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Aim:To study the effects of carvedilol on the transmural heterogeneity of ven-tricular repolarization in rabbits with congestive heart failure(CHF).Methods:Rabbits were randomly divided into 3 groups:control,CHF and carvedilol treatedCHF group.Monophasic action potential duration(MAPD)in the 3 myocardiallayers was simultaneously recorded.Results:All the rabbits in the CHF grouphad signs of severe CHF.Compared with the control group,the mean bloodpressure and cardiac output were significantly decreased,while peripheral resis-tance was significantly increased in the CHF group.This proved that the CHFmodel was successful created with adriamycin in this study.Compared to thecontrol group,the ventricular fibrillation threshold(VFT)was remarkably decreasedand all MAPD of the 3 myocardial layers were extended in rabbits with CHF.However,the extension of MAPD in the midmyocardium was more obvious.Thetransmural dispersion of repolarization(TDR)was significantly increased in CHF.Low-dose carvedilol(0.25 mg/kg,twice daily)had no effects on ventricularremodeling.Treatment with low-dose carvedilol significantly increased VFT.Al-though the MAPD of the 3 myocardial layers were further prolonged in the carvediloltreated CHF group,the prolongation of MAPD in the midmyocardium was shorterthan those in the epicardium and endocardium.Treatment with low-dose carvedilolsignificantly decreased TDR in CHF.Conclusion:In the present study,the trans-mural heterogeneity of ventricular repolarization increased in the rabbits withCHF.Low-dose carvedilol decreased the transmural heterogeneity of ventricularrepolarization in CHF,which may be related to its direct electropbysiological pro-perty rather than its effect on ventricular remodeling.
Aim: To study the effects of carvedilol on the transmural heterogeneity of ven-tricular repolarization in rabbits with congestive heart failure (CHF). Methods: Rabbits were randomly divided into 3 groups: control, CHF and carvedilol treated CHF group. Monophasic action potential duration ( MAPD) in the 3 myocardiallayers was simultaneously recorded. Results: All the rabbits in the CHF grouphad signs of severe CHF. Compared with the control group, the mean blood pressure and cardiac output were significantly decreased, while peripheral resis- tance was significantly increased in the CHF group. This demonstrated that the CHF model was was created with adriamycin in this study. Compared to thecontrol group, the ventricular fibrillation threshold (VFT) was remarkably decreasedand all MAPD of the 3 myocardial layers were extended in rabbits with CHF.However, the extension of MAPD in the midmyocardium was more significantly. The transmural dispersion of repolarization (TDR) was significantly increased in CHF. Low-dose carvedi lol (0.25 mg / kg, twice daily) had no effects on ventricular remodeling. Treatment with low-dose carvedilol significantly increased VFT. Al-though the MAPD of the 3 myocardial layers were prolonged in the carvediloltreated CHF group, the prolongation of MAPD in the midmyocardium was shorterthan those in the epicardium and endocardium. Treatment with low-dose carvedilolsignificantly decreased TDR in CHF. Conlusion: In the present study, the trans-mural heterogeneity of ventricular repolarization increased in the rabbits with CHF. Low-dose carvedilol decreased the transmural heterogeneity of ventricular repolarization in CHF, which may be related to its direct electropbysiological pro-perty rather than its effect on ventricular remodeling.