There are few reports about the incidence and predictors of silent cerebral thromboembolic lesions (SCLs) after atrial fibrillation (AF) ablation in patients treated with direct oral anticoagulants (DOACs). The purpose of this study is to evaluate the incidence and predictors of SCLs after AF ablation with cerebral magnetic resonance imaging (C-MRI) in patients treated with DOACs. We enrolled 117 consecutive patients who underwent first AF ablation and received DOACs, including apixaban, dabigatran, edoxaban, and rivaroxaban. DOACs were discontinued after administration 24 h before the procedure, and restarted 6 h after the procedure. During the procedure, activated clotting time (ACT) was measured every 15 min, and intravenous heparin infusion was performed to maintain ACT at 300-350 s. All patients underwent C-MRI the day after the procedure. SCLs were detected in 28 patients (24%) after AF ablation. Age, female sex, the presence of persistent AF, left atrial volume, procedure time, radiofrequency energy, electrical cardioversion, and mean ACT showed no correlations with the incidence of SCLs. Multivariate analysis revealed independent predictors of SCLs were CHADSVASc scores ≥3, left atrial appendage (LAA) emptying velocity ≤39 cm/s, and minimum ACT ≤260 s. Patients with both CHADSVASc scores ≥3 and LAA flow velocity ≤39 cm/s had the highest incidence of SCLs 15 of 26 patients (58%). In patients treated with DOACs, CHADSVASc score ≥3, minimum ACT ≤260 s, and LAA emptying velocity ≤39 cm/s were independent risk factors for the SCLs after AF ablation.
Several trials demonstrated that a long detection interval and a high-rate cutoff reduced implantable cardioverter-defibrillator (ICD) therapy in primary prevention patients. However, only a few data are available for secondary prevention (SP) patients. The aim of this study was to evaluate whether these ICD programming would be effective in reducing ICD therapies in SP patients. We enrolled 65 SP patients under ICD or cardiac resynchronization therapy with the defibrillator programmed with the same setting (conventional setting). During follow-up, we changed detection rates in each zone; cycle length (CL) ≤400 to ≤370 ms for ventricular tachycardia (VT) zone, CL ≤350 to ≤320 ms for fast VT zone, CL ≤300 to ≤270 ms for ventricular fibrillation (VF) zone, and number of intervals to detect ventricular tachyarrhythmia in VF zone: 12-24. We retrospectively compared the incidences of ICD therapies, syncope, and hospitalization due to slow VT under the detection rate between both settings. Median follow-up periods were 5.0 (interquartile range 2.5-7.8) and 2.5 years (interquartile range 2.3-2.7) in conventional and strategic settings, respectively. The incidence of appropriate ATP and shock significantly decreased in strategic setting (conventional and strategic settings: 21.2 and 4.8 ATPs per year, respectively, OR 0.18, 95 % CI 0.06-0.54, p = 0.002, 26.1 and 7.8 shocks per year, respectively, OR 0.29, 95 % CI 0.09-0.88, p = 0.03). The incidence of overall inappropriate therapy significantly decreased (conventional and strategic settings: 17.6 and 2.8 therapies per year, respectively, OR 0.14, 95 % CI 0.05-0.44, p = 0.01). The incidence of syncope and slow VT was not significantly different between both settings. In conclusion, ICD programming-combined long detection interval with high-rate cutoff was effective in reducing appropriate shock and inappropriate therapy without increasing the incidence of syncope and slow VT in SP patients.
Non-invasive risk stratification for ventricular fibrillation (VF) in Brugada syndrome (BrS) has not been fully evaluated. The aim of this study was to assess the utility of signal-averaged Holter electrocardiogram (Holter SAECG) and 12-lead Holter electrocardiogram (Holter ECG) after a pilsicainide provocation test for non-invasive risk stratification in BrS. We enrolled 30 consecutive patients with BrS [divided into 2 groups: the VF group, those with a previous history of VF (n = 10); and the non-VF group, those without a history of VF (n = 20)] and 10 control subjects without type 1 ECG. We evaluated late potentials [LP: filtered QRS (f-QRS), RMS40, and LAS40] on the Holter SAECG for 4 h after the pilsicainide provocation and in the same patients on another day without performing the pilsicainide provocation. Furthermore, we measured QRS duration and QTc interval in leads V2 and V5, and J amplitude in lead V2 on the Holter ECG after the pilsicainide provocation. On the Holter SAECG, the f-QRS at 1 h and LAS40 at 3 h after the pilsicainide provocation were significantly larger in the VF group than in the non-VF group (f-QRS at 1 h: 113.9 ± 8.9 vs. 104.9 ± 8 ms; p = 0.01, LAS40 at 3 h: 45.4 ± 5.9 vs. 35.5 ± 7.4 ms; p < 0.001). The receiver-operating characteristic curve analysis for a single parameter of VF occurrence was determined [f-QRS at 1 h: area under the curve (AUC) 0.8, with sensitivity 80% and specificity 80%; and LAS40 at 3 h: AUC 0.87, with sensitivity 90% and specificity 75%]. On the Holter ECG, there were no significant differences in these parameters between the VF and non-VF groups. In conclusion, the LP after the pilsicainide provocation using Holter SAECG may be useful for risk stratification of VF episodes in patients with BrS.
Several trials demonstrated that frequent right ventricular apical pacing (RVAP) was associated with cardiac dysfunction and an increased rate of heart failure hospitalization. However, there are few reports about the 12-lead electrocardiogram (12-ECG) parameters at the time of device implantation to predict deterioration of LVEF in patients with frequent RVAP. We retrospectively studied 115 consecutive patients undergoing pacemaker or implantable cardioverter-defibrillator implantation with RVAP, with rate of ventricular pacing ≥ 40% and LVEF ≥ 50% at the time of implantation. We compared the 12-ECG characteristics at the time of device implantation between patients with deterioration of LVEF (≥ 10% reduction) and those without. Twenty-nine patients (25%) had deteriorated LVEF with a decrease in mean LVEF from 59 to 40% during a median follow-up period of 8.9 [4.6-13.7] years. Multivariate logistic regression analysis showed that cumulative % of ventricular pacing [odds ratio (OR) 1.04 per 1% increase, 95% confidence interval (CI) 1.01-1.09, p = 0.04], notching of baseline paced QRS in limb leads (OR 5.04, 95% CI 1.59-19.6, p = 0.005) and the QS pattern in all precordial leads (OR 3.56, 95% CI 1.21-10.8, p = 0.02) were independently associated with deterioration of LVEF. The QS pattern of baseline paced QRS in all precordial leads had 58% sensitivity, 93% specificity for the RV lead position at the tip of RV apex. In conclusion, considering OR by multivariate analysis, notching of baseline paced QRS in limb leads and the QS pattern in all precordial leads at device implantation may be simple and useful predictors to identify patients who are at risk for deterioration of cardiac function during long-term RVAP. 12-ECG monitoring at device implantation and avoidance of the RVAP site showing a QS pattern may be important to prevent deterioration of cardiac function in patients with frequent RVAP.
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