Initial experience of left bundle branch area pacing using stylet-driven pacing leads: A multicenter study.

BACKGROUND: Left bundle branch area pacing (LBBAP) has been performed exclusively using lumen-less pacing leads (LLL) with fixed helix design. This registry study explores the safety and feasibility of LBBAP using stylet-driven leads (SDL) with extendable helix design in a multicenter patient population. METHODS: This study prospectively enrolled consecutive patients who underwent LBBAP for bradycardia pacing or heart failure indications at eight Belgian hospitals. LBBAP was attempted using SDL (Solia S60; Biotronik) delivered through dedicated delivery sheath (Selectra3D). Implant success, complications, procedural, and pacing characteristics were recorded at implant and follow-up. RESULTS: The study enrolled 353 patients (mean age 76 ± 39 years, 43% female). The mean number of implants per center was 25 (range: 5-162). Overall, LBBAP with SDL was successful in 334/353 (94%), varying from 93% to 100% among centers. Pacing response was labeled as left bundle branch pacing in 73%, whereas 27% were labeled as myocardial capture. Mean paced QRS duration and stimulus to left ventricular activation time measured 126 ± 21 ms and 74 ± 17. SDL-LBBAP resulted in low pacing thresholds (0.6 ± 0.4 V at 0.4 ms), which remained stable at 12 months follow-up (0.7 ± 0.3, p = .291). Lead revisions for SDL-LBBAP occurred in 5 (1.4%) patients occurred during a mean follow up of 9 ± 5 months. Five (1.4%) septal coronary artery fistulas and 8 (2%) septal perforations occurred, none of them causing persistent ventricular septal defects. CONCLUSION: The use of SDL to achieve LBBAP is safe and feasible, characterized by high implant success in low and high volume centers, low complication rates, and stable low pacing thresholds.

Cryoballoon ablation of atrial fibrillation in octogenarians: one year outcomes from the cryo global registry.

BACKGROUND: Limited information is available on the safety and efficacy of cryoballoon ablation (CBA) in elderly patients with atrial fibrillation (AF). Moreover, global utilization of CBA in this population (≥ 80 years old) has not been reported. This study's objectives were to determine the use, efficacy, and safety of CBA to treat octogenarians suffering from AF. METHODS: In this sub-analysis of the Cryo Global Registry, 12-month outcomes of treating AF via CBA in octogenarians were compared to patients < 80 years old. Efficacy was evaluated as time to a ≥ 30 s atrial arrhythmia (AA) recurrence. Healthcare utilization was determined via repeat ablations and hospitalizations. Improvement upon disease burden was evaluated through patient reporting of symptoms and the EQ-5D-3L quality of life (QoL) survey. RESULTS: The octogenarian cohort (n = 101) had a higher prevalence of females (51.5% vs 35.7%) and CHA2DS2-VASc scores (4.2 ± 1.3 vs 2.0 ± 1.5) compared to the control cohort (n = 1573, both p < 0.01). Even when adjusting for baseline characteristics and antiarrhythmic drug usage, freedom from AA recurrence at 12 months (80.6% vs 78.9%, HRadj:0.97 [95% CI:0.59-1.58], p = 0.90) was comparable between octogenarians and control, respectively. Similar serious adverse event rates were observed between octogenarians (5.0%) and control (3.2%, p = 0.38). The groups did not differ in healthcare utilization nor reduction of AF-related symptoms from baseline to follow-up, but both experienced an improvement in QoL at 12 months. CONCLUSIONS: Despite more age-related comorbidities, CBA is a safe and effective treatment for AF in octogenarians, with efficacy and adverse events rates akin to ablations performed in younger patients. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT02752737.

Adenosine plus dipyridamole: a novel strategy to enhance adenosine-induced conduction recovery after pulmonary vein isolation.

AIMS: Intravenous administration of adenosine after a pulmonary vein (PV) isolation procedure can unmask residual, so-called 'dormant', conduction that would otherwise remain unnoticed. Elimination of these dormant potentials is challenging because of the transient effect of adenosine, often requiring repeated injections. We tested the hypothesis that dipyridamole, a drug which inhibits adenosine deamination, can provoke longer-lasting unmasking of dormant conduction. METHODS AND RESULTS: In 191 patients with drug refractory paroxysmal atrial fibrillation, a bolus of 12-24 mg of adenosine was administered after all 764 PVs were isolated. In the case of transient dormant conduction, a short infusion of dipyridamole 50 mg was given and a bolus of adenosine was repeated. In all cases, re-isolation was attempted guided by the activation pattern in the PV on a circular mapping catheter. Duration of adenosine-induced dormant conduction before and after dipyridamole was recorded as the time between administration of adenosine and cessation of dormant conduction either spontaneously or by catheter ablation. Transient dormant conduction was re-established by a single bolus of adenosine in 24 of 191 patients (12.6%). Mean duration of adenosine-induced dormant conduction before dipyridamole was 13.1 ± 6.4 s, whereas it was significantly longer at 218.9 ± 165.6 s after dipyridamole (P < 0.0001). Eighteen of the 24 PVs were re-isolated by catheter ablation before spontaneous cessation of dormant conduction, and in 6 cases dormant conduction disappeared spontaneously before PV re-isolation was achieved. CONCLUSION: Dipyridamole significantly prolongs the effect of adenosine to unmask dormant conduction after PV isolation and may thus facilitate its elimination by catheter ablation.

Cibenzoline induced Brugada ECG pattern.

We report a case of a 61-year-old female patient who presented with palpitations. The baseline electrocardiogram showed incomplete right bundle branch block with saddle back pattern of the ST segment in one precordial lead, but without any significant ST elevation. She was treated with oral cibenzoline. The subsequent ECG showed a coved Brugada ECG (type I) pattern, which resolved following the discontinuation of cibenzoline. An ajmaline test reproduced the coved type Brugada ECG pattern. Our case is the first report of oral cibenzoline therapy unmasking the diagnostic coved Brugada ECG pattern in a patient with a baseline normal ECG. Cibenzoline, a class I sodium channel blocker antiarrhythmic drug, should probably be avoided in the treatment of patients with Brugada syndrome.