scholarly journals Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea

2021 ◽  
Vol 10 (15) ◽  
pp. 3413
Author(s):  
Afrouz Behboudi ◽  
Tilia Thelander ◽  
Duygu Yazici ◽  
Yeliz Celik ◽  
Tülay Yucel-Lindberg ◽  
...  

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1176
Author(s):  
Yeliz Celik ◽  
Hale Yapici-Eser ◽  
Baran Balcan ◽  
Yüksel Peker

Excessive daytime sleepiness (EDS) is a factor associated with both obstructive sleep apnea (OSA) and depressive symptoms. Continuous positive airway pressure (CPAP) treatment may decrease EDS in adults with OSA; however, the modulatory role of depressive symptoms on the improvement of EDS is not known. We aimed to explore the association between subscales of the Zung Self-rated Depression Scale (SDS) and Epworth Sleepiness Scale (ESS) over a 2-year period in coronary artery disease (CAD) patients with OSA. This was a post-hoc analysis of the RICCADSA cohort, in which 399 adults with CAD (155 sleepy OSA [apnea–hypopnea index ≥ 15/h] and ESS score ≥ 10, who were offered CPAP; and 244 nonsleepy OSA [ESS < 10]), randomized to CPAP [n = 122] or no-CPAP [n = 122]) were included. Three factors were extracted from the Zung SDS, based on the principal component analysis: F1, cognitive symptoms and anhedonia; F2, negative mood; and F3, appetite. In a mixed model, the ESS score decreased by 3.4 points (p < 0.001) among the sleepy OSA phenotype, which was predicted by the decline in the F2, but not in the F1 and F3 scores. The fixed effects of time were not significant in the nonsleepy OSA groups, and thus, further analyses were not applicable. Additional within-group analyses showed a significant decrease in all subscales over time both in the sleepy and nonsleepy OSA patients on CPAP whereas there was a significant increase in the nonsleepy OSA group randomized to no-CPAP. We conclude that the improvement in negative mood symptoms of depression, but not changes in cognitive symptoms and anhedonia as well as appetite, was a significant predictor of decline in the ESS scores over a 2-year period in this CAD cohort with sleepy OSA on CPAP treatment.


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


2015 ◽  
Vol 16 (1) ◽  
pp. 160-167 ◽  
Author(s):  
Helena Glantz ◽  
Erik Thunström ◽  
Magnus C. Johansson ◽  
Cecilia Wallentin Guron ◽  
Harun Uzel ◽  
...  

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