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

2021 ◽  
Vol 12 ◽  
Author(s):  
Ling Zhang ◽  
Yankai Guo ◽  
Jiasuoer Xiaokereti ◽  
Guiqiu Cao ◽  
Hongliang Li ◽  
...  

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.

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.


2020 ◽  
Vol 7 (12) ◽  
pp. 1850
Author(s):  
Govind Narayan Srivastava ◽  
Deepanjali Sharma ◽  
Mrityunjay Sharma ◽  
Aiyush Jain

Background: With the emergence of lifestyle diseases in epidemic proportions in developing nations like India, Obstructive sleep apnea syndrome (OSAS) is increasing consistently. OSA brings many adverse consequences, such as systemic hypertension, cardiovascular diseases, obesity, diabetes mellitus, behavioral changes and many other comorbid conditions.  Methods: This is a prospective study of 46 polysomnography proven patients with OSA apnea hypopnea index (AHI) ≥5/h. The study period was from 1st October, 2017 to 31st March, 2019. Subjects were divided into three subgroups according to AHI: mild OSAS: 5<AHI<15, moderate OSAS: 15<AHI<30 and severe OSAS: AHI >30. The patients were thoroughly examined and evaluated for associated comorbidities.  Results: We evaluated 25 men and 21 women with OSA, mean age of 57.7 years (range 30–86). Average weight and body mass index (BMI) of the patients were 86.1 kg (range 65-132) and 33.1 kg/m2 (range 25-46.9) respectively. On evaluation of comorbidities hypertension was on the top 30 (65%) followed by obesity 28 (61%), left ventricular hypertrophy 23 (50%), diabetes mellitus 21 (46%), dyslipidemia and chronic obstructive pulmonary disease in 12 (26%) each. Total no. of comorbidities and multiple comorbidities in a single patient were highest in severe OSA group.Conclusions: OSA predominantly affects middle-aged (>55 years) individuals who are overweight with many having high neck circumference. There is statistically significant positive correlation between AHI and BMI and between number of comorbidities and severity of OSAS. Awareness regarding OSA among the general population and clinicians, wider availability of PSG studies will help in identifying and treating these patients.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
F Dalgaard ◽  
R North ◽  
K Pieper ◽  
B A Steinberg ◽  
K W Mahaffey ◽  
...  

Abstract Background Obstructive sleep apnea (OSA) is common in patients with atrial fibrillation (AF). It is not well understood if OSA impacts cardiovascular outcomes in patients with AF. Purpose To investigate patient characteristics and major adverse cardiovascular and neurological events (MACNE) in patients with AF and OSA. Methods Using the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF I) and ORBIT-AF II we compared the adjusted risk of the composite of cardiovascular death, myocardial infarction, stroke/transient ischemic attack/non-CNS embolism (stroke/SE), and new-onset heart failure (MACNE) according to the presence or absence of OSA, using multivariable adjusted Cox proportional hazard models. Secondary outcomes were the individual components of MACNE. Results Among 22,760 patients with AF, there were 4,045 (17.8%) with OSA at baseline. Median follow-up time was 1.5 (IQR: 1–2.2) years. OSA patients were younger (median [IQR] 68 [61–75] years vs. 74 [66–81] years, were more likely to be male (70.7% vs. 55.3%), and had markedly increased body mass index (BMI) (median 34.6 kg/m2 [29.8–40.2] vs. 28.7 kg/m2 [25.2–33.0]). Those with OSA had a higher prevalence of diabetes (39.2% vs. 25.2%), chronic obstructive pulmonary disease (COPD) (20% vs. 12%), heart failure (32.2% vs. 25.1%), and hyperlipidemia (73.2% vs. 66.7%). After adjustment, the presence of OSA was significantly associated with MACNE (HR: 1.16 [95% CI: 1.03–1.31], p=0.011) [Figure]. Stroke/SE was higher in patients with OSA (HR: 1.38 [95% CI 1.12–1.70], p=0.003). Addition of OSA to a model containing the CHA2DS2-VASc risk factors slightly improved discrimination for stroke/SE: CHA2DS2-VASc risk factors alone C-index (Standard Error) was 0.6867 (0.0125) vs. CHA2DS2-VASc risk factors plus OSA 0.6876 (0.0124), p=0.022. Figure 1. Hazard ratios with 95% confidence intervals and event rates for the association between obstructive sleep apnea and major adverse cardiovascular and neurological events combined and separately. Abbreviations: OSA; obstructive sleep apnea MACNE; major adverse cardiovascular and neurological events, CV; cardiovascular, TIA; transient ischemic attack. Conclusion One in five patients with AF in community practice had OSA. The presence of OSA was associated with higher risk of MACNE and stroke/SE. Addition of OSA to CHA2DS2-VASc risk factors only slightly improved discrimination for the occurrence of stroke. Acknowledgement/Funding The Danish Heart Foundation, T32 NIH Grant HL079896. The ORBIT-AF registry is sponsored by Janssen.


