Introduction. The mechanism(s) whereby atrial ectopy induces atrial fibrillation (AF) is still poorly understood.
Methods and Results. In 12 dogs, we determined the refractory period (RP) along the ...right atrium (RA) and right superior pulmonary vein (RSPV), and AF inducibility with and without concurrent stimulation of the anterior right ganglionated plexi (ARGP) at the base of the RSPV. Multielectrode catheters were attached to the RSPV and RA with the distal electrodes close to ARGP. The RP and window of vulnerability (WOV), i.e., the longest S1–S2 minus the shortest S1–S2 at which AF was induced, were measured before and during incremental levels of ARGP stimulation. Mapping of the onset of AF was performed using the EnSite® mapping system (St. Jude Medical, St. Paul, MN, USA) positioned in the RA.
A single premature depolarization (PD) from the RSPV that did not induce AF without ARGP stimulation could do so with ARGP stimulation. The onset of AF consistently arose at the myocardium subtending the ARGP. With GP stimulation, the average WOV at the RSPV‐atrial junction was significantly wider than at the RA appendage (65 ± 27 vs. 8 ± 17 msec, P < 0.05) or further along the RSPV sleeve (48 ± 39 vs. 10 ± 20 msec, P < 0.05). Even without GP stimulation, high intensity (10–20 mA) premature stimuli delivered at the RA appendage induced AF, originating from atrial tissue subtending the ARGP, presumably due to axonal conduction that activated the ARGP.
Conclusion. GP stimulation, subthreshold for atrial excitation, converts isolated PDs into AF‐inducing PDs, suggesting that autonomic tone may play a critical role in the initiation of paroxysmal AF.
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and is associated with significant morbidity and mortality. Obstructive sleep apnoea (OSA) is common among patients with AF. Growing ...evidence suggests that OSA is associated with the initiation and maintenance of AF. This association is independent of obesity, body mass index and hypertension. OSA not only promotes initiation of AF but also has a significant negative impact on the treatment of AF. Patients with untreated OSA have a higher AF recurrence rate with drug therapy, electrical cardioversion and catheter ablation. Treatment with continuous positive airway pressure (CPAP) has been shown to improve AF control in patients with OSA. In this article, we will review and discuss the pathophysiological mechanisms of OSA that may predispose OSA patients to AF as well as the standard and emerging therapies for patients with both OSA and AF.
The authors intended to investigate if 28-mm cryoballoon (CB) ablation also modifies the 4 major atrial ganglionaated plexi (GP).
The major atrial GP facilitate the initiation and maintenance of ...atrial fibrillation (AF). The 28-mm CB covers a large surface area of the left atrium and probably the GP areas.
High-frequency stimulation (20 Hz) was delivered to the area of anterior right GP (ARGP), inferior right GP, superior left (SLGP), and inferior left GP (ILGP). Positive GP sites were defined as a prolongation of R-wave to R-wave (RR) interval during AF by >50%. The area of each GP before and after CB ablation was compared.
A total of 18 patients with paroxysmal AF who underwent CB and radiofrequency ablation and had positive GP sites were reviewed. The Wilcoxon signed-rank test was used to assess the effects of CB ablation on each GP. There was a statistically significant difference in the area of all 4 GP after CB ablation: 1) ARGP area: 2.9 cm2 (interquartile range IQR: 2.1 to 3.5 cm2) pre-CB, 0.1 cm2 (IQR: 0 to 0.6 cm2) post-CB, p = 0.0002; 2) inferior right GP area: 2.1 cm2 (IQR: 0.9 to 2.9 cm2) pre-CB, 0.5 cm2 (IQR: 0 to 1.7 cm2) post-CB, p = 0.001; 3) SLGP area: 1.4 cm2 (IQR: 0.6 to 2.4 cm2) pre-CB, 0 cm2 (IQR: 0 to 0 cm2) post-CB, p = 0.0002; and 4) ILGP area: 1.3 cm2 (IQR: 0.3 to 2.2 cm2) pre-CB, 0.3 cm2 (IQR: 0 to 1.6 cm2) post-CB, p = 0.008.
The surface area of all 4 of the major atrial GP was substantially reduced by CB ablation. The SLGP and ARGP had the largest, whereas the ILGP had the least percent of reduction following CB ablation. Part of the therapeutic effects of CB ablation may result from modifying the 4 major atrial GP.
