Patients with obstructive sleep apnea exhibit impaired endothelial function after myocardial infarction.
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ABSTRACT:
SUBMITTER: Sert Kuniyoshi FH
PROVIDER: S-EPMC3130528 | biostudies-other | 2011 Jul
REPOSITORIES: biostudies-other
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Project description:Objectives: Obstructive Sleep Apnea (OSA) is related to repeated upper airway collapse, intermittent hypoxia, and intestinal barrier dysfunction. The resulting damage to the intestinal barrier may affect or be affected by the intestinal microbiota. Methods: A prospective case-control was used, including 48 subjects from Sleep Medicine Center of Nanfang Hospital. Sleep apnea was diagnosed by overnight polysomnography. Fecal samples and blood samples were collected from subjects to detect intestinal microbiome composition (by 16S rDNA gene amplification and sequencing) and intestinal barrier biomarkers – intestinal fatty acid-binding protein (I-FABP) and D-lactic acid (D-LA) (by ELISA and colorimetry, respectively). Results: The severity of OSA was related to differences in the structure and composition of the intestinal microbiome. Enriched Fusobacterium, Megamonasa, Lachnospiraceae_UCG_006, and reduced Anaerostipes was found in patients with severe OSA. Enriched Ruminococcus_2, Lachnoclostridium, Lachnospiraceae_UCG_006, and Alloprevotella was found in patients with high intestinal barrier biomarkers. Lachnoclostridium and Lachnospiraceae_UCG_006 were the common dominant bacteria of OSA and intestinal barrier damage. Fusobacterium and Peptoclostridium was independently associated with apnea-hypopnea index (AHI). The dominant genera of severe OSA were also related to glucose, lipid, neutrophils, monocytes and BMI. Network analysis identified links between the intestinal microbiome, intestinal barrier biomarkers, and AHI. Conclusions: The study confirms that changes in the intestinal microbiota are related to intestinal barrier biomarkers among patients in OSA. These changes may play a pathophysiological role in the systemic inflammation and metabolic comorbidities associated with OSA, leading to multi-organ morbidity of OSA.
2023-08-30 | GSE181270 | GEO
Project description:Study objectivesObstructive sleep apnea (OSA) is strongly associated with cardiovascular disease, including stroke and acute coronary syndromes. Plasminogen activator inhibitor-1 (PAI-1), the principal inhibitor of tissue-type plasminogen activator (t-PA), has a pronounced circadian rhythm and is elevated in both OSA and cardiovascular disease and may be an important link between the two conditions. Endothelial dysfunction is one of the underlying pathophysiological mechanisms of cardiovascular disease, and may be altered in OSA. Our primary aim was to compare circadian variability of PAI-1 and t-PA in patients with OSA and normal controls by determining the amplitude (peak level) and mesor (rhythm adjusted mean) of PAI-1 and t-PA in serial blood samples over a 24-h period. The secondary aim was to measure markers of endothelial function (brachial and radial artery flow) in patients with OSA compared with normal controls.SettingCross-sectional cohort study.Patients or participantsSubjects age 18 y or older, with a body mass index of 25-45 kg/m(2), with or without evidence of untreated OSA.InterventionsPlasma samples were collected every 2 h, in OSA patients and matched controls, over a 24-h period. PAI-1 and t-PA antigen and activity were measured. The presence or absence of OSA (apnea-hypopnea index of 5 or greater) was confirmed by overnight polysomnography. Endothelial function was measured via brachial artery flow mediated vasodilatation and computerized arterial pulse waveform analysis.Measurements and resultsThe rhythm-adjusted mean levels of PAI-1 antigen levels in the OSA group (21.8 ng/mL, 95% confidence level [CI], 18 to 25.7) were significantly higher as compared to the non-OSA group (16 ng/mL, 95% CI, 12.2 to 19.8; P = 0.03). The rhythm-adjusted mean levels of PAI-1 activity levels in the OSA group (23.9 IU/mL, 95% CI, 21.4 to 26.5) were also significantly higher than in the non-OSA group (17.2 IU/ mL, 95% CI, 14.6 to 19.9; P < 0.001).There were strong correlations between amplitude of PAI-1 activity and severity of OSA as measured by AHI (P = 0.02), and minimum oxygen levels during sleep (P = 0.04). Endothelial function parameters did not differ significantly between the two groups.ConclusionThe presence of obstructive sleep apnea adversely affects circadian fibrinolytic balance with higher mean plasminogen activator inhibitor-1 activity and antigen, and significantly lower mean tissue-type plasminogen activator activity compared with controls. This perturbation may be an important mechanism for increased cardiovascular events in patients with obstructive sleep apnea. Intermittent hypoxia and changes in circadian clock gene activity in obstructive sleep apnea may be responsible for these findings and warrant further study. Favorable changes in fibrinolytic balance may underlie the reduction in cardiovascular events observed with the treatment of obstructive sleep apnea.
