone (P<0.05). The mean values of AERP and AVNERP in the group were decreased as well. Atrial flutter and atrial fibrillation were induced during stimulation of the experimental group. In the other pigs of the experimental group, singular and paired ventricular extrasystolic were observed. In the EPS 3, AERP and AVNERP were statistically shorter in pigs with hyperthyreosis. A significant difference in Wenckebach CL between the control and experimental groups were observed. SNRT was shorter in the group with hyperthyreosis. In all pigs with hyperthyreosis, atrial fibrillation was induced. In one pig, non-sustained ventricular tachycardia was observed. During EPS 4, AERP remained shorter in group with hyperthyreosis. In two pigs of the group, atrial fibrillation was induced during pacing, and in two pigs, ventricular fibrillation was observed. The assessment of the heart's weight revealed a significant increase in its mass in pigs with hyperthyreosis. An increase in the thickness of the right and left ventricle free walls (P<0.01) and interventricular septum (P<0.01) was found in pigs with hyperthyreosis. At the same time, the inner diameter of the left ventricle was significantly smaller in this group (P<0.01) due to a concentric hypertrophy of the ventricle. In view of these findings, experimental hyperthyreosis caused shortening of refractory periods of different parts of the conducting system and enhanced susceptibility to supraventricular and ventricular arrhythmias, both spontaneous and induced during electrical stimulation. The mechanism of these arrhythmias can differ as a consequence of the hypertrophy of the left ventricle.