Background
Epicardial ganglionated plexuses (GP) have an important role in the pathogenesis of atrial fibrillation (AF). The relationship between anatomical, histological and functional effects of GP is not well known. We previously described atrioventricular (AV) dissociating GP (AVD-GP) locations. In this study, we hypothesised that ectopy triggering GP (ET-GP) are upstream triggers of atrial ectopy/AF and have different anatomical distribution to AVD-GP.
Objectives
We mapped and characterised ET-GP to understand their neural mechanism in AF and anatomical distribution in the left atrium (LA).
Methods
26 patients with paroxysmal AF were recruited. All were paced in the LA with an ablation catheter. High frequency stimulation (HFS) was synchronised to each paced stimulus for delivery within the local atrial refractory period. HFS responses were tagged onto CARTO™ 3D LA geometry. All geometries were transformed onto one reference LA shell. A probability distribution atlas of ET-GP was created. This identified high/low ET-GP probability regions.
Results
2302 sites were tested with HFS, identifying 579 (25%) ET-GP. 464 ET-GP were characterised, where 74 (16%) triggered ≥30s AF/AT. Median 97 (IQR 55) sites were tested, identifying 19 (20%) ET-GP per patient. >30% of ET-GP were in the roof, mid-anterior wall, around all PV ostia except in the right inferior PV (RIPV) in the posterior wall.
Conclusion
ET-GP can be identified by endocardial stimulation and their anatomical distribution, in contrast to AVD-GP, would be more likely to be affected by wide antral circumferential ablation. This may contribute to AF ablation outcomes.
Twenty-one-hour melatonin plasma profiles were studied in 15 normal elderly volunteers from the community, and eight who had been in hospital for more than six weeks and who had not been exposed to strong natural lighting. The hospital group had significantly higher daytime plasma melatonin levels, an earlier nocturnal rise, and the timing of their secretory profiles was more variable. These results suggest that currently used artificial and supplementary natural lighting may not be sufficient to suppress melatonin secretion adequately during daylight hours nor act efficiently to entrain day/night secretion of melatonin in a physiological circadian manner. Raised melatonin levels by day and variable secretory profiles at night may account for certain mood and sleep disorders observed in institutionalized people.
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