Catheter-Based Renal Denervation Reduces Hypoxia-Triggered Nocturnal Blood Pressure Peak in Obstructive Sleep Apnea Syndrome.
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ABSTRACT:
SUBMITTER: Kario K
PROVIDER: S-EPMC8031979 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Obstructive sleep apnea (OSA) causes blood pressure (BP) surges during sleep, which may lead to increased sleep-onset cardiovascular events. The authors recently developed a triggered nocturnal BP monitoring system that initiates BP measurements when oxygen desaturation falls below a variable threshold. The distribution and reproducibility of hypoxia-triggered nocturnal BP parameters compared with those of fixed-interval nocturnal BP parameters for two consecutive nights in 147 OSA patients (mean age 59.4 years, 86.4% men) were evaluated. The mean and distribution (standard deviation [SD]) of the hypoxia-peak systolic BP (SBP) were significantly greater than that of the mean nocturnal SBP (mean±SD: 148.8±20.5 vs 123.4±14.2 mm Hg, P<.001). The repeatability coefficient (expressed as %MV) of hypoxia-peak SBP between night 1 and night 2 was comparable to that of mean nocturnal SBP (43% vs 32%). In conclusion, hypoxia-peak nocturnal BP was much higher than mean nocturnal BP, and it was as reproducible as mean nocturnal BP.
| S-EPMC8031313 | biostudies-literature
Project description:In obese subjects with obstructive sleep apnea (OSA), chronic intermittent hypoxia (CIH) may be linked to systemic and adipose tissue inflammation.We obtained abdominal subcutaneous adipose tissue biopsies from OSA and non-OSA obese (BMI > 35) subjects at baseline and after 24 weeks (T1) of weight-loss intervention plus continuous positive airway pressure (c-PAP) or weight-loss intervention alone, respectively. OSA subjects were grouped according to good (therapeutic) or poor (subtherapeutic) adherence to c-PAP.At baseline, anthropometric and metabolic parameters, serum cytokines, and adipose tissue mRNA levels of obesity-associated chemokines and inflammatory markers were not different in OSA and non-OSA subjects. At T1, body weight was significantly reduced in all groups. Serum concentrations of IL-2, IL-4, IL-6, MCP-1, PDGF?, and VEGF? were reduced by therapeutic c-PAP in OSA subjects and remained unaltered in non-OSA and subtherapeutic c-PAP groups. Similarly, adipose tissue mRNA levels of macrophage-specific (CD68, CD36) and ER stress (ATF4, CHOP, ERO-1) gene markers, as well as of IL-6, PDGF?, and VEGF?, were decreased only in the therapeutic c-PAP group.CIH does not represent an additional factor increasing systemic and adipose tissue inflammation in morbid obesity. However, in subjects with OSA, an effective c-PAP therapy improves systemic and obesity-associated inflammatory markers.Ministero dell'Università e della Ricerca and Progetti di Rilevante Interesse Nazionale.
| S-EPMC5621882 | biostudies-other
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:A growing body of evidence links obstructive sleep apnea (OSA) with hypertension. The authors performed a retrospective cohort study using the University Hospital of Larissa Sleep Apnea Database (1501 patients) to determine predictors of in-laboratory diagnosed OSA for development of hypertension. Differences in continuous variables were assessed via independent samples t test, whereas discrete variables were compared by Pearson's chi-square test. Multivariate analysis was performed via discriminant function analysis. There were several significant differences between hypertensive and normotensive patients. Age, body mass index, comorbidity, daytime oxygen saturation, and indices of hypoxia during sleep were deemed the most accurate predictors of hypertension, whereas apnea-hypopnea index and desaturation index were not. The single derived discriminant function was statistically significant (Wilk's lambda=0.771, χ(2) =289.070, P<.0001). Daytime and nocturnal hypoxia as consequences of chronic intermittent hypoxia play a central role in OSA-related hypertension and should be further evaluated as possible severity markers in OSA.
| S-EPMC8032090 | biostudies-literature
Project description:Background Chronic intermittent hypoxia ( CIH ) is a distinct pathological mechanism of obstructive sleep apnea ( OSA ), which is recognized as an independent risk factor for cardiovascular diseases. The aims of this study were to ascertain whether CIH induces atrial fibrillation ( AF ), to determine whether cardiac sympathetic denervation ( CSD ) can prevent it and suppress blood pressure, and to explore the potential molecular mechanisms involved. Methods and Results Sixty Sprague-Dawley male rats were randomly divided into 4 groups: sham, CSD , CIH , CIH + CSD . The rats were exposed either to CIH 8 hours daily or normoxia for 6 weeks. Cardiac pathology and structure were analyzed by hematoxylin and eosin staining and echocardiogram. ECG, blood pressure, body weight, and blood gas were recorded. Connexin 43 and tyrosine hydroxylase were detected by western blot, immunohistochemistry, and immunofluorescence. CIH induced atrial remodeling, and increased AF inducibility. CSD treatment reduced postapneic blood pressure rises and AF susceptibility, which could attenuate CIH -associated structural atrial arrhythmogenic remodeling. In addition, CIH -induced sympathetic nerve hyperinnervation and CSD treatment reduced sympathetic innervation, which may affect CIH -induced AF -associated sympathovagal imbalance. Connexin 43 was specifically downregulated in CIH , whereas CSD treatment increased its expression. Conclusions These results suggested CIH induces atrial remodeling, increases AF inducibility, results in sympathetic nerve hyperinnervation, and decreases connexin 43 expression, but CSD treatment reduces AF susceptibility, postapneic blood pressure increase, sympathetic innervation, and the alteration of Cx43, which may be a key point in the genesis of CIH -induced AF .
