scholarly journals Effects and Mechanisms of Cutting Upper Thoracic Sympathetic Trunk on Ventricular Rate in Ambulatory Canines with Persistent Atrial Fibrillation

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Jie Cai ◽  
Min Tang ◽  
Hao Liu ◽  
Shiao Ding ◽  
Rongxin Lu ◽  
...  

Objective. The purpose is to observe the effects and neural mechanism of cutting upper thoracic sympathetic trunk (TST) on the ventricular rate (VR) during persistent atrial fibrillation (AF). Methods. Twelve beagle dogs were halving to the control group and experimental group, 6 dogs for each group. Both groups were performed with left atrial rapid pacing (600 beats/min) to induce sustained AF. The experimental group underwent cutting upper TST  after a sustained AF model was established, while the control group received thoracotomy without cutting TST. Bilateral stellate ganglion (SG) and left atrial myocardium were harvested for tyrosine-hydroxylase (TH) immunohistochemical staining. Results. After cutting upper TST for 30 minutes, the average VR was 121.5 ± 8.7 bpm (95% CI, 114.8 to 128.0) in the experimental group, which was significantly slower than that of the control group (144.5 ± 4.2 bpm (95% CI, 141.5 to 148.0)) ( P < 0.001 ). After cutting upper TST for 1 month, the average VR of the experimental group (106.5 ± 4.9 bpm (95% CI, 102.0 to 110.0)) was also significantly slower versus that of the control group (139.2 ± 5.6 bpm (95% CI, 135.0 to 143.8)) ( P < 0.001 ). Compared with the control group, both left stellate ganglion (LSG) and right stellate ganglion (RSG) of the experimental group caused neural remodeling characterized by decreased ganglionic cell density and reduced TH staining. TH-positive component was significantly decreased in the left atrium of the experimental group compared with the control group. Conclusions. Cutting upper TST could reduce fast VR during persistent AF. Cutting upper TST induced bilateral SG neural remodeling and reduced sympathetic nerve density in the left atrium, which could contribute to the underlying mechanism of VR control during AF.

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247308
Author(s):  
Jiasuoer Xiaokereti ◽  
Yan-Kai Guo ◽  
Zhen-Yu Dong ◽  
Mei Ma ◽  
Yan-Mei Lu ◽  
...  

Objective Autonomic imbalance plays a crucial role in obstructive sleep apnea (OSA) associated atrial fibrillation (AF). Here, we investigated the potential neural mechanism of AF induced by OSA. Methods Ten dogs were divided into control group (n = 5) and OSA group (n = 5). The chronic OSA model was established by repeat apnea-ventilation cycles for 4 hours a day for 12 weeks. During the process of model establishment, arterial blood gases, atrial effective refractory period (AERP), AF inducibility, normalized low-frequency power (LFnu), normalized high-frequency power (HFnu), and LFnu/ HFnu were evaluated at baseline, 4th week, 8th week, and 12th week. Nerve activities of left stellate ganglion (LSG) and left vagal nerve(LVN) were recorded. Tyrosine hydroxylase(TH), choline acetyltransferase(CHAT), PGP9.5, nerve growth factor(NGF), and c-Fos were detected in the left atrium, LSG, and LVN by immunohistochemistry and western blot. Moreover, high-frequency stimulations of LSG and LVN were conducted to observe the AF inducibility. Results Compared with the control group, the OSA group showed significantly enhanced neural activity of the LSG, increased AF inducibility, and shortened AERP. LFnu and LFnu/HFnu were markedly increased in the OSA group, while no significant difference in HFnu was observed. TH-positive and PGP9.5-positive nerve densities were significantly increased in the LSG and left atrium. Additionally, the protein levels of NGF, c-Fos, and PGP9.5 were upregulated both in the LSG and left atrium. AF inducibility was markedly increased under LSG stimulation without a stimulus threshold change in the OSA group. Conclusions OSA significantly enhanced LSG and left atrial neural remodeling, and hyperactivity of LSG may accelerate left atrial neural remodeling to increase AF inducibility.


