Obstructive sleep apnea and self-reported functional impairment in revascularized patients with coronary artery disease in the RICCADSA trial.
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ABSTRACT:
SUBMITTER: Baniak LM
PROVIDER: S-EPMC6391726 | biostudies-literature | 2018 Dec
REPOSITORIES: biostudies-literature
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Obstructive sleep apnea and self-reported functional impairment in revascularized patients with coronary artery disease in the RICCADSA trial.
Baniak Lynn M LM Chasens Eileen R ER Luyster Faith S FS Strollo Patrick J PJ Thunström Erik E Peker Yüksel Y
Sleep & breathing = Schlaf & Atmung 20181015 4
<h4>Purpose</h4>Daytime sleepiness, a frequent symptom of obstructive sleep apnea (OSA), can impact functional status. In patients with coronary artery disease (CAD) and concomitant OSA, the distinction between sleep-related functional impairment from underlying CAD versus OSA is unclear. This study evaluated the impact of OSA on sleep-related functional impairment in patients with CAD and compared the effect of 1-year continuous positive airway pressure (CPAP) use on change in impairment betwee ...[more]
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Project description:Study objectivesRecent studies show that obstructive sleep apnea (OSA) is a possible contributor to abnormal cognitive decline in older adults. These new observations create the need to identify older adults with OSA who are at risk of the developing dementia if not treated. This study's goal was to verify whether self-reported cognitive complaints could become a useful tool to screen for objective cognitive deficits in late middle-aged and older adults with OSA.MethodsFifty-seven participants with OSA with an apnea-hypopnea index (AHI) ≥ 15 events/h (3% or arousal) and aged between 55 and 85 years were compared to 54 participants in a mild/non-OSA group on their ability to evaluate their objective cognitive functioning. They underwent overnight polysomnography followed by a comprehensive neuropsychological assessment. We recruited a similar proportion of participants with mild cognitive impairment (MCI) in both groups (OSA: 36.8%; mild/non-OSA: 35.2%). They filled out questionnaires assessing mood, sleep, and cognition. Group (OSA versus mild/non-OSA) × cognitive status (MCI versus non-MCI) analyses of variance were performed on cognitive complaint questionnaires.ResultsWe found that among participants without objective cognitive deficits, participants in the OSA group reported more cognitive complaints compared to those in the mild/non-OSA group. Among participants with objective cognitive deficits, those in the OSA group reported less cognitive complaints compared to those in the mild/non-OSA group.ConclusionsParticipants with OSA and MCI were less aware of their deficits compared to those in the mild/non-OSA group, possibly reflecting a distinctive OSA-associated cognitive impairment. Our results underscore the importance of referring patients with OSA for a comprehensive neuropsychological assessment when an abnormal cognitive decline is suspected.
| S-EPMC6411171 | biostudies-literature
Project description:Coronary artery disease (CAD) and obstructive sleep apnea (OSA) are both complex and significant clinical problems. The pathophysiological mechanisms that link OSA with CAD are complex and can influence the broad spectrum of conditions caused by CAD, from subclinical atherosclerosis to myocardial infarction. OSA remains a significant clinical problem among patients with CAD, and evidence suggesting its role as a risk factor for CAD is growing. Furthermore, increasing data support that CAD prognosis may be influenced by OSA and its treatment by continuous positive airway pressure (CPAP) therapy. However, stronger evidence is needed to definitely answer these questions. This paper focuses on the relationship between OSA and CAD from the pathophysiological effects of OSA in CAD, to the clinical implications of OSA and its treatment in CAD patients.
| S-EPMC3649685 | biostudies-literature
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.
| S-EPMC5097675 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO
Project description:BackgroundThe aim of this study was to explore the underlying impact of obstructive sleep apnea (OSA) on postoperative parameters of multi-organ function among coronary heart disease (CHD) patients following elective coronary artery bypass grafting (CABG).MethodsElectronic literature databases were searched manually and automatically for relevant English articles. All of the included articles focused on a comparison of the incidence of postoperative parameters of multi-organ function in CHD patients undergoing elective CABG with and without OSA. Studies were excluded if they met any one of the following criteria: (I) duplicate publication; (II) ongoing or unpublished studies; (III) only published as abstracts or conference proceedings; and (IV) less than 30 patients in the patient cohort.ResultsA total of 13 articles met our inclusion criteria. The current study demonstrated OSA significantly increased the incidence of major adverse cardiac and cerebrovascular events (MACCEs) in CHD patients undergoing elective CABG compared with the controls [odds risk (OR), 1.97; 95% CI, 1.50 to 2.59, P<0.0001]. In addition, OSA was associated with an increased risk of new revascularization in CHD patients undergoing elective CABG (OR, 9.47; 95% CI, 2.69 to 33.33, P<0.0001). Moreover, reintubation and tracheostomy in the OSA group was increased 243% (OR, 3.43; 95% CI, 1.35 to 8.71; P=0.009) and 372% (OR, 4.72; 95% CI, 1.23 to 18.13; P=0.024), respectively, compared with the control group. Besides, we also confirmed OSA significantly increased the acute kidney injury (AKI) incidence by 124% (OR, 2.24; 95% CI, 1.07 to 4.72; P<0.0001).ConclusionsOSA may contribute to postoperative multi-organ dysfunction among CHD patients undergoing elective CABG by increasing the incidence of MACCEs, especially new revascularization, as well as respiratory, and renal complications.
