The Association of Obstructive Sleep Apnea in Ischemia with No Obstructive Coronary Artery Disease – A Pilot Study.

Author(s):  
Eng Lee Ooi ◽  
Sharmalar Rajendran ◽  
Dian Andina Munawar ◽  
Khin Hnin ◽  
Gnanadevan Mahadavan ◽  
...  
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 ◽  
...  

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.


2018 ◽  
Vol 23 (4) ◽  
pp. 331-339 ◽  
Author(s):  
Daniel Shpilsky ◽  
Sebhat Erqou ◽  
Sanjay R Patel ◽  
Kevin E Kip ◽  
Oluremi Ajala ◽  
...  

Studies have reported an association between obstructive sleep apnea (OSA) and cardiovascular disease (CVD) morbidity and mortality. Proposed mechanisms include endothelial dysfunction and atherosclerosis. We aimed to investigate the associations of OSA with endothelial dysfunction and subclinical atherosclerotic coronary artery disease (CAD), and assess the impact of race on these associations. We used data from the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) study, a community-based prospective cohort with approximately equal representation of black and white participants. OSA severity was measured in 765 individuals using the apnea-hypopnea index (AHI). Endothelial dysfunction was measured using the Endo-PAT device, expressed as Framingham reactive hyperemia index (F_RHI). Coronary artery calcium (CAC), a marker of subclinical CAD, was quantified by electron beam computed tomography. There were 498 (65%) female participants, 282 (37%) black individuals, and 204 (26%) participants with moderate/severe OSA (AHI ≥15). In univariate models, moderate/severe OSA was associated with lower F_RHI and higher CAC, as well as several traditional CVD risk factors including older age, male sex, hypertension, diabetes, higher body mass index, and lower high-density lipoprotein cholesterol levels. In a multivariable model, individuals with moderate/severe OSA had 10% lower F_RHI and 35% higher CAC, which did not reach statistical significance ( p=0.08 for both comparisons). There was no significant interaction of race on the association of OSA with F_RHI or CAC ( p-value >0.1 for all comparisons). In a community-based cohort comprised of black and white participants, moderate/severe OSA was modestly associated with endothelial dysfunction and subclinical atherosclerotic CAD. These associations did not vary by race.


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