2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Yingming Zhao ◽  
Kangting Tang ◽  
Xu Tianbao ◽  
Junhong Wang ◽  
Jin Yang ◽  
...  

Atrial fibrillation (AF) progression is generally accompanied by increased atrial fibrosis and atrial structural remodeling. Lysyl oxidase-like 2 (LOXL2) is known to play an important role in many fibrotic conditions, including cardiac fibrosis. The present study aimed to explore the relationship between serum LOXL2 levels and AF. Fifty-four AF patients and 32 control subjects were enrolled in the study. High-density three-dimensional electroanatomic mapping was performed, and mean bipolar voltage was assessed in AF patients. LOXL2 levels were measured by enzyme-linked immunosorbent assay. All patients underwent echocardiography to assess left atrium size and left ventricle function. Serum LOXL2 levels were significantly elevated in AF patients compared with the control group (526.81 ± 316.82 vs 240.94 ± 92.51 pg/ml, P<0.01). In addition, serum LOXL2 level was significantly correlated with the size of the left atrium (LAD) (r2 = 0.38, P<0.01). Furthermore, the serum LOXL2 levels were significantly higher in AF patients with LAD ≥ 40 mm compared with those with LAD < 40 mm (664.34 ± 346.50 vs 354.90 ± 156.23 pg/ml, P<0.01). And the Spearman’s correlation analysis further revealed that the mean bipolar left atrial voltage was inversely correlated with the LOXL2 (r2 = −0.49, P<0.01) in AF patients. Multivariate regression analysis further demonstrated that serum LOXL2 [odds ratio (OR) 1.013, 95% confidence interval (CI) 1.002–1.024, P<0.05] and LAD (OR 1.704, 95% CI 1.131–2.568, P<0.01) were independent predictors of AF. In conclusion, serum LOXL2 levels were significantly elevated and were correlated with the degree of left atrial fibrosis in AF patients.


Kardiologiia ◽  
2021 ◽  
Vol 61 (5) ◽  
pp. 17-22
Author(s):  
E. S. Mazur ◽  
V. V. Mazur ◽  
N. D. Bazhenov ◽  
Yu. A. Orlov

Aim      To compare the incidence of cardiovascular complications (CVC) in patients with persistent atrial fibrillation (AF) following thrombus dissolution in the left atrial appendage (LAA) and in patients with persistent AF without preceding LAA thrombosis.Material and methods  The main group included 43 patients who had been diagnosed with LAA thrombosis on the first examination, transesophageal echocardiography, and who showed dissolution of the thrombus on a repeated study performed after 7.1+2.0 weeks of the anticoagulant treatment. The control group consisted of 123 patients with a risk score >0 for men without LAA thrombosis and score >1 for women without LAA thrombosis according to the CHA2DS2‑VASc scale. The patients were followed up for 47.3±17.9 months. The following unfavorable outcomes were recorded: all-cause mortality, ischemic stroke or systemic thromboembolism, hemorrhagic stroke or severe bleeding, and myocardial infarction (MI).Results Unfavorable clinical outcomes were observed in 39.5 % of patients in the main group and in 3.3 % of patients in the control group (p<0.001). Furthermore, the incidence of ischemic stroke (relative risk (RR), 12.9; 95 % confidence interval (CI), 2.89–57.2), and MI (RR, 5.72; 95 % CI, 1.09–30.1) was higher in the main group. However, the number of MI cases in both groups and the number of stroke cases in the control group increased during the entire follow-up period, while the number of stroke cases rapidly increased only during the first year of follow-up.Conclusion      In patients with persistent AF, the risk of CVC after LAA thrombus dissolution remains significantly higher than in patients with AF without LAA thrombosis.


EP Europace ◽  
2017 ◽  
Vol 19 (12) ◽  
pp. 1958-1966 ◽  
Author(s):  
Alex J.A. McLellan ◽  
Sandeep Prabhu ◽  
Alex Voskoboinik ◽  
Michael C.G. Wong ◽  
Tomos E. Walters ◽  
...  

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