Concurrent cardiac sarcoidosis and obstructive sleep apnea presenting as arrhythmias.
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ABSTRACT:
SUBMITTER: Malli F
PROVIDER: S-EPMC7210663 | biostudies-literature | 2020 May
REPOSITORIES: biostudies-literature
Publications
Concurrent cardiac sarcoidosis and obstructive sleep apnea presenting as arrhythmias.
Malli Foteini F Bardaka Fotini F Gourgoulianis Konstantinos I KI Daniil Zoe Z
BMC pulmonary medicine 20200508 1
<h4>Background</h4>Cardiac involvement is a rare and potentially fatal presentation of sarcoidosis. Obstructive sleep apnea may complicate sarcoidosis.<h4>Case presentation</h4>We report a case of a sarcoidosis patient with cardiac involvement presenting with ventricular arrhythmias. Besides medical and invasive measures of therapy, the patient failed to respond fully. The patient was subjected to overnight polysomnography and diagnosed with concurrent obstructive sleep apnea syndrome. Following ...[more]
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Project description:Obstructive sleep apnea (OSA) is common among patients with cardiac rhythm disorders. OSA may contribute to arrhythmias due to acute mechanisms, such as generation of negative intrathoracic pressure during futile efforts to breath, intermittent hypoxia, and surges in sympathetic activity. In addition, OSA may lead to heart remodeling and increases arrhythmia susceptibility. Atrial distension and remodeling, that has been shown to be associated with OSA, is a well-known anatomical substrate for atrial fibrillation (AF). AF is the arrhythmia most commonly described in patients with OSA. Several observational studies have shown that the treatment of OSA with continuous positive airway pressure (CPAP) reduces recurrence of AF after electrical cardioversion and catheter ablation. There is also evidence that nocturnal hypoxemia, a hallmark of OSA, predicts sudden cardiac death (SCD) independently of well-established cardiovascular risk factors. Among patients with an implantable cardiac defibrillator, those with OSA have a higher risk of receiving treatment for life-threatening arrhythmias. Nocturnal hypoxemia may also increase vagal tone, which increases susceptibility to bradycardic and conduction rhythm disorders that have also been described in patients with OSA. In conclusion, there are several biological pathways linking OSA and increased cardiac arrhythmogenesis propensity. However, the independent association is derived from observational studies and the direction of the association still needs clarification due to the lack of large clinical trials. This review focuses on the current scientific evidence linking OSA to cardiac rhythm disorders and point out future directions.
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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:Rationale:An increased incidence of Obstructive Sleep Apnea (OSA) in sarcoidosis has been described in small sample size studies. Fatigue is common in sarcoidosis and OSA could be a relevant, treatable comorbidity. To date, the effect of Continuous Positive Airway Pressure (CPAP) on fatigue has never been assessed. Objectives:To investigate the prevalence of OSA in sarcoidosis, fatigue status and daytime sleepiness in patients of our center. To explore the effect of CPAP in fatigue and daytime sleepiness after 3 months using validated questionnaires. Method:Single group, one center, open-label prospective cohort study. Measurements and main result:We enrolled 68 patients and OSA was diagnosed in 60 (88.2%): 25 (36.8%) were mild while 35 (51.5%) were moderate-to-severe. 38 (55.9%) patients received CPAP but only 20 (30.9%) were compliant at 3-month evaluation. Questionnaires demonstrated fatigue in 34 (50%) and daytime sleepiness in 21 (30.9%). In multivariate regression analysis, Scadding stage and FAS behave as predictors of Apnea-Hypopnea Index (AHI) severity while sleepiness and steroids weren't associated. FAS score (?FAS = 6.3; p = 0.001) and ESS score (?ESS = 2.8; p = 0.005) improved after three months of CPAP. Conclusions:OSA is highly prevalent in patients affected by sarcoidosis. ESS questionnaire is not reliable for OSA screening and other pre-test probability tool should be evaluated in further studies. CPAP leads to a significative reduction of fatigue and daytime sleepiness at three-month. Further studies are needed to confirm the high prevalence of OSA in sarcoidosis and the positive role of CPAP in fatigue. (Sarcoidosis Vasc Diffuse Lung Dis 2020; 37 (2): 169-178).
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Project description:Illumina MiSeq next generation sequencing chip was used to identify differentially expressed miRs by comparing peripheral blood mononuclear cell samples between OSA patients and healthy non-snorers.
2021-12-01 | GSE174245 | GEO
Project description:OBJECTIVES:The number of studies on the frequency of obstructive sleep apnea (OSA) in subjects with sarcoidosis is low. Therefore, we aimed to investigate the frequency and predictors of OSA in subjects with clinically stable stage I and II sarcoidosis who were not taking corticosteroid and/or immunosuppressive drugs. We also evaluated restless legs syndrome (RLS) and periodic leg movements in sleep (PLMS). MATERIALS AND METHODS:Subjects with clinically stable stage I and II sarcoidosis and not receiving corticosteroid and/or immunosuppressive therapy were included in the study. Upper airway examination, lung function tests (forced vital capacity [FVC], forced expiratory volume in 1 second [FEV1], diffusing capacity of the lungs for carbon monoxide [DLCO]), and polysomnography were performed on all subjects. In addition, subjects' Epworth Sleepiness Scale (ESS) scores and the Pittsburgh Sleep Quality Index (PSQI) were recorded. RESULTS:Of the total number of 46 sarcoidosis subjects (35 women, 11 men; age: 44.4±10.7 years; body mass index (BMI): 29.3±5 kg/m2), 28 (60.9%) were detected with OSA (67.8% mild OSA). The recorded ESS score of the subjects was low (2.6±3.2), whereas the sleep quality was poor in 36.9% of these subjects. Rapid eye movements (REM) related OSA was diagnosed in 14.2% of the OSA subjects. Age was the only factor related to OSA diagnosis in a logistic regression analysis (p=0.048). None of the subjects were diagnosed with RLS and PLMS. CONCLUSION:OSA is common in stage I and II sarcoidosis subjects who did not receive corticosteroid therapy. The frequency of OSA diagnosis increases as the age of the subjects increases. Therefore, sarcoidosis subjects should be evaluated for OSA throughout the follow-up.
