Effect of fluoroscopy frame rate on radiation exposure and in-hospital outcomes in three-dimensional electroanatomic mapping guided procedures.

BACKGROUND: Fluoroscopic imaging involves exposure of the patients and the laboratory staff to ionizing radiation. One of the strategies that reduce such exposure in an electrophysiology laboratory is using a three-dimensional electroanatomic mapping (3D EAM) system for performing these procedures. In this analysis, we have analyzed the effect of fluoroscopy frame rate on the radiation exposure and in-hospital outcomes in ablation procedures performed under 3D EAM guidance. METHODS: We retrospectively analyzed all the ablation procedures performed under 3D EAM guidance at our institute from September 2015 to December 2018. The procedures were divided into two groups based on whether the procedures were performed before (pre) or after (post) January 26, 2018. After January 2018, fluoroscopy was used at a frame rate of 3.75 frames per second (fps). Radiation exposure indices and in-hospital outcomes were compared between the two groups. RESULTS: Ablation procedures included in the analysis were ventricular arrhythmias (n = 192), atrial flutter (115), atrial tachycardia (AT) (43), and atrial fibrillation (AF) (30). Over the study period, there was a significant reduction in procedure time, fluoroscopy time, dose area product, and effective dose (ED) (P < .001). Except for AT and AF ablation procedures, there was a significant reduction in the radiation exposure indices when the "post" group was compared with the "pre" group (P ≤ .02). The decrease in the frame rate had no significant effect on in-hospital outcomes. CONCLUSION: The use of 3D EAM combined with decreasing the fluoroscopy frame rate significantly reduced the total radiation exposure without adversely affecting in-hospital outcomes.

Clinical and Electrophysiological Correlates of Incessant Ivabradine-Sensitive Atrial Tachycardia.

BACKGROUND: Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT. METHODS: The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine. RESULTS: Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites (P=0.046). CONCLUSIONS: Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.