Rhythmia zero-fluoroscopy workflow with high-power, short-duration ablation: retrospective analysis of procedural data.

BACKGROUND: Fluoroscopy is commonly used during atrial fibrillation (AF) ablation to guide catheter navigation and placement. Technology improvements have significantly reduced fluoroscopy time, and subsequent radiation dose, necessary to perform successful ablations. However, there is still no amount of radiation exposure known to be completely safe. The aim of this manuscript is to describe a detailed zero-fluoroscopy RHYTHMIA HDx workflow for AF ablation. METHODS: This was an observational, single-center experience to describe the technique, acute procedural success, and safety using a novel zero-fluoroscopy workflow with the RHYTHMIA HDx mapping system and intracardiac echocardiography (ICE). Seventy-two consecutive patients undergoing de novo or redo AF ablation were retrospectively analyzed. Venous access was guided with ultrasound. ICE combined with the mapping system's magnetic tracking and sheath detection was used for precise catheter placement in the coronary sinus, at the transseptal puncture, and in the left atrium. A high-power, short-duration ablation strategy guided by local impedance was used. Pulmonary vein isolation was performed or touched up for all patients with additional lines added at the operator's discretion. RESULTS: Using this zero-fluoroscopy workflow, all patients achieved acute isolation with no significant procedure-related complications. Average procedure time was 73.7 ± 16.2 min, which included persistent (58%) and paroxysmal (42%) AF cases, and no procedures required conversion to fluoroscopy. CONCLUSIONS: In this experience, a zero-fluoroscopy workflow using the RHYTHMIA HDx mapping system combined with ICE was feasible and safe for ablation in a heterogenous AF population. This approach, in the appropriate patient population, can eliminate radiation exposure to patients and staff.

Slow Conduction Corridors and Pivot Sites Characterize the Electrical Remodeling in Atrial Fibrillation.

OBJECTIVES: This study aimed to evaluate the progression of electrophysiological phenomena in a cohort of patients with paroxysmal atrial fibrillation (PAF) and persistent atrial fibrillation (PsAF). BACKGROUND: Electrical remodeling has been conjectured to determine atrial fibrillation (AF) progression. METHODS: High-density electroanatomic maps during sinus rhythm of 20 patients with AF (10 PAF, 10 PsAF) were compared with 5 healthy control subjects (subjects undergoing ablation of a left-sided accessory pathway). A computational postprocessing of electroanatomic maps was performed to identify specific electrophysiological phenomena: slow conductions corridors, defined as discrete areas of conduction velocity <50 cm/s, and pivot points, defined as sites showing high wave-front curvature documented by a curl module >2.5 1/s. RESULTS: A progressive decrease of mean conduction velocity was recorded across the groups (111.6 ± 55.5 cm/s control subjects, 97.1 ± 56.3 cm/s PAF, and 84.7 ± 55.7 cm/s PsAF). The number and density of slow conduction corridors increase in parallel with the progression of AF (8.6 ± 2.2 control subjects, 13.3 ± 3.2 PAF, and 20.5 ± 4.5 PsAF). In PsAF the atrial substrate is characterized by a higher curvature of wave-front propagation (0.86 ± 0.71 1/s PsAF vs 0.74 ± 0.63 1/s PAF; P = 0.003) and higher number of pivot points (25.1 ± 13.8 PsAF vs 9.5 ± 6.7 PAF; P < 0.0001). Slow conductions: corridors were mostly associated with pivot sites tending to cluster around pulmonary veins antra. CONCLUSIONS: The electrical remodeling hinges mainly on corridors of slow conduction and higher curvature of wave-front propagation. Pivot points associated to SC corridors may be the major determinants for functional localized re-entrant circuits creating the substrate for maintenance of AF.

Comparison of Coronary Atherosclerotic Plaque Burden and Composition of Culprit Lesions Between Cigarette Smokers and Non-Smokers by In Vivo Virtual Histology Intravascular Ultrasound.

Cigarette smoking is a major risk factor in the progression of atherosclerosis and has been shown to cause endothelial dysfunction, inflammation, and modification of lipid profile. However, its role in the pathogenesis of vulnerable coronary plaque remains unknown. We investigated the relationship between cigarette smoking and the development of vulnerable coronary artery plaque using virtual histology intravascular ultrasound (VH-IVUS). Data from consecutive patients who underwent VH-IVUS assessment of native coronary artery stenosis during clinically indicated cardiac catheterization at our institution over a 2-year period were analyzed. Baseline demographic and study characteristics were collected on all patients. Coronary plaque compositions of the culprit lesion were compared on bivariate and multivariate analysis. We analyzed data on 160 patients with a mean age of 60 ± 11 years. Sixty-nine percent of these patients were admitted for acute coronary syndrome, 31% were smokers, and the mean plaque burden was 66%. On average, 58% of these plaques were fibrous, 19% were fibro-fatty, 18.3% had a necrotic core, and 5.4% were composed of dense calcium. Cigarette smokers had a higher burden of necrotic core (20.7% vs 17.2%; P=.04). On multivariate analysis, cigarette smoking was independently associated with a 4.54% increase in the burden of necrotic core (P=.01). Older age (>80 years) was also a predictor of higher necrotic core burden (P=.02). In conclusion, cigarette smoking is associated with a higher burden of necrotic core in coronary atherosclerotic plaques. This may represent one of the mechanisms for increased cardiovascular events.