| S-EPMC6405657 | biostudies-literature
Project description:Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.To examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Randomized crossover trial of CPAP vs CPAP withdrawal.Thirty-one patients with moderate to severe OSA acclimated to CPAP.Patients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ?20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.CPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.OSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.
| S-EPMC5587067 | biostudies-literature
Project description:Study Objectives:To assess the effect of adenotonsillectomy for relieving obstructive sleep apnea syndrome (OSAS) symptoms in children on cardiac autonomic modulation. Methods:In 354 children enrolled in the Childhood Adenotonsillectomy Trial, randomized to undergo either early adenotonsillectomy (eAT; N = 181) or a strategy of watchful waiting with supportive care (WWSC; N = 173), nocturnal heart rate control was analyzed during quiet, event-free sleep at baseline and at 7 months using overnight polysomnography (PSG). The relative frequency of patterns indicating monotonous changes in heart rate was quantified. Results:Children who underwent eAT demonstrated a significantly greater reduction in heart rate patterns postsurgery than the WWSC group. On assessing those heart rate patterns regarding normalization of clinical PSG, heart patterns were reduced to a similar level in both groups. In children whose AHI normalized spontaneously, heart rate patterns were already significantly less frequent at baseline, suggesting that upper airway obstruction was milder in this group at the outset. Conclusions:Adenotonsillectomy reduces monotonous heart rate patterns throughout quiet event-free sleep, reflecting a reduction in cardiac autonomic modulation. Heart rate pattern analysis may help quantifying the effect of OSAS on autonomic nervous system activity in children. Clinical Trial Registration: The study was registered at Clinicaltrials.gov (#NCT00560859).
| S-EPMC6231530 | biostudies-literature
Project description:We set to measure the interatrial pressure gradient during simulated obstructive sleep apnea (OSA).OSA occurs when a sleeping patient attempts to inhale against an obstructed airway. How this event affects the interatrial pressure gradient has not been defined. We hypothesized that simulated OSA in a conscious subject (Mueller maneuver [MM], inspiration against obstruction) would promote increased right-to-left pressure gradient, and then the substrate for right-to-left atrial shunting.Selected patients underwent simultaneous measurement of airway and atrial pressures (both left and right atrium [LA, RA]) using high-fidelity micromanometry at rest, during MM, and during VM, during right heart catheterization.Ten patients (age 55?±?11 years, two women) were successfully studied. During the onset of MM, RA pressure transiently but consistently exceeded LA pressure in response to the steep decline in intrathoracic pressure (maximum RA-LA pressure gradient increased from 0.1?±?1.4 mm Hg at baseline to 7.0?±?4.3 mm Hg during MM, P?<?0.001). The maximum right-to-left atrial pressure gradient during Mueller maneuver was higher than that achieved during the Valsalva maneuver release (P?<?0.007).The onset of MM increased right-to-left pressure gradient across the atrial septum, likely as a result of greater blood return to the RA from extrathoracic veins. The RA-LA pressure gradient achieved during MM was greater than that observed during VM. These findings delineate the hemodynamic substrate for right to left shunting during OSA.
| S-EPMC4244266 | biostudies-literature
Project description:Obstructive sleep apnea causes blood pressure (BP) surges during sleep, which may lead to increased sleep-onset cardiovascular events. The authors recently developed an oxygen-triggered nocturnal BP monitoring system that initiates BP measurements when oxygen desaturation (SpO2 ) falls below a variable threshold. The association between nocturnal BP parameters obtained by nocturnal BP monitoring and simultaneously examined polysomnography-derived sleep parameters in 116 patients with obstructive sleep apnea (mean age 57.9 years, 85.3% men) was studied. In multivariable analysis with independent factors of age, body mass index, sex, and polysomnography-derived measures (apnea-hypopnea index, apnea index, arousal index, lowest SpO2 , and SpO2 < 90%), apnea-hypopnea index (β = .26, P = .02) and lowest SpO2 (β = -.34, P < .001) were independent determinants of hypoxia-peak systolic BP (SBP), defined as the maximum SBP value measured by nocturnal BP monitoring. Similarly, apnea-hypopnea index (β = .21, P = .04) and lowest SpO2 (β = -.49, P < .001) were independent determinants of nocturnal SBP surge, defined as the difference between the hypoxia-peak SBP and the average of the SBP values within 30 minutes before and after the hypoxia-peak SBP, measured by the fixed-interval function in the manner of conventional ambulatory BP monitoring. In conclusion, in polysomnography-derived parameters, lowest SpO2 , defined as the minimum SpO2 value during sleep, is the strongest independent determinant of hypoxia-peak SBP and nocturnal SBP surge measured by nocturnal BP monitoring. Our findings suggest that the severity of the decrease in SpO2 and the frequency of such decreases would be important indicators to identify high-risk patients who are likely to develop cardiovascular events specifically during sleep.
| S-EPMC8031332 | biostudies-literature