Neuromodulatory Approaches for Atrial Fibrillation Ablation

In this review, the authors describe evolving alternative strategies for the management of AF, focusing on non-invasive and percutaneous autonomic modulation. This modulation can be achieved – among other approaches – via tragus stimulation, renal denervation, cardiac afferent denervation, alcohol injection in the vein of Marshall, baroreceptor activation therapy and endocardial ganglionated plexi ablation. Although promising, these therapies are currently under investigation but could play a role in the treatment of AF in combination with conventional pulmonary vein isolation in the near future.

Potential value of the low frequency/high frequency ratio of heart rate variability to guide atrial fibrillation ablation procedures

Funding Acknowledgements Type of funding sources: None. Background. The differentiation between vagally and non-vagally mediated atrial fibrillation (AF) could be useful to decide adding ganglionated plexi ablation (GPA) to pulmonary vein isolation (PVI) in patients with vagally mediated AF onset. The role of the autonomic nervous system in triggering paroxysmal AF can be analyzed through heart rate variability (HRV) parameters. The low frequency/high frequency ratio (LF/HF) is used as an index of sympatho-vagal interaction. Based on clinical criteria, values of LF/HF <1.5 are considered to reflect an increase of vagal modulation. Purpose Identify patients with paroxysmal AF who may benefit from GPA in addition to PVI, based on analysis of HRV parameters Material and methods From our database of unselected Holter recordings containing paroxysmal AF episodes, 199 analyzable AF onsets were labelled. We analyzed HRV frequential parameters by segments every 300 RR intervals to identify adrenergic and vagal onsets of AF episodes. We categorized AF onsets, depending of their respective values of LF/HF. We also checked the relationship of these parameters to heart rate (HR). We followed the evolution of the mean normalized values of LF/HF from the beginning of the recordings to the AF onsets (see figure). Results We found a progressive increase of LF/HF in normalized units (mean [95% confidence interval]) from 2.44 [2.12-2.76] to 3.12 [2.85-3.39] in the adrenergic group (n = 113) and a progressive decrease of LF/HF from 1.51 [1.28-1.75] to 1.02 [0.95-1.09] in the vagal group (n = 86). Differences between adrenergic and vagal AF were highly significant using Mann-Whitney test (p < 0.001). A given patient shows the same type of AF in 80% of cases. We found no correlation between frequential parameters and HR. Conclusions Our data show potential added value of frequential HRV analysis to guide additional ganglionated plexi ablation to PVI. This remains to be demonstrated in a prospective study. The ratio LF/HF should be considered to optimize the decision-making process for the ablation procedure. Abstract Figure. Frequential HRV parameters before AF

Ganglionated Plexi Ablation Suppresses Chronic Obstructive Sleep Apnea-Related Atrial Fibrillation by Inhibiting Cardiac Autonomic Hyperactivation

Background: Previous studies have reported that right pulmonary artery ganglionated plexi (GP) ablation could suppress the onset of atrial fibrillation (AF) associated with obstructive sleep apnea (OSA) within 1 h.Objective: This study aimed to investigate the effect of superior left GP (SLGP) ablation on AF in a chronic OSA canine model.Methods and Results: Fifteen beagles were randomly divided into three groups: control group (CTRL), OSA group (OSA), and OSA + GP ablation group (OSA + GP). All animals were intubated under general anesthesia, and ventilation-apnea events were subsequently repeated 4 h/day and 6 days/week for 12 weeks to establish a chronic OSA model. SLGP were ablated at the end of 8 weeks. SLGP ablation could attenuate the atrial effective refractory period (ERP) reduction and decrease ERP dispersion, the window of vulnerability, and AF inducibility. In addition, chronic OSA leads to left atrial (LA) enlargement, decreased left ventricular (LV) ejection fraction, glycogen deposition, increased necrosis, and myocardial fibrosis. SLGP ablation reduced the LA size and ameliorated LV dysfunction, while myocardial fibrosis could not be reversed. Additionally, SLGP ablation mainly reduced sympathovagal hyperactivity and post-apnea blood pressure and heart rate increases and decreased the expression of neural growth factor (NGF), tyrosine hydroxylase (TH), and choline acetyltransferase (CHAT) in the LA and SLGP. After SLGP ablation, the nucleotide-binding oligomerization domain (NOD)-like receptor signaling pathway, cholesterol metabolism pathway, and ferroptosis pathway were notably downregulated compared with OSA.Conclusions: SLGP ablation suppressed AF in a chronic OSA model by sympathovagal hyperactivity inhibition. However, there were no significant changes in myocardial fibrosis.