The aim of our work was not to

The aim of our work was not to advocate for performing LAA occlusion and AF ablation concomitantly. Indeed, given the potential benefits of a successful catheter ablation procedure for stroke buy Birinapant [3–5], some would appropriately advocate performing these procedures in a staged fashion. The aim of this report was simply to provide an objective characterization of the LAA after PV isolation and additional substrate modification. Our findings will provide reassurance to interventional cardiac electrophysiologists contemplating concomitant AF ablation and percutaneous LAA occlusion. This knowledge is important, as combined procedures may have theoretical advantages including a reduction in the number of procedures requiring transseptal catheterization, truncation of the total required duration of oral anticoagulation (as post-procedure anticoagulation would serve a dual purpose of preventing both post-ablation stroke and acute thrombus formation on the LAA occlusion device), and the potential for a long-term reduction in stroke risk without the need for oral anticoagulation. While our current pilot study is important and addresses an important gap in clinical knowledge, it merely provides radiographic data and is no substitute for the additional larger clinical studies needed to elucidate the feasibility and safety of performing these procedures concomitantly prior to the widespread uptake of combined procedures. Limitations to our work must be noted. First, our sample size was small and comprised patients without severe LA dilation, which may have prevented the detection of statistically significant changes in LAA dimensions. While we suspect that changes in LAA dimension may not be of a sufficient magnitude to affect LAA occlusion device placement, we cannot fully exclude this possibility in all patients and for all ablation strategies and ablation energies. Second, our approach to PV isolation involved ablation along the venous side of the ridge, frequently with the precision of robotic navigation. Deliberate ablation along the pulmonary venous ridge itself, the appendage side of the ridge, or even ablation resulting in LAA electrical isolation may have a more prominent influence on the LAA. Despite this, given the recent uptake of circular ablation techniques that result in more ostial ablation, our findings are applicable [25]. Third, LAA imaging was not performed immediately after ablation. This delay in imaging may have resulted in an underestimation of acute RF injury, which may have resolved during the short waiting period. In addition, our measurements obtained at 24h post ablation may not reflect acute LAA dimensions due to changes in fluid status. Finally, while tropism may be argued that the absence of gadolinium uptake in the LAA may reflect technical limitations of DE-MRI and not the absence of actual LAA injury, we suspect that this is not the case as all patients had gadolinium enhancement in other areas of the LA post ablation.
Conclusion
Conflict of interest
Case report A 29-year-old man was referred to our institution with recurrent implantable cardioverter-defibrillator (ICD) shocks (<3 shocks over 24h) for ventricular tachycardia (VT) and ventricular fibrillation (VF) that were repeatedly initiated by closely coupled premature ventricular beats (Fig. 1). He had experienced 18 appropriate shocks since the ICD implantation. He had suffered an out-of-hospital cardiac arrest 5 years previously. No cardiac risk factors or family history of sudden cardiac death was found. Echocardiography and cardiac magnetic resonance findings were normal. Coronary angiography demonstrated normal coronary arteries. Ajmaline and adrenaline provocation test findings were unremarkable. A secondary prevention single-chamber ICD device was implanted at a local district general hospital (Atlas model V-168; St. Jude Medical, Inc., St. Paul, MN, USA). Resting 12-lead electrocardiography (ECG) revealed a clear ER pattern described as J point elevation in inferolateral leads (Fig. 2). Ambulatory 12-lead ECG monitoring was arranged to guide future catheter ablation but was unable to capture any triggering premature ventricular beats. He then underwent an electrophysiology study, which was unable to initiate any clinical ectopics or VT. The patient was started on oral quinidine in addition to beta-blockers to reduce the risk of recurrent VF and ICD shocks.