Incidence of Left Atrial Appendage Triggers in Patients With Atrial Fibrillation Undergoing Catheter Ablation.

OBJECTIVE: This study sought to investigate incidence of left atrial appendage (LAA) triggers of atrial fibrillation (AF) and/or organized atrial tachycardias (OAT) in patients undergoing AF ablation and to evaluate outcomes after ablation. BACKGROUND: Although LAA isolation is being increasingly performed during AF ablation, the true incidence of LAA triggers for AF remains unclear. METHODS: All patients with LAA triggers of AF and/or OAT during AF ablation from 2001 to 2017 were included. LAA triggers were defined as atrial premature depolarizations from the LAA, which initiated sustained AF and/or OAT. RESULTS: Out of 7,129 patients undergoing AF ablation over 16 years, LAA triggers were observed in 21 (0.3%) subjects (age 60 ± 9 years; 57% males; 52% persistent AF). Twenty (95%) patients were undergoing repeat ablation. The LAA was the only nonpulmonary vein trigger in 3 patients; the remaining 18 patients had both LAA and other nonpulmonary vein triggers. LAA triggers were eliminated in all patients (focal ablation in 19 patients; LAA isolation in 2 patients). Twelve months after ablation, 47.6% remained free from recurrent arrhythmia. After overall follow-up of 5.0 ± 3.6 years (median: 3.7 years; interquartile range: 1.4 to 8.9 years), 38.1% were arrhythmia-free. All 3 patients with triggers limited to the LAA remained free of AF recurrence. One patient undergoing LAA isolation developed LAA thrombus during follow-up. CONCLUSIONS: The incidence of true LAA triggers is very low (0.3%). Most patients with LAA triggers have additional nonpulmonary vein triggers, and despite elimination of LAA triggers, long-term arrhythmia recurrence rates remain high. Potential risks of empiric LAA isolation during AF ablation (especially first-time AF ablation) may outweigh benefits.

Characterization of Structural Changes in Arrhythmogenic Right Ventricular Cardiomyopathy With Recurrent Ventricular Tachycardia After Ablation: Insights From Repeat Electroanatomic Voltage Mapping.

BACKGROUND: Data characterizing structural changes of arrhythmogenic right ventricular (RV) cardiomyopathy are limited. METHODS: Patients presenting with left bundle branch block ventricular tachycardia in the setting of arrhythmogenic RV cardiomyopathy with procedures separated by at least 9 months were included. RESULTS: Nineteen consecutive patients (84% males; mean age 39±15 years [range, 20-76 years]) were included. All 19 patients underwent 2 detailed sinus rhythm electroanatomic endocardial voltage maps (average 385±177 points per map; range, 93-847 points). Time interval between the initial and repeat ablation procedures was mean 50±37 months (range, 9-162). No significant progression of voltage was observed (bipolar: 38 cm2 [interquartile range (IQR), 25-54] versus 53 cm2 [IQR, 25-65], P=0.09; unipolar: 116 cm2 [IQR, 61-209] versus 159 cm2 [IQR, 73-204], P=0.36) for the entire study group. There was a significant increase in RV volumes (percentage increase, 28%; 206 mL [IQR, 170-253] versus 263 mL [IQR, 204-294], P<0.001) for the entire study population. Larger scars at baseline but not changes over time were associated with a significant increase in RV volume (bipolar: Spearman ρ, 0.6965, P=0.006; unipolar: Spearman ρ, 0.5743, P=0.03). Most patients with progressive RV dilatation (8/14, 57%) had moderate (2 patients) or severe (6 patients) tricuspid regurgitation recorded at either initial or repeat ablation procedure. CONCLUSIONS: In patients with arrhythmogenic RV cardiomyopathy presenting with recurrent ventricular tachycardia, >10% increase in RV endocardial surface area of bipolar voltage consistent with scar is uncommon during the intermediate term. Most recurrent ventricular tachycardias are localized to regions of prior defined scar. Voltage indexed scar area at baseline but not changes in scar over time is associated with progressive increase in RV size and is consistent with adverse remodeling but not scar progression. Marked tricuspid regurgitation is frequently present in patients with arrhythmogenic RV cardiomyopathy who have progressive RV dilation.

