Outcomes of posterior wall isolation with pulmonary vein isolation for paroxysmal atrial fibrillation.

INTRODUCTION: Prior studies have shown that addition of posterior wall isolation (PWI) may reduce atrial fibrillation recurrence in patients with persistent atrial fibrillation. No data on PWI in paroxysmal AF (pAF) patients with normal left atrial voltage is available, to date. OBJECTIVE: This study sought to evaluate the efficacy of PWI in addition to pulmonary vein isolation (PVI) in patients presenting with pAF and normal left atrial voltage. METHODS: Consecutive patient registry analysis was performed on all patients with pAF and normal left atrial voltage undergoing initial radiofrequency ablation from November 1, 2018 to November 15, 2019. Primary endpoint was recurrence of atrial arrhythmia including AF, atrial tachycardia (AT), or atrial flutter (AFL). RESULTS: A total of 321 patients were studied, 214 in the PVI group and 107 in the PWI + PVI group. Recurrence of any atrial arrhythmia occurred in 18.2% of patients in the PVI group and 16.8% in the PVI + PWI cohort (p = 0.58). At 1 year, recurrence was 14.0% in the PVI group and 15.0% in the PWI + PVI group (p = 0.96). There was a lower AT/AFL recurrence in the PVI + PWI group, not reaching significance (3.7% in the PWI + PVI group vs. 7.9% in PVI group, p = 0.31). Need for carina lesions predicted recurrence in the PVI-only group. CONCLUSIONS: Addition of PWI to PVI in pAF patients undergoing their first ablation did not reduce the frequency of atrial arrhythmia recurrence. This warrants further study in a prospective trial.

QT interval dynamics and triggers for QT prolongation immediately following cardiac arrest.

BACKGROUND: The prolongation in QT interval typically observed following cardiac arrest is considered to be multifactorial and induced by external triggers such as hypothermia therapy and exposure to antiarrhythmic medications. OBJECTIVE: To evaluate the corrected QT interval (QTc) dynamics in the first 10 days following cardiac arrest with respect to the etiology of arrest, hypothermia and QT prolonging medications. METHODS: We enrolled 104 adult survivors of cardiac arrest, where daily ECG was available for at least 3 days. We followed their QT and QRS intervals for the first 10 days of hospitalization. We used both Bazett and Fridericia formulas to correct for heart rate. For patients with QRS < 120 we analyzed the QTc interval (n = 90) and for patients with QRS > 120 ms we analyzed the JTc (n = 104) vs. including only the narrow QRS samples (n = 89). We stratified patients by 3 groups: (1) presence of ischemic heart disease (IHD) (2) treatment with hypothermia protocol, and (3) treatment with QTc prolonging medications. Additionally, genetic information obtained during hospitalization was analyzed. RESULTS: QTc and JTc intervals were significantly prolonged in the first 6 days. Maximal QTc/JTc prolongation was observed in day 2 (QTcB = 497 ± 55). There were no differences in daily QTc/JTc and QRS intervals in the first 2 days post arrest between patients with or without hypothermia induction but such difference was found with QT prolonging medications. All subgroups demonstrated significantly prolonged QTc/JTc interval regardless of the presence of IHD, hypothermia protocol or QTc prolonging medication exposure. Our results were consistent for both Bazetts' and Frediricia correction and for any QRS duration. Prolongation of the JTcB beyond 382 ms after day 3 predicted sustained QTc/JTc prolongation beyond day 6 with an ROC of 0.78. CONCLUSIONS: QTc/JTc interval is significantly and independently prolonged post SCA, regardless of known QT prolonging triggers. Normalization of the QTc post cardiac arrest should be expected only after day 6 of hospitalization. Assessment of the QTc for adjudication of the etiology of arrest or for monitoring the effect of QT prolonging medications may be unreliable.