OTO Open ◽  
2021 ◽  
Vol 5 (1) ◽  
pp. 2473974X2198959
Author(s):  
Ahmed Yassin Bahgat

Objective Plasma is formed by creating a high-density energy field within an electrically conductive fluid such as saline. Sometimes ablated bits of tissue get stuck between the electrodes of the wand, obstructing the suction channel. The purpose of this study is to investigate the effect of cooling the irrigating saline during ablation of the hypertrophied tongue base in patients with obstructive sleep apnea. Study Design Prospective randomized controlled trial. Setting An otorhinolaryngology department in Main University hospitals. Methods Sixty adult patients with obstructive sleep apnea and tongue base hypertrophy underwent tongue base ablation surgery. Patients were randomly divided into 2 groups of 30 patients each: cooled saline and room temperature saline. The Coblation wand used was the EVac 70 Xtra HP (Smith & Nephew). Results In this study, a significant difference in operative time (mean ± SD) was seen between groups: 21.2 ± 5.5 minutes in the cold group and 47 ± 9.5 minutes in the control group ( P = .001). The wands in the cold group did not obstruct, while all the wands in the control group were obstructed by tissue clogs with variable degrees, hence wasting more time to clean the wands’ tips. Conclusion Cooling the irrigating saline overcame the problem of wand clogs, and the wand tip did not occlude at all during the procedures, thus saving time lost in wand cleaning and demonstrating a faster and safer surgical procedure. Further studies are needed to identify the hemostatic effect of the cooled saline over the regular one.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
X Wang ◽  
Z Li ◽  
Y Du ◽  
L Jia ◽  
J Fan ◽  
...  

Abstract Background Obstructive sleep apnea (OSA) is closely related to the incidence and progression of coronary artery disease (CAD), but the mechanisms linking OSA and CAD are unclear. C1q/TNF-related protein-9 (CTRP9) is a novel adipokine that protects the heart against ischemic injury and ameliorates cardiac remodeling. Purpose We aimed to ascertain the clinical relevance of CTRP9 with OSA prevalence in patients with CAD. Methods From August 2016 to March 2019, consecutive eligible patients with CAD (n=154; angina pectoris, n=88; acute myocardial infarction [AMI], n=66) underwent cardiorespiratory polygraphy during hospitalization. OSA was defined as an apnea-hypopnea index (AHI) ≥15 events h–1. Plasma CTRP9 concentrations were measured by ELISA method. Results OSA was present in 89 patients (57.8%). CTRP9 levels were significantly decreased in the OSA group than in the non-OSA group (4.7 [4.1–5.2] ng/mL vs. 4.9 [4.4–6.0] ng/mL, P=0.003). The difference between groups was only observed in patients with AMI (3.0 [2.3–4.9] vs. 4.5 [3.2–7.9], P=0.009), but not in patients with AP (5.0 [4.7–5.3] ng/mL vs. 5.1 [4.7–5.9] ng/mL, P=0.571) (Figure 1). Correlation analysis showed that CTRP9 levels were negatively correlated with AHI (r=−0.238, P=0.003) and oxygen desaturation index (r=−0.234, P=0.004), and positively correlated with left ventricular ejection fraction (r=0.251, P=0.004) in all subjects. Multivariate analysis showed that male gender (OR 3.099, 95% CI 1.029–9.330, P=0.044), body mass index (OR 1.148, 95% CI 1.040–1.268, P=0.006), and CTRP9 levels (OR 0.726, 95% CI 0.592–0.890, P=0.002) were independently associated with the prevalence of OSA. Conclusions Plasma CTRP9 levels were independently related to the prevalence of OSA in patients with CAD, suggesting that CTRP9 might play a role in the pathogenesis of CAD exacerbated by OSA. Figure 1. CTRP9 levels in OSA and non-OAS groups Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Natural Science Foundation of China


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