Dataset Information

Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease.

ABSTRACT: Background:Obstructive sleep apnea (OSA) is closely related to the incidence and progression of coronary artery disease (CAD), and the mechanisms linking OSA and CAD are multifactorial. C1q/TNF-related protein-9 (CTRP9) is a novel adipokine that protects the heart against ischemic injury and ameliorates cardiac remodeling. 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. OSA was defined as an apnea-hypopnea index (AHI) ?15 events·h-1. Plasma CTRP9 concentrations were measured by ELISA method. Results:Moderate/severe OSA was present in 89 patients (57.8%). CTRP9 levels were significantly decreased in the moderate/severe OSA group than in the no/mild 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). 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), BMI (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 moderate/severe OSA. Conclusions:Plasma CTRP9 levels were independently related to the prevalence of moderate/severe OSA in patients with CAD, suggesting that CTRP9 might play a role in the pathogenesis of CAD exacerbated by OSA.

SUBMITTER: Li Z

PROVIDER: S-EPMC7426787 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease.

Li Zexuan Z Du Yunhui Y Jia Lixin L Fan Jingyao J Guo Ruifeng R Ma Xinliang X Wang Xiao X Nie Shaoping S Wei Yongxiang Y

Mediators of inflammation 20200805

<h4>Background</h4>Obstructive sleep apnea (OSA) is closely related to the incidence and progression of coronary artery disease (CAD), and the mechanisms linking OSA and CAD are multifactorial. C1q/TNF-related protein-9 (CTRP9) is a novel adipokine that protects the heart against ischemic injury and ameliorates cardiac remodeling. We aimed to ascertain the clinical relevance of CTRP9 with OSA prevalence in patients with CAD.<h4>Methods</h4>From August 2016 to March 2019, consecutive eligible pat ...[more]

PMID: 32831639

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Project description:Obstructive sleep apnea (OSA) is prevalent in obese subjects. Plasma adiponectin level in obese subjects is decreased. Whether reduced adiponectin level is associated with OSA is unknown. Participants without a previous diagnosis of OSA or who have not been treated with continuous positive airway pressure were enrolled and parameters of interest were collected. Polysomnography was performed to evaluate the presence of OSA and the severity of OSA as indexed by the apnea-hypopnea index (AHI). Between-group differences were analyzed. Pearson correlation analysis was used to evaluate the association between body mass index (BMI) with plasma levels of adiponectin and C-reactive protein (CRP) and AHI; and the association between plasma adiponectin level with CRP and AHI was also evaluated. Logistic regression analysis was conducted to evaluate the association between per 1-SD standardized decrease of plasma adiponectin level and the prevalence of OSA using stepwise adjustment models. A total of 486 participants were enrolled and the mean BMI was 26.9 ± 6.2 kg/m with obesity prevalence of 28%; and the mean AHI was 12.6 ± 8.9 per sleep hour with OSA prevalence of 42%. The mean adiponectin level was 18.4 ± 10.6 μg/mL. Compared with the nonobese group, participants in the obese group had higher BMI, neck girth, waist circumference, and AHI (P < .05 for all comparisons). The prevalence of OSA (51% vs 37%) and the proportion of moderate OSA (49% vs 42%) were also significantly higher, while adiponectin level (14.6 ± 8.7 μg/mL vs 20.7 ± 10.5 μg/mL) was significantly lower. In the obese group, plasma adiponectin level was decreased gradually with the increasing severity of OSA, which was not observed in the nonobese group. BMI was negatively correlated with adiponectin while positively correlated with CRP and AHI; and adiponectin was negatively correlated with both CRP and AHI. After adjusted for covariates including BMI and waist circumference, adiponectin remained significantly associated with OSA prevalence with odds ratio of 1.20 (95% confidence interval 1.12-1.65). In summary, our preliminary study suggests that in obese subjects, plasma adiponectin level is associated with the prevalence of OSA.

Project description:RationaleWe recently demonstrated that patients with coronary artery disease (CAD) and obstructive sleep apnea (OSA) carrying the tumor necrosis factor-alpha (TNF-α) A allele had increased circulating TNF-α levels compared with the ones carrying the TNF-α G allele. In the current study, we addressed the effect of TNF-α (-308G/A) gene polymorphism on circulating TNF-α levels following continuous positive airway pressure (CPAP) therapy.MethodsThis study was a secondary analysis of the RICCADSA trial (NCT00519597) conducted in Sweden. CAD patients with OSA (apnea-hypopnea index) of ≥15 events/h and an Epworth Sleepiness Scale (ESS) score of <10 were randomized to CPAP or no-CPAP groups, and OSA patients with an ESS score of ≥10 were offered CPAP treatment. Blood samples were obtained at baseline and 12-month follow-up visits. TNF-α was measured by immunoassay (Luminex, R&D Systems). Genotyping of TNF-α-308G/A (single nucleotide polymorphism Rs1800629) was performed by polymerase chain reaction-restriction fragment length polymorphism.ResultsIn all, 239 participants (206 men and 33 women; mean age 64.9 (SD 7.7) years) with polymorphism data and circulating levels of TNF-α at baseline and 1-year follow-up visits were included. The median circulating TNF-α values fell in both groups between baseline and 12 months with no significant within- or between-group differences. In a multivariate linear regression model, a significant change in circulating TNF-α levels from baseline across the genotypes from GA to GA and GA to AA (standardized β-coefficient -0.129, 95% confidence interval (CI) -1.82; -0.12; p = 0.025) was observed in the entire cohort. The association was more pronounced among the individuals who were using the device for at least 4 h/night (n = 86; standardized β-coefficient -2.979 (95% CI -6.11; -1.21); p = 0.004)), whereas no significant association was found among the patients who were non-adherent or randomized to no-CPAP. The participants carrying the TNF-α A allele were less responsive to CPAP treatment regarding the decline in circulating TNF-α despite CPAP adherence (standardized β-coefficient -0.212, (95% CI -5.66; -1.01); p = 0.005).ConclusionsOur results suggest that TNF-α (-308G/A) gene polymorphism is associated with changes in circulating TNF-α levels in response to CPAP treatment in adults with CAD and OSA.

