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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
VENTRICULAR REPOLARIZATION IN DOXORUBICIN-INDUCED CARDIOMYOPATHY
Abstract number: P23
KHARIN1 SN, STRELKOVA1 MV, SHUMIKHIN2 KV, SOBOLEV2 AS, KRANDYCHEVA1 VV, TSVETKOVA1 AS, SHMAKOV1 DN
1Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, Syktyvkar, Russia,
2Komi Branch of the Kirov State Medical Academy, Syktyvkar, Russia
Anthracycline chemotherapy produces cardiac remodeling, electrocardiographic abnormalities, and arrhythmias. Doxorubicin was administered to adult female Wistar rats (six equal intraperitoneal injections of the drug in a cumulative dose of 15 mg/kg for two weeks) in order to examine ventricular repolarization alterations by electrophysiological mapping of the ventricular epicardium in situ six weeks after treatment. There were the inhomogeneous prolongation of activation-recovery intervals (ARIs) and the increase in repolarization heterogeneity across the epicardium. Intraregional repolarization heterogeneity was increased. Meanwhile, interregional differences in repolarization heterogeneity were lost. The apex-to-base ARI gradient was significantly greater compared with controls. The increase in the apex-to-base ARI gradient within the right ventricle was greater than within the left ventricle. The interventricular ARI gradient was not different from controls, although the regional interventricular ARI gradients were altered: the interventricular ARI gradient on the base was increased, and that on the apex was decreased. The right ventricle was more vulnerable to doxorubicin than the left one. Doxorubicin treatment produced a twofold decrease in cardiac output. There was histological evidence of fibrosis in the ventricular myocardium. These results indicate that doxorubicin produces inhomogeneous, significant, and persisted alterations of ventricular repolarization, which can explain electrocardiographic repolarization abnormalities in doxorubicin-induced cardiomyopathy. The study was supported by the Ural Branch of the Russian Academy of Sciences (project No. 12-P-4-1003).
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :P23