Combined use of electro-anatomic mapping system and intracardiac echocardiography to achieve zero-fluoroscopy catheter ablation for treatment of paroxysmal atrial fibrillation: a single centre experience.

Fluoroscopy is the principal imaging method for catheter ablation (CA) of atrial fibrillation (AF). However, radiation exposure carries potential health risk to patients and operators alike. Our aim was to study safety and efficacy of zero-fluoroscopy CA of paroxysmal AF with a combined use of electroanatomic mapping system (EAM) and intracardiac echocardiography (ICE). In addition, impact of ICE/EAM automatic integration system and contact force (CF) sensing technology on procedural times were assessed. We included 144 consecutive patients (69% males, age 60 ± 10 years, BMI 29 ± 4,6) referred for CA of symptomatic paroxysmal AF. All procedures were performed only with EAM system and ICE. No fluoroscopy was used. The acute procedural success of complete pulmonary vein isolation was achieved in all patients (100%) and adverse events were detected in eight patients (5.6%). In 53 (37%) patients the use of ICE/EAM automatic integration system shortened procedural times compared to those performed without it (148 ± 35 vs. 187 ± 44 min, p < 0.05). Similarly, 89 (60%) procedures where CF sensing catheter was used were shorter compared to those performed without it (163 ± 41 vs. 188 ± 46 min, p < 0.05). Zero-fluoroscopy approach for treatment of paroxysmal AF seems feasible, safe, and acutely effective. Additional reduction of procedural times could be achieved with the use of ICE/EAM automatic integration system and CF sensing technology.

The tip of the muscle is a dominant location of ventricular ectopy originating from papillary muscles in the left ventricle.

INTRODUCTION: Frequent ventricular premature complexes (VPCs) may cause symptoms and/or lead to deterioration of LV systolic function. Although frequent VPCs may be abolished by catheter ablation, it may be challenging in case of their origin from the LV papillary muscles (PMs). Our collaborative study aimed to analyze in detail the site of origin and the outcome of ablation. METHODS: Consecutive 34 patients (males: 68%; aged 62 ± 12 years; LV ejection fraction: 50 ± 9%) undergoing catheter ablation of VPCs originating from PMs were included. All procedures were guided by intracardiac echocardiography. RESULTS: The size and shape of PMs were highly variable. The length of anterolateral and posteromedial PM was 23 ± 4 mm and 28 ± 7 mm, respectively. In about one-third of patients, the PM was formed by two distinctly separate heads. The ectopic foci were located on anterolateral, posteromedial or both PM in 35%, 56% and 9% of cases, respectively. Their location was found within the distal, mid, or proximal (basal) third of PM in the 67%, 19%, and 14%, respectively. A total of 86% of PM foci were acutely abolished and long-term success was achieved in 65% of patients. Absence of VPCs of other morphologies and a high burden of ectopic activity before ablation were associated with favorable clinical outcome. CONCLUSION: VPCs originate predominantly from the distal portion of the PM. This knowledge may facilitate the mapping in patients with infrequent ectopic beats. Intracardiac echocardiography is of crucial importance for navigation of the ablation catheter and for assessment of its stability at PM target sites.

Electrophysiology of anterograde right-atrial and left-atrial inputs to the atrioventricular node in patients with atrioventricular nodal re-entrant tachycardia.

AIMS: To study anterograde atrioventricular (A-V) nodal electrophysiological properties through the right-atrial (Ri) and left-atrial inputs (Li) under the pharmacological autonomic blockade (AUB) in patients with slow-fast A-V nodal re-entrant tachycardia (AVNRT) and in controls. METHODS AND RESULTS: Twenty-nine patients with slow-fast AVNRT and 15 control subjects were included. Programmed stimulation with single extrastimulus was performed from the right atrial appendage to test the Ri, and from the posterolateral coronary sinus to test the Li. The AUB was induced with intravenous atropine (0.04 mg/kg) and metoprolol (0.15 mg/kg). The A-V nodal conduction times, refractoriness, discontinuous conduction (≥ 40 ms atrial-His interval 'jump'), and inducibility of AVNRT or reciprocating beats were compared. The A-V nodal conduction times were longer: (i) through the Ri than Li, (ii) in patients than controls, and (iii) in baseline than after AUB--at slow rates in both groups and at fast rates in patients through the right input only (P < 0.05-0.001). A significantly longer slow pathway effective refractory period was demonstrated through the Li than the Ri in patients in baseline (P < 0.05). The discontinuous conduction was demonstrated 94 times in 25 of 29 (83%) patients and 15 times in 6 of 15 (40%) controls (P < 0.01), and was most frequently encountered with the Ri testing. Likewise, inducibility was manifested most frequently with the Ri testing (P = 0.08), and decreased after AUB during this testing only (P = 0.05). CONCLUSION: The inherent magnitude of discordance of A-V nodal conduction velocity, refractoriness, and parasympathetic modulation between the Ri and Li to the A-V node may play a role in the aetiology of AVNRT.