Idiopathic monomorphic ventricular tachycardia and premature ventricular complexes (PVCs) commonly arise from the right and left ventricular outflow tracts (VOT). Their mechanism is most commonly triggered activity fr...Idiopathic monomorphic ventricular tachycardia and premature ventricular complexes (PVCs) commonly arise from the right and left ventricular outflow tracts (VOT). Their mechanism is most commonly triggered activity from delayed after-depolarizations and successful ablation is performed at the site of earliest endocardial activation. Re-entrant mechanisms have been rarely described. We report a case of an otherwise healthy patient who ultimately underwent six electro-physiology studies (EPS) and suffered numerous implantable cardiac defibrillator (ICD) discharges prior to the successful radiofrequency ablation (RFA) of two idiopathic VOT tachycardias. During the sixth EPS, a proximal aortogram demonstrated a left aortic sinus of valsalva (LASV) aneurysm. Subsequntly, a novel and successful RFA strategy of aneurysm isolation was undertaken. The presence of multiple clinical or inducible VT morphologies and the characterization of a VT as re-entrant should raise concerns that a complex arrhythmogenic substrate is present and defining the anatomy with angiography or an alternative imaging modality is essential in achieving a successful ablation strategy.展开更多
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
The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are ...The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this because of the technical difficulties associated with examining this theory. The L-type calcium current (ICa-L), an important inward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological characteristics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and ICa-L were investigated using the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolarization (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a higher current density for ICa-L than RV myocytes (RVOT (13.16±0.87) pA pF-1, RV (8.59±1.97) pA pF-1; P<0.05). The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 μmol L-1), which blocks the ICa-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.展开更多
文摘Idiopathic monomorphic ventricular tachycardia and premature ventricular complexes (PVCs) commonly arise from the right and left ventricular outflow tracts (VOT). Their mechanism is most commonly triggered activity from delayed after-depolarizations and successful ablation is performed at the site of earliest endocardial activation. Re-entrant mechanisms have been rarely described. We report a case of an otherwise healthy patient who ultimately underwent six electro-physiology studies (EPS) and suffered numerous implantable cardiac defibrillator (ICD) discharges prior to the successful radiofrequency ablation (RFA) of two idiopathic VOT tachycardias. During the sixth EPS, a proximal aortogram demonstrated a left aortic sinus of valsalva (LASV) aneurysm. Subsequntly, a novel and successful RFA strategy of aneurysm isolation was undertaken. The presence of multiple clinical or inducible VT morphologies and the characterization of a VT as re-entrant should raise concerns that a complex arrhythmogenic substrate is present and defining the anatomy with angiography or an alternative imaging modality is essential in achieving a successful ablation strategy.
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.
文摘The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this because of the technical difficulties associated with examining this theory. The L-type calcium current (ICa-L), an important inward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological characteristics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and ICa-L were investigated using the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolarization (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a higher current density for ICa-L than RV myocytes (RVOT (13.16±0.87) pA pF-1, RV (8.59±1.97) pA pF-1; P<0.05). The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 μmol L-1), which blocks the ICa-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.
