Ventricular fibrillation （VF） is a malignant arrhythmia, usually initiated by a ventricular premature contraction （VPC） during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been desc...Ventricular fibrillation （VF） is a malignant arrhythmia, usually initiated by a ventricular premature contraction （VPC） during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPCs preceded by Purkinje potentials or from the right ventricular outflow tract （RVOT） in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. The most important issue before the ablation session is the recording of the 12-lead ECG of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pace mapping. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.展开更多
文摘Ventricular fibrillation （VF） is a malignant arrhythmia, usually initiated by a ventricular premature contraction （VPC） during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPCs preceded by Purkinje potentials or from the right ventricular outflow tract （RVOT） in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. The most important issue before the ablation session is the recording of the 12-lead ECG of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pace mapping. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.