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Aging of the cardiovascular regulatory function manifests as an imbalance between the sympathetic and parasympathetic (vagal) components of the autonomic nervous system (ANS). The most characteristic ...change is sympathetic overdrive, which is manifested by an increase in the muscle sympathetic nerve activity (MSNA) burst frequency with age. Age-related changes that occur in vagal nerve activity is less clear. The resting tonic parasympathetic activity can be estimated noninvasively by measuring the increase in heart rate occurring in response to muscarinic cholinergic receptor blockade; animal study models have shown this to diminish with age. Humoral, cellular, and neural mechanisms work together to prevent non-resolving inflammation. This review focuses on the mechanisms underlying age-related alternations in the ANS and how an imbalance in the ANS, evaluated by MSNA and heart rate variability (HRV), potentially facilitates inflammation when the homeostatic mechanisms between reflex neural circuits and the immune system are compromised, particularly the dysfunction of the cholinergic anti-inflammatory reflex. Physiologically, the efferent arm of this reflex acts via the
α
7 nicotinic acetylcholine receptors expressed in macrophages, monocytes, dendritic cells, T cells, and endothelial cells to curb the release of inflammatory cytokines, in which inhibition of NF‑κB nuclear translocation and activation of a JAK/STAT-mediated signaling cascade in macrophages and other immune cells are implicated. This reflex is likely to become less adequate with advanced age. Consequently, a pro-inflammatory state induced by reduced vagus output with age is associated with endothelial dysfunction and may significantly contribute to the development and propagation of atherosclerosis, heart failure, and hypertension. The aim of this review is to summarize the relationship between ANS dysfunction, inflammation, and endothelial dysfunction in the context of aging. Meanwhile, this review also attempts to describe the role of HRV measures as a predictor of the level of inflammation and endothelial dysfunction in the aged population and explore the possible therapeutical effects of vagus nerve stimulation.
The present study investigated the safety and efficacy of mapping and ablating isolated premature atrial contractions (PACs) in patients with a structurally normal heart, as well as whether the ...elimination of PACs by radiofrequency catheter ablation (RFCA) improved symptoms and the quality of life.
Forty-three consecutive patients with frequent, symptomatic, and drug-refractory PACs, but without atrial tachyarrhythmias (≥5 beats), were enrolled. In all patients, we performed physical, laboratory, and imaging examinations to exclude structural heart disease. The quality of life questionnaire SF-36 before and 3 months after RFCA was performed in each patient.
Twenty-three men and 20 women with an average age of 52.6 ± 17.6 years were finally enrolled. The mean number of PACs was 21,685 ± 9,596 per 24 h, and the mean PACs' burden was 28.9 ± 13.7%. Short runs of tachycardia (<5 atrial beats) were observed in 32 patients (74.4%). All patients underwent successful RFCA without complications. The activation time at the successful ablation sites preceded the onset of the P-wave by 36 ± 7.6 ms. During 15 ± 8 months of follow-up, the recurrence of PACs was observed in 2 patients. The 24-h PAC burden was significantly reduced 3 months after RFCA (mean 0.5%,
< 0.05). The quality of life scores were significantly increased 3 months after RFCA (all
< 0.05).
RFCA was feasible, safe, and effective to eliminate isolated frequent, symptomatic, and drug-refractory PACs in patients with a structurally normal heart. The elimination of PACs by RFCA significantly improved symptoms and the quality of life.
Reply: Vagal Modulation of Atrial Fibrillation Stavrakis, Stavros; Humphrey, Mary Beth; Po, Sunny S.
Journal of the American College of Cardiology,
08/2015, Letnik:
66, Številka:
8
Journal Article
The ganglionated plexi (GP) located at the junction of the superior vena cava, aorta, and right pulmonary artery (SVC-Ao GP) was proposed to be the "head station" between the extrinsic and the ...intrinsic cardiac autonomic nervous system (ECANS and ICANS, respectively).
To investigate the chronic effects after interrupting the ECANS-ICANS connections by ablating the SVC-Ao GP.
A right thoracotomy in 10 dogs allowed stimulation at the right superior and inferior pulmonary veins (RSPV and RIPV, respectively), right atrial appendage (RAA), and SVC to determine effective refractory period (ERP) and atrial fibrillation (AF) inducibility in the first operation. Group 1 (n = 5) received SVC-Ao GP ablation; group 2 (n = 5) received no ablation. A second operation and the same measurements were made 10 weeks later. A pacemaker with lead implanted at the RSPV recorded atrial fibrillation or tachycardia (AF/AT).
During the first operation in group 1, ERPs increased significantly in the SVC but not at the RSPV, RIPV, or RAA site immediately after ablation, whereas ERPs decreased significantly in the RSPV, RIPV, and RAA but not the SVC in the second operation performed 10 weeks later (compared to the ERP in the first operation). ERPs decreased and AF/AT burden increased significantly from weeks 4 and 5, respectively, after the first operation in group 1 dogs. The ERP and AF/AT burden in group 2 remained unchanged between operations.
Ablation of the head station GP between the ECANS and the ICANS prolonged the ERP acutely, but shortened regional ERPs and increased AF/AT burden chronically, suggesting that the ECANS may tonically inhibit the ICANS activity.
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