Project description:Background and aimsObstructive sleep apnea (OSA) is characterized by intermittent airway obstruction and systemic hypoxia during sleep, which can contribute to an increase in reactive oxygen species, vascular remodeling, vasoconstriction and ultimately cardiovascular disease. Continuous positive airway pressure (CPAP) is a clinical therapy that maintains airway patency and mitigates several symptoms of OSA. However, it is currently unknown whether CPAP therapy also reduces the overall inflammatory potential in the circulation; to address this in an unbiased manner, we applied a novel endothelial biosensor approach, the serum cumulative inflammatory potential (SCIP) assay.MethodsWe studied healthy controls (n = 7), OSA subjects receiving no treatment, (OSA controls) (n = 7) and OSA subjects receiving CPAP for 3 months (n = 8). Serum was obtained from OSA subjects before and after CPAP or no treatment. A battery of quantitative and functional assays was performed to assess the serum inflammatory potential, in terms of endothelial responses. For the SCIP assay, human coronary artery endothelial cells (hCAECs) were incubated with 5% serum in media from individual subjects for 4 h. qPCR was performed to assess endothelial inflammatory transcript (ICAM-1, VCAM-1, IL-8, P-selectin, CCL5, and CXCL12) responses to serum. Additionally, transendothelial resistance was measured in serum-incubated hCAECs following leukocyte challenge.ResultshCAECs exhibited significant increases in VCAM-1, ICAM-1, IL-8 and P-selectin mRNA when incubated with serum from OSA patients compared to serum from healthy control subjects. Furthermore, compared to no treatment, serum from CPAP-treated individuals was less potent at inducing inflammatory gene expression in the SCIP assay. Similarly, in a leukocyte adhesion assay, naïve cells treated with serum from patients who received CPAP exhibited improved endothelial barrier function than cells treated with OSA control serum.ConclusionsOSA results in greater serum inflammatory potential, thereby driving endothelial activation and dysfunction.

Project description:Importance:While much has been reported on the relationship between floppy eyelid syndrome and obstructive sleep apnea (OSA), the diagnostic criteria of floppy eyelid syndrome are often subjective and vague. Objective:To evaluate the association between OSA and quantitative markers of eyelid laxity or secondary ocular surface disease in a sleep clinic population. Design, Setting, and Participants:This investigation was a cross-sectional observational study at the Center for Sleep Medicine at Icahn School of Medicine at Mount Sinai. Participants were individuals referred for overnight polysomnography from March 1 to August 30, 2015. Main Outcomes and Measures:Eyelid laxity and ocular surface disease were assessed on bedside ophthalmologic examination. The presence and severity of OSA were determined from polysomnography results. Initial correlation between OSA and ocular surface and eyelid markers was calculated through bivariate linear regression analysis, and the association between ocular symptoms was obtained through bivariate ordered logistic regression. Analysis was repeated adjusting for known associations between OSA and sex, age, body mass index, and medical comorbidities through multivariable analysis. Results:In total, 201 individuals (402 eyes) were enrolled in the study. Their mean (SD) age was 53.2 (13.5) years, 43.3% (n?=?87) were female, 56.7% (n?=?114) were of white race/ethnicity, 26.9% (n?=?54) were black/African American, 4.0% (n?=?8) were Asian, 8.0% (n?=?16) were multiracial or other, and 4.5% (n?=?9) were of unknown race/ethnicity, with 21.9% (n?=?44) of all individuals self-identifying as Hispanic and 75.1% (n?=?151) self-identifying as non-Hispanic. After adjustment, no association was observed between OSA severity and an eyelid laxity score (regression coefficient, 0.85; 95% CI, -0.33 to 0.62; P?=?.40) or an ocular surface score (regression coefficient, 1.09; 95% CI, -0.32 to 0.29; P?=?.93). Through subset analysis, male sex was associated with a higher ocular surface score, while older age and diabetes were associated with a higher eyelid laxity score. Only one patient (0.5%) exhibited findings of floppy eyelid syndrome. Conclusions and Relevance:Among individuals referred for overnight polysomnography, quantitative markers of eyelid laxity were not associated with the presence or severity of OSA. Subset analysis suggests that prior studies may have been limited by confounding variables or the technique of identifying eyelid laxity.

Dataset Information

Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease.

Publications

Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease.

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