Identification of exit block after ostial PV ablation provides a clear endpoint for electrical isolation of the PVs. Isolation of the PVs can be performed during sustained AF without the need to apply excess RF lesions. Applying a 20-minute waiting period after electrical isolation will identify reconnection in approximately 10% of PVs.
Using the described techniques, PV electrical isolation of PVs demonstrating spontaneous and/or provoked triggers is superior to focal PV ablation, with marked differences in outcome by 2 months. MEAM confirmed the noncircumferential nature of ostial ablation for effective isolation of most PVs and may play a role in the low risk and good outcome observed. The good outcome of targeted PV isolation as described suggests the need for a prospective comparison of targeted versus empiric PV isolation techniques.
Background-Identifying the septal versus lateral site of origin of ventricular tachycardia (VT) with a right bundle-branch block (RBBB)-type pattern and an R-S ratio Ͼ1 in lead V 1 is difficult with the 12-lead ECG, especially in patients with prior apical infarction. Methods and Results-We prospectively evaluated 58 patients with VT. Sixteen patients had apical infarcts (group 1), 29 had nonapical infarcts (group 2), and 13 had no heart disease (group 3). QRS complex onset to activation at the right ventricular apex (stim-RVA) was measured during left ventricular (LV) apical septal and lateral pacing, and 47 RBBB-type VTs (QRS-RVA) were localized to the septal or lateral apex by using entrainment techniques. Pacing and VT site of origin were confirmed by electroanatomic mapping. The stim-RVA time was 59Ϯ16 ms for septal versus 187Ϯ24 ms for lateral sites in group 1, PϽ0.001; 70Ϯ14 ms for septal versus 169Ϯ19 ms for lateral sites in group 2, PϽ0.001; and 42Ϯ15 ms for septal versus 86Ϯ16 ms for lateral sites in group 3, PϽ0.005. The QRS-RVA time was 50Ϯ13 ms for apical septal VTs versus 178Ϯ21 ms for lateral VTs in group 1, PϽ0.001; 71Ϯ17 ms for apical septal versus 157Ϯ20 ms for lateral VTs in group 2, PϽ0.001; and 32Ϯ12 ms for septal versus 71Ϯ16 ms for lateral VTs in group 3, PϽ0.01. Conclusions-The QRS-RVA differs for the VT site of origin from the LV septal versus lateral apex. These data prove useful in rapidly regionalizing the VT site of origin with a V 1 R-S ratio Ͼ1, particularly in instances of an apical infarct, where surface ECG distinctions are less identifiable.
A MAD score >12% between RVOT VT and a pace-map at any site suggests sufficient dissimilarity to dissuade ablation at that site. The MAD score can be used to standardize 12-lead ECG waveform morphology comparisons among different laboratories, and may be useful for guiding ablation of VT.
Manifest NFV pathways presented with variable QRS expression dependent on the ventricular insertion site and often coexisted with other tachycardia mechanisms (atrioventricular nodal reentry tachycardia and atrioventricular reentrant tachycardia). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.
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