Clinical and electrophysiological characteristics of idiopathic ventricular arrhythmias originating from the slow pathway region.

BACKGROUND: The slow pathway region (SPR) is commonly targeted during ablation of atrioventricular nodal reentrant tachycardia. However, its role in idiopathic ventricular arrhythmias (IVAs) remains unknown. OBJECTIVE: The purpose of this study was to describe the electrocardiographic and electrophysiological characteristics of IVAs that were successfully ablated from the SPR. METHODS: Medical records of consecutive patients undergoing ablation of IVAs in the para-Hisian region between 2010 and 2018 were reviewed to identify subjects whose ventricular arrhythmias were targeted from the SPR. RESULTS: Among 63 patients with para-Hisian IVAs undergoing ablation, the SPR was targeted in 12 (20%; mean age 64 ± 7 years; 9 men). All patients presented with ventricular premature depolarizations manifesting left bundle branch block morphology with variable precordial transition (leads V2-V5) and a mean QRS duration of 131 ± 11 ms. In all cases, leads I and aVL had positive forces (R or Rs) and lead aVR had negative forces (QS or Qr). In the majority of cases, lead II had positive forces (R or Rs; n = 9 [75%]) and lead III had negative forces (rS or QS; n = 9 [75%]). Mean activation at the SPR was 31 ± 5 ms pre-QRS. All patients had initial ablation with radiofrequency, resulting in junctional rhythm in 9 (75%); 3 (25%) patients required additional cryoablation. Ablation was successful in 11 patients (92%). One patient required a permanent pacemaker for heart block but subsequently recovered intrinsic conduction. CONCLUSION: The SPR can be a source of IVAs, which can be safely and successfully ablated in most cases using radiofrequency energy. IVAs arising from this location manifest unique electrocardiographic features.

Class I Histone Deacetylase Inhibition for the Treatment of Sustained Atrial Fibrillation.

Current therapies are less effective for treating sustained/permanent versus paroxysmal atrial fibrillation (AF). We and others have previously shown that histone deacetylase (HDAC) inhibition reverses structural and electrical atrial remodeling in mice with inducible, paroxysmal-like AF. Here, we hypothesize an important, specific role for class I HDACs in determining structural atrial alterations during sustained AF. The class I HDAC inhibitor N-acetyldinaline [4-(acetylamino)-N-(2-amino-phenyl) benzamide] (CI-994) was administered for 2 weeks (1 mg/kg/day) to Hopx transgenic mice with atrial remodeling and inducible AF and to dogs with atrial tachypacing-induced sustained AF. Class I HDAC inhibition prevented atrial fibrosis and arrhythmia inducibility in mice. Dogs were divided into three groups: 1) sinus rhythm, 2) sustained AF plus vehicle, and 3) sustained AF plus CI-994. In group 3, the time in AF over 2 weeks was reduced by 30% compared with group 2, along with attenuated atrial fibrosis and intra-atrial adipocyte infiltration. Moreover, group 2 dogs had higher atrial and serum inflammatory cytokines, adipokines, and atrial immune cells and adipocytes compared with groups 1 and 3. On the other hand, groups 2 and 3 displayed similar left atrial size, ventricular function, and mitral regurgitation. Importantly, the same histologic alterations found in dogs with sustained AF and reversed by CI-994 were also present in atrial tissue from transplanted patients with chronic AF. This is the first evidence that, in sustained AF, class I HDAC inhibition can reduce the total time of fibrillation, atrial fibrosis, intra-atrial adipocytes, and immune cell infiltration without significant effects on cardiac function.