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Project description:To characterize the prospective associations of obstructive sleep apnea (OSA) with future echocardiographic measures of adverse cardiac remodeling.This was a prospective long-term observational study. Participants had overnight polysomnography followed by transthoracic echocardiography a mean (standard deviation) of 18.0 (3.7) y later. OSA was characterized by the apnea-hypopnea index (AHI, events/hour). Echocardiography was used to assess left ventricular (LV) systolic and diastolic function and mass, left atrial volume and pressure, cardiac output, systemic vascular resistance, and right ventricular (RV) systolic function, size, and hemodynamics. Multivariate regression models estimated associations between log10(AHI+1) and future echocardiographic findings. A secondary analysis looked at oxygen desaturation indices and future echocardiographic findings.At entry, the 601 participants were mean (standard deviation) 47 (8) y old (47% female). After adjustment for age, sex, and body mass index, baseline log10(AHI+1) was associated significantly with future reduced LV ejection fraction and tricuspid annular plane systolic excursion (TAPSE) ? 15 mm. After further adjustment for cardiovascular risk factors, participants with higher baseline log10(AHI+1) had lower future LV ejection fraction (? = -1.35 [standard error = 0.6]/log10(AHI+1), P = 0.03) and higher odds of TAPSE ? 15 mm (odds ratio = 6.3/log10(AHI+1), 95% confidence interval = 1.3-30.5, P = 0.02). SaO2 desaturation indices were associated independently with LV mass, LV wall thickness, and RV area (all P < 0.03).OSA is associated independently with decreasing LV systolic function and with reduced RV function. Echocardiographic measures of adverse cardiac remodeling are strongly associated with OSA but are confounded by obesity. Hypoxia may be a stimulus for hypertrophy in individuals with OSA.
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Project description:Chronic intermittent hypoxia, platelet activation and inflammation all play roles in the pathogenesis of obstructive sleep apnea syndrome (OSAS), which may increase the risk of cardiovascular disease (CVD). The aim of this study was to evaluate the relationship of the platelet-to-lymphocyte ratio (PLR) as a new biomarker showing systemic inflammation and platelet distribution width (PDW) as an indicator of platelet activation to the severity of OSAS.A total of 290 patients suspected with OSAS who underwent a full night of polysomnography were included. The patients were placed into 4 separate groups according to their apnea-hypopnea index (AHI) scores; the control group (AHI <5), mild OSAS group (AHI 5-15), moderate OSAS group (AHI 16-30), and severe OSAS group (AHI >30). CVD risk was defined by the presence of hypertension, diabetes mellitus, current smoking, and dyslipidemia.Higher AHI groups were significantly correlated with increasing age, body mass index, systolic blood pressure and male sex. PLR and PDW were also significantly associated with AHI (r = 0.417 for PLR and r = 0.227 for PDW, all p-values < 0.001) and the Epworth sleepiness scale (r = 0.160 for PLR and r = 0.189 for PDW, all p-values <0.05). Multivariate regression analysis revealed that AHI ≥9.2 (adjusted odds ratios [OR] 5.03, 95 % confidential interval (CI) = 1.67-15.2, p = 0.004) and PLR ≥159 (adjusted OR 2.81, 95 % CI = 1.34-5.91, p = 0.006) were independently associated with the presence of hypertension.PLR and PDW are associated with OSAS severity. PLR may also be useful as a systemic biomarker for the concurrent hypertension in OSAS patients.
| S-EPMC4750799 | biostudies-other
Project description:Obstructive sleep apnea (OSA) has been linked to dysregulated metabolic states and treatment of sleep apnea may improve these conditions. Subcutaneous adipose tissue is a readily samplable fat depot that plays an important role in regulating metabolism. However, neither the pathophysiologic consequences of OSA nor the effects of continuous positive airway pressure (CPAP) in altering this compartment’s molecular pathways are understood. This study aimed to systematically identify subcutaneous adipose tissue transcriptional programs modulated in OSA and in response to its effective treatment with CPAP. Two subject groups were investigated: Study Group 1 was comprised of 10 OSA and 8 controls; Study Group 2 included 24 individuals with OSA studied at baseline and following CPAP. For each subject, genome-wide gene expression measurement of subcutaneous fat was performed. Differentially activated pathways elicited by OSA (Group 1) and in response to its treatment (Group 2) were determined using network and Gene Set Enrichment Analysis (GSEA). In Group 2, treatment of OSA with CPAP improved apnea hypopnea index, daytime sleepiness, and blood pressure, but not anthropometric measures. In Group 1, GSEA revealed many up-regulated gene sets in OSA subjects, most of which were involved in immuno-inflammatory (e.g., interferon-γ signaling), transcription, and metabolic processes such as adipogenesis. Unexpectedly, CPAP therapy in Group 2 subjects was also associated with up-regulation of several immune pathways as well as cholesterol biosynthesis. Collectively, our findings demonstrate that OSA alters distinct inflammatory and metabolic programs in subcutaneous fat, but these transcriptional signatures are not reversed with short-term effective therapy.
2019-12-21 | GSE135917 | GEO