| S-EPMC7656408 | biostudies-literature
Project description:BackgroundObstructive sleep apnea (OSA) is an independent risk factor for the development of cardiovascular diseases. Aim of this present study was to evaluate and extend recent research on the influence of obstructive sleep apnea on vascular strain.MethodsA total number of 98 patients were integrated in the study. Patients were grouped according to the Apnea-Hypopnea-Index (AHI) in patients with mild-to-moderate OSA (5/h ≤ AHI < 30/h), severe OSA (AHI ≥ 30/h) and controls (AHI < 5/h). Groups were matched in age, body-mass-index and cardiovascular risks. Vascular strain of common carotid arteries was assessed by ultrasound speckle-tracking. A minor group of 30 patients and controls further underwent assessment of vascular strain of brachial and femoral arteries. Additionally, all patients underwent blood testing to reveal potential influences of inflammatory markers on arterial stiffness. In additional analysis we examined the effect of statin therapy on vascular strain.ResultsPatients with OSA showed significantly reduced values of vascular strain of common carotid arteries. Radial and circumferential strains were significantly lower in both patients with mild-to-moderate (p = .05) and patients with severe OSA (p = .001) compared to control. Vascular strain parameters of brachial and femoral arteries showed no consistent results. There were no significant correlations of inflammatory markers with vascular strain parameters. No significant differences in vascular strain were detected between statin and non-statin groups.ConclusionPatients with OSA show significantly reduced vascular strain assessed by ultrasound-based speckle-tracking. Vascular stiffness increases with the severity of the disease. Target vessels to assess vascular strain in patients with OSA are common carotid arteries, whereas other sites of the arterial tree are not reliable. No significant impact of current statin therapy on vascular strain was found. Further studies are needed to evaluate potential benefit of statins in secondary prevention of atherosclerosis in OSA.
| S-EPMC5831412 | biostudies-literature
Project description:BackgroundExcessive daytime sleepiness is a frequent symptom of obstructive sleep apnea (OSA) and has been proposed as a motivator for adherence to continuous positive airway pressure (CPAP) therapy. However, excessive daytime sleepiness is absent in many patients with coronary artery disease (CAD) and concomitant OSA. We evaluated long-term use of CPAP and predictors of CPAP use in nonsleepy and sleepy OSA patients from a CAD cohort.HypothesisLong-term CPAP use is lower in CAD patients with nonsleepy OSA vs sleepy OSA.MethodsNonsleepy (Epworth Sleepiness Scale [ESS] score < 10) OSA patients randomized to CPAP (n = 122) and sleepy (ESS ≥10) OSA patients offered CPAP (n = 155) in the RICCADSA trial in Sweden were included in this substudy. The median follow-up was 4.8 years for the main trial, with a predefined minimum follow-up of 2 years.ResultsThe probability of remaining on CPAP at 2 years was 60% in nonsleepy patients and 77% in sleepy patients. Multivariate analyses indicated that age and hours of CPAP use per night at 1 month were independently associated with long-term CPAP use in nonsleepy patients. In the sleepy phenotype, body mass index, acute myocardial infarction at baseline, and hours of CPAP use per night at 1 month were predictors of long-term CPAP use.ConclusionsLong-term use of CPAP is likely to be challenging for CAD patients with nonsleepy OSA. Early CPAP use is an important predictor of continued long-term use of CPAP, so optimizing patients' initial experience with CPAP could promote adherence.
| S-EPMC6490397 | biostudies-literature
Project description:BackgroundObstructive 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.MethodsFrom 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.ResultsModerate/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.ConclusionsPlasma 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.
| S-EPMC7426787 | biostudies-literature
Project description:BackgroundEndothelial dysfunction is one of the most important early indicators of atherosclerosis in obstructive sleep apnea (OSA) patients. Endothelial cell specific molecules-1 (ESM-1), which is a novel endothelial dysfunction marker that may be linked to cardiovascular disease. We investigated to assess whether circulating ESM-1 levels are correlated with the presence of coronary artery disease (CAD) in patients with OSA.MethodsWe performed a cross-sectional study in 228 Chinese OSA subjects, including 185 patients with OSA and 43 controls. The Gensini stenosis scoring system was used to assess the severity of CAD. Circulating ESM-1 levels were measured by Human Magnetic Luminex Screening Assay. The associations between circulating ESM-1 levels and CAD were determined by multivariate logistic regression analysis. The association between ESM-1 levels and Gensini scores was determined by multivariate linear regression analysis.ResultsCAD patients had significantly higher circulating ESM-1 levels compared with non-CAD patients (1279.01[918.52-1770.71] pg/ml vs 585.46[423.61-812.56] pg/ml, P < 0.001). After adjusting for confounding factors, we found that circulating ESM-1 levels were an independent risk factor for CAD (OR = 1.633/100 pg ESM-1, 95%CI =1.179-2.262, P = 0.003), while circulating ESM-1 levels have no significant correlation with the Gensini score. Furthermore, circulating ESM-1 showed higher discriminatory accuracy in predicting the presence of OSA (AUC:0.910).ConclusionsCirculating ESM-1 might function as a useful biomarker for monitoring the development and progression of CAD in OSA patients.
| S-EPMC6701084 | biostudies-literature