Longitudinal electrocardiographic assessment in Brugada syndrome.

Background: The type 1 electrocardiographic (ECG) pattern diagnostic of Brugada syndrome (BrS) can be dynamic. Limited studies have rigorously evaluated the temporal stability of the Brugada ECG pattern. Objective: We sought to evaluate fluctuations of the Brugada pattern in serial resting ECGs from BrS patients managed within a large health care system. Methods: In our cohort of BrS patients with at least 2 standard, resting ECGs recorded on separate clinical encounters, we evaluated serial changes in the Brugada pattern and categorized patients into 1 of 3 groups: dynamic was defined as the presence of both type 1 and non-type 1 patterns in available ECGs; the provoked-only group was defined as having a non-type 1 Brugada pattern across resting ECGs; and the persistent group was defined as having a type 1 pattern on all ECGs. We also evaluated the clinical risk in this cohort according to the Shanghai risk score. Results: In 72 patients with BrS (mean age 46 ± 15 years, 69% male), 828 standard, resting ECGs were recorded over a median duration of 30.2 (interquartile range 6.3-68.1) months. The dynamic group comprised 50 (69% of the cohort) patients, the provoked-only group consisted of 17 patients (24% of the cohort), and the persistent group included 5 patients. No significant differences were detected in the total number of ECGs evaluated during the follow-up period between any of the groups. Only sinus node dysfunction and a prior cardiac arrest were associated with the persistent type 1 group. The majority of patients had a low annualized risk of lethal arrhythmic events. Conclusion: Most BrS patients have a dynamic Brugada pattern noted on longitudinal, resting ECGs. Expert consensus statements should provide clarity on the frequency of obtaining resting ECGs in patients suspected of having BrS during follow-up.

Long-term outcome of surgical cryoablation for refractory ventricular tachycardia in patients with non-ischemic cardiomyopathy.

Aims: Limited data exist on the long-term outcome of patients (pts) with non-ischemic cardiomyopathy (NICM) and ventricular tachycardia (VT) refractory to conventional therapies undergoing surgical ablation (SA). We aimed to investigate the long-term survival and VT recurrence in NICM pts with VT refractory to radiofrequency catheter ablation (RFCA) who underwent SA. Methods and results: Consecutive pts with NICM and VT refractory to RFCA who underwent SA were included. VT substrate was characterized in the electrophysiology lab and targeted by RFCA. During SA, previous RFCA lesions/scars were identified and targeted with cryoablation (CA; 3 min/lesion; target -150 °C). Follow-up comprised office visits, ICD interrogations and the social security death index. Twenty consecutive patients with NICM who underwent SA (age 53 ± 16 years, 18 males, LVEF 41 ± 20%; dilated CM = 9, arrhythmogenic right ventricular CM = 3, hypertrophic CM = 2, valvular CM = 4, and mixed CM = 2) were studied. Percutaneous mapping/ablation in the electrophysiology lab was performed in 18 and 2 pts had primary SA. During surgery, 4.9 ± 4.0 CA lesions/pt were delivered to the endocardium (2) and epicardium (11) or both (7). VT-free survival was 72.5% at 1 year and over 43 ± 31 months (mos) (range 1-83mos), there was only one arrhythmia-related death. There was a significant reduction in ICD shocks in the 3-mos preceding SA vs. the entire follow-up period (6.6 ± 4.9 vs. 2.3 ± 4.3 shocks/pt, P = 0.001). Conclusion: In select pts with NICM and VT refractory to RFCA, SA guided by pre-operative electrophysiological mapping and ablation may be a therapeutic option.

Risk of stroke or transient ischemic attack after atrial fibrillation ablation with oral anticoagulant use guided by ECG monitoring and pulse assessment.

INTRODUCTION: We sought to gain insight into stroke risk after atrial fibrillation (AF) ablation. METHODS AND RESULTS: We followed 1,990 patients for >1 year (49 ± 29 months) who underwent AF ablation. Prior to stopping oral anticoagulants (OAC), we performed 3-week transtelephonic ECG monitoring (TTM) and taught patients heart rate and pulse assessment. Documented AF or inability to do monitoring or assess pulse precluded stopping OAC in CHADS2 ≥1 patients. OAC was stopped in 546/840 (65%) with CHADS2  = 0; 384/796 (48%) with CHADS2  = 1 and 101/354 (40%) with CHADS2 ≥ 2. Sixteen strokes or TIAs occurred (0.2%/patient-year); 5 in CHADS2  = 0 patients (all off OAC); 5 in CHADS2  = 1 (1 off and 4 on OAC); and 6 in CHADS2 ≥2 (2 off and 4 on OAC). Twelve of 16 patients (75%) with stroke or TIA had documented AF. In patients "off " OAC, stroke rate/year stratified by the CHADS2 score was similar (CHADS2  = 0: 0.28%; CHADS2  = 1: 0.07%; CHADS2 ≥2: 0.50%; P = NS). There was no difference in stroke risk "on" versus "off " OAC in CHADS2  = 1 (0.48% vs. 0.07%) or CHADS2 ≥2 (0.39% vs. 0.50%). Risk of major bleeding per patient year "on" OAC was > "off " OAC (13/1,138 (1.14%) versus 1/832 (0.1%); P<0.016). CONCLUSIONS: Post-AF ablation with OAC guided by TTM and pulse assessment: (1) Overall stroke or TIA rate risk is low and risk is due to recurrent AF and (2) OAC can be stopped in 40% of CHADS2 ≥2 patients with low stroke and hemorrhagic risk.