| S-EPMC3900618 | biostudies-literature
Project description:IntroductionObstructive Sleep Apnea Syndrome (OSAS) is the most common respiratory disorder during sleep. Many studies have shown an association between obstructive sleep apnea syndrome and stroke, and OSAS has not been adequately considered in Vietnam compared to the actual clinical dangers. This study aims to assess the prevalence and general characteristics of obstructive sleep apnea syndrome in patients with cerebral infarction and investigate the relationship between obstructive sleep apnea syndrome and the severity of cerebral infarction.MethodsDescriptive cross-sectional study. We identified 56 participants from August 2018 to July 2019. Subacute infarcts were identified by neuroradiologists. For each participant, vascular risk factors, medications, clinical symptoms, and neurological examination were abstracted from the medical record. Patients were taken for history and clinical examination. The patients were divided into two groups according to their AHI (Apnea-Hypopnea Index) (<5 and ≥5).ResultsA total of 56 patients were registered for the study. The mean age is 67.70 ± 11.07. The proportion of men is 53.6%. AHI has a positive correlation with neck circumference (r = 0.4), BMI (r = 0.38), the Epworth Sleepiness Scale (r = 0.61), LDL cholesterol (r = 0.38), the Modified Rankin Scale (r = 0.49), NIHSS (National Institutes of Health Stroke Scale) (r = 0.53), and an inverse correlation with SpO2 (r = 0.61).ConclusionObstructive sleep apnea Syndrome is a factor in the prognosis of cerebral infarction as well as cardiovascular diseases such as hypertension. Thus, understanding the risk of stroke in people with sleep apnea is necessary and working with a doctor to diagnose and treat sleep apnea is important.
| S-EPMC10321128 | biostudies-literature
Project description:ObjectiveObstructive sleep apnea (OSA) is a potential cardiovascular risk. We aimed to investigate the association of OSA with heart rhythm disorders and prognosis in elderly patients with new-onset acute myocardial infarction (AMI).MethodsWe prospectively enrolled 252 AMI elderly patients (mean age, 68.5 ± 6.9 years) who were undergoing revascularization and completed a sleep study during their hospitalization. All subjects were categorized into non-OSA (apnea-hypopnea index (AHI) < 15, n = 130) and OSA (AHI ≥ 15, n = 122) groups based on the AHI. The changes in the autonomic nervous system, incidence of arrhythmia during nocturnal sleep, and major adverse cardiovascular and cerebrovascular events (MACCEs) were compared between the groups.ResultsThe mean AHI value in all AMI patients was 22.8 ± 10.9. OSA patients showed higher levels of body mass index and peak high-sensitivity C-reactive protein and lower levels of minimum nocturnal oxygen saturation (MinSaO2), as well as greater proportion of multivessel coronary artery disease (all P < 0.05). The OSA group also showed significant increases in heart rate variability and heart rate turbulence onset (both P < 0.05) and higher incidence of arrhythmia (including sinus, atrial, and ventricular in origin). At a median follow-up of 6 months (mean 0.8-1.6 years), OSA (AHI ≥ 15) combined with hypoxia (MinSaO 2 ≤ 80%) was independently associated with the incidence of MACCEs (hazard ratio [HR]: 4.536; 95% confidence interval [CI]: 1.461-14.084,P = 0.009) after adjusting for traditional risk factors.ConclusionsOSA and OSA-induced hypoxia may correlate with the severity of myocardial infarction, increase the occurrence of heart rhythm disorders in elderly subacute MI patients, and worsen their short-term poor outcomes.
| S-EPMC7868912 | 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:Obstructive sleep apnea (OSA) is a syndrome characterized by repeated pauses in breathing induced by a partial or complete collapse of the upper airways during sleep. Intermittent hypoxia (IH), a hallmark characteristic of OSA, has been proposed to be a major determinant of cancer development, and patients with OSA are at a higher risk of tumors. Both OSA and healthy monocytes have been found to show enhanced HIF1? expression under IH. Moreover, these cells under IH polarize toward a tumor-promoting phenotype in a HIF1?-dependent manner and influence tumor growth via vascular endothelial growth factor (VEGF). Monocytes from patients with OSA increased the tumor-induced microenvironment and exhibited an impaired cytotoxicity in a 3D tumor in vitro model as a result of the increased HIF1? secretion. Adequate oxygen restoration both in vivo (under continuous positive airway pressure treatment, CPAP) and in vitro leads the monocytes to revert the tumor-promoting phenotype, demonstrating the plasticity of the innate immune system and the oxygen recovery relevance in this context.
