One of the most important proarrhythmic complications after left atrial (LA) ablation is regular atrial tachycardia (AT) or flutter. Those tachycardias that occur after atrial fibrillation (AF) ablation can cause even more severe symptoms than those from the original arrhythmia prior to the index ablation procedure since they are often incessant and associated with rapid ventricular response. Depending on the method and extent of LA ablation and on the electrophysiological properties of underlying LA substrate, the reported incidence of late ATs is variable. To establish the exact mechanism of these tachycardias can be difficult and controversial but correlates with the ablation technique and in the vast majority of cases the mechanism is reentry related to gaps in prior ablation lines. When tachycardias occur, conservative therapy usually is not effective, radiofrequency ablation procedure is mostly successful, but can be challenging, and requires a complex approach.
Dissociated firing in isolated PVs is associated with their role in the initiation and maintenance of PAF.
Background or purpose Episodes of left atrial (LA) pressure increase predispose to atrial fibrillation (AF). The adaptation of LA mechanical function and electrophysiology to pressure elevation in healthy adults, and in patients with AF, is largely unknown. Methods Eleven patients with left-sided accessory pathway (controls) and 16 patients with paroxysmal AF undergoing catheter ablation were studied. LA pressure (LAP) was recorded through transseptal catheterization, while speckle trackingderived peak LA longitudinal strain (PALS) was measured using transthoracic echocardiography. Stiffness index (SI) was calculated as mean LAP/PALS. Effective refractory period (ERP) of the LA was determined during simultaneous atrioventricular (AV) pacing and during atrial pacing. Results At baseline, AF patients had higher LA pressure (mean LAP 8.3±4.7 vs. 5.1±3.1 mmHg, p=0.048), reduced LA mechanical function (PALS 15.1±5.1 vs. 21.6±6.2 %, p=0.006, SI 0.69±0.75 vs. 0.28±0.22, p=0.015), and longer LA ERP (242.3±33.4 vs. 211.7±15.6 ms, p=0.017). Mean LAP was increased to the same extent by AV pacing in controls and AF patients (mean change 12.6± 7.4 vs. 12.6± 7.5 mmHg, p=0.980). At the same time PALS decreased (from 15.1±5.1 to 11.6±3.3 %, p=0.008), SI increased (from 0.69±0.75 to 1.29±1.17, p<0.001) and ERP shortened (from 242.3±33.4 to 215.9±26.3 ms, p=0.003) in AF patients, while they remained unchanged in controls. ConclusionsThe stiffened LA in patients with AF responds to acute pressure elevation with an exaggerated increase in wall tension and decrease in ERP, which is not seen in the normal LA. This may underlie the propensity for AF during episodes of atrial stretch in these patients.
Introduction: Both isoproterenol (Iso) and adenosine (Ado) are used to induce atrial fibrillation (AF) in the electrophysiology lab. However, the utility of Ado has not been systematically established.Objective: The purpose of this study was to compare Ado to Iso for the induction of paroxysmal AF.Methods: Forty patients (16 women; mean age, 60 ± 12 years) with paroxysmal AF, presenting for ablation were prospectively included of whom 36 (90%) received Ado (18-36 mg) and/or Iso (3-20 µg/min incremental dose) in a randomized order (26 [72%] received both drugs).Results: AF was induced with Iso in 15 of 32 (47%) and with Ado in 12 of 30 (40%) patients (P = 0.9). Iso-triggered AF started from the left pulmonary veins (PVs) in 11 of 15 (73%), from the right PVs in 3 of 15 (20%), and from the coronary sinus (CS) in 1 of 15 (7%) cases. Ado-induced AF episodes originated from the left PVs in 6 of 12 (50%), from the right atrium (RA) in 4 of 12 (33%), and from the CS in 2 of 12 (17%) cases. Altogether, Iso-induced AF was more likely initiated from the PVs (93%) compared with Ado (50%) (P = 0.02). Ado-induced non-PV triggers were not predictive of arrhythmia recurrence after PV isolation.Conclusion: Ado much more frequently induces non-PV triggers, especially from the RA. The clinical significance of these foci, however, is questionable. K E Y W O R D S adenosine, atrial fibrillation, isoproterenol, pulmonary vein, triggers 1 | INTRODUCTION Elimination of initiating triggers has become the cornerstone of atrial fibrillation (AF) treatment. Most of these triggers reside in the pulmonary veins (PVs) 1 ; however, non-PV triggers are an important source of recurrence after PV isolation (PVI). Triggers can be identified during the electrophysiology study if spontaneously occurring or can be induced by a drug challenge. Owing to the spurious nature of spontaneous triggers and the laboriousness of AF provocation, empirical isolation of all PVs has become the standard in AF ablation, despite the fact that selective isolation of only the triggering PV can achieve similar success in selected patients. 2 Even if total PV isolation is pursued as a first step, identification of non-PV triggers gains importance when AF occurs despite isolated PVs. 3,4The role of high dose isoproterenol (Iso) infusion to elicit AF triggers is well established. 5,6 Besides Iso, adenosine (Ado) or adenosine triphosphate (ATP) is increasingly used for the induction of AF, despite the lack of systematic studies on the sensitivity and
Purpose Various ventricular pacing maneuvers have been developed to differentiate orthodromic reciprocating tachycardia (ORT) from atrioventricular nodal reentry tachycardia (AVNRT). We aimed to evaluate the diagnostic value of ventricular pacing maneuvers in patients undergoing catheter ablation for AVNRT/ORT. Methods Sixty patients with supraventricular tachycardia (SVT) undergoing invasive EP study were included (ORT: 31, typical AVNRT: 18, atypical AVNRT: 11). Ventricular overdrive pacing (VOP) and resetting by premature ventricular stimulation (PVS) during SVT were analyzed by 3 independent observers blinded to the ultimate diagnosis. We determined intraclass correlation coefficient (ICC) for interobserver agreement and the diagnostic accuracy of consensual results. Results Although specificity of all parameters was high (96-100%) for ORT, semi-quantitative parameters of VOP (requiring the recognition of specific ECG patterns) had lower interobserver reliability (ICC: 0.32-0.66) and sensitivity (16.1-77.4%). In contrast, most quantitative measurements of VOP and PVS showed good reproducibility (ICC: 0.93-0.95) and sensitivity (74.2-89.3%), but post-pacing interval after VOP needed correction with AV nodal conduction slowing. False negative results for diagnosing ORT were more common with left free wall vs. right free wall or septal, and slowly vs. fast-conducting septal APs. False positivity was only seen with a bystander, concealed nodo-fascicular/nodo-ventricular (NF/NV) AP in a case of AVNRT. Conclusions No single maneuver is 100% sensitive for ORT. Semi-quantitative features have limited reproducibility and all parameters can be misleading in the case of rate-dependent delay during VOP/PVS, ORT circuits remote from the pacing site, or a bystander, concealed NF/NV AP.
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