| S-EPMC5994578 | biostudies-literature
Project description:Maxillomandibular advancement (MMA) is effective for the treatment of obstructive sleep apnea (OSA). In previous studies, the airway was increased in the anteroposterior and transverse dimensions after MMA. However, the effect of the opposite of mandibular movement (mandibular setback) on the airway is still controversial. Mandibular setback surgery has been suggested to be one of the risk factors in the development of sleep apnea. Previous studies have found that mandibular setback surgery could reduce the total airway volume and posterior airway space significantly in both the one-jaw and two-jaw surgery groups. However, a direct cause-and-effect relationship between the mandibular setback and development of sleep apnea has not been clearly established. Moreover, there are only a few reported cases of postoperative OSA development after mandibular setback surgery. These findings may be attributed to a fundamental difference in demographic variables such as age, sex, and body mass index (BMI) between patients with mandibular prognathism and patients with OSA. Another possibility is that the site of obstruction or pattern of obstruction may be different between the awake and sleep status in patients with OSA and mandibular prognathism. In a case-controlled study, information including the BMI and other presurgical conditions potentially related to OSA should be considered when evaluating the airway. In conclusion, the preoperative evaluation and management of co-morbid conditions would be essential for the prevention of OSA after mandibular setback surgery despite its low incidence.
| S-EPMC7078420 | biostudies-literature
Project description:Obstructive sleep apnea (OSA) is a risk factor for cardiovascular disease. We hypothesized that patients with OSA and no cardiovascular disease have oxidant-related microcirculatory endothelial dysfunction.To evaluate the microcirculation in OSA.This study included seven patients with OSA and seven age- and weight-matched control subjects (mean age, 38 yr; mean body mass index, 32.5 kg/m²). All participants were free of cardiovascular risk factors. Participants received measurement of brachial artery flow-mediated dilation and forearm subcutaneous biopsy. Patients underwent repeated tests 12 weeks after treatment. Microcirculatory endothelial cells were isolated, and immunohistochemistry staining for peroxynitrite in the microcirculation was performed.Flow-mediated dilation was lower in patients than in control subjects at baseline (mean ± SEM: 5.7 ± 0.5 vs. 9.5 ± 0.6; P = 0.02) and increased after treatment (5.7-7.3; change, 1.7 ± 0.6; P = 0.04). Microcirculatory peroxynitrite deposit was higher in patients compared with control subjects (44.0 ± 1.6 vs. 21.8 ± 1.9 stain density units; P < 0.001) and decreased after treatment from 44.0 to 30.5 stain density units (change, -13.5 ± 2.9; P = 0.009). In patients, transcription of endothelial nitric oxide synthase decreased from 5.2 to -1.3 after treatment (change, 6.5 ± 2.5; P = 0.05), and transcription of superoxide dismutase1 decreased from -4.0 to -12.3 after treatment (change, -8.3 ± 2.1; P = 0.01). These changes persisted after adjustment for weight and underlying severity of OSA.This is the first direct evaluation of the microcirculation in OSA. Patients with OSA with low cardiovascular risk status had increased oxidant production in the microcirculation and endothelial dysfunction, both of which improved with treatment. Endothelial nitric oxide synthase transcription decreased with treatment.
| S-EPMC3029939 | 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-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:Obstructive sleep apnea (OSA) is an independent risk factor for many cardiovascular conditions such as coronary artery disease, myocardial infarction, systemic hypertension, pulmonary hypertension, and stroke. However, the association of OSA with outcomes in patients hospitalized for ST-elevation myocardial infarction remains controversial. We used the nation-wide inpatient sample between 2003 and 2011 to identify patients with a primary discharge diagnosis of ST-elevation myocardial infarction and then used the International Classification of Diseases, Clinical Modification code 327.23 to identify a group of patients with OSA. The primary outcome of interest was in-hospital mortality, and secondary outcomes were in-hospital cardiac arrest, length of stay and hospital charges. Our cohort included 1 850 625 patients with ST-elevation myocardial infarction, of which 1.3% (24 623) had documented OSA. OSA patients were younger and more likely to be male, smokers, and have chronic pulmonary disease, depression, hypertension, known history of coronary artery disease, dyslipidemia, obesity, and renal failure (P<0.001 for all). Patients with OSA had significantly decreased in-hospital mortality (adjusted odds ratio, 0.78 [95% CI, 0.73-0.84]), longer hospital stay (5.00±4.68 versus 4.85±5.96 days), and incurred greater hospital charges ($79 460.12±70 621.91 versus $62 889.91±69 124.15). There was no difference in incidence of in-hospital cardiac arrest (adjusted odds ratio, 0.93 [95% CI, 0.84-1.03]) between these 2 groups. ST-elevation myocardial infarction patients with recognized OSA had significantly decreased mortality compared with patients without OSA. Although patients with OSA had longer hospital stays and incurred greater hospital charges, there was no difference in incidence of in-hospital cardiac arrest.
| S-EPMC5586313 | biostudies-literature