Obstructive sleep apnea and metabolic syndrome.

Metabolic syndrome (MS) is a heterogeneous condition associated with increased cardiovascular risk. There is growing evidence from experimental, translational, and clinical investigations that has suggested that obstructive sleep apnea (OSA) is associated with prevalent and incident components of MS and MS itself. The biological plausibility is supportive, primarily related to one of the main features of OSA, namely intermittent hypoxia: increased sympathetic activation with hemodynamic repercussions, increased hepatic glucose output, insulin resistance through adipose tissue inflammation, pancreatic ß-cell dysfunction, hyperlipidemia through the worsening of fasting lipid profiles, and the reduced clearance of triglyceride-rich lipoproteins. Although there are multiple related pathways, the clinical evidence relies mainly on cross-sectional data preventing any causality assumptions. The overlapping presence of visceral obesity or other confounders such as medications challenges the ability to understand the independent contribution of OSA on MS. In this review, we revisit the evidence on how OSA/intermittent hypoxia could mediate adverse effects of MS parameters independent of adiposity. Particular attention is devoted to discussing recent evidence from interventional studies. This review describes the research gaps, the challenges in the field, perspectives, and the need for additional high-quality data from interventional studies addressing the impact of not only established but promising therapies for OSA/obesity.

Effect of continuous positive airway pressure on atrial remodeling and diastolic dysfunction of patients with obstructive sleep apnea and metabolic syndrome: a randomized study.

OBJECTIVE: The aim of this study was to evaluate the role of obstructive sleep apnea (OSA) treatment on heart remodeling and diastolic dysfunction in patients with metabolic syndrome (MS). METHODS: This study is a prespecified analysis of a randomized placebo-controlled trial that enrolled patients with a recent diagnosis of MS and moderate-to-severe OSA to undergo continuous positive airway pressure (CPAP) or nasal dilators (placebo) for 6 months. Patients were invited to perform a transthoracic echocardiogram by a single investigator blinded to treatment assignment. RESULTS: A total of 99 (79% men; mean [SD], age: 48 [9] years; BMI: 33 [4] kg/m2 ) completed the study. At follow-up, in the placebo group, patients had a significant increase in atrial diameter: from 39.5 (37.0-43.0) mm to 40.5 (39.0-44.8) mm (p = 0.003). CPAP prevented atrial enlargement: from 40.0 (38.0-44.0) to 40.0 (39.0-45.0) mm (p = 0.194). In patients with diastolic dysfunction at baseline, almost half had diastolic dysfunction reversibility with CPAP (in comparison with only two patients in the placebo group, p = 0.039). In the regression analysis, the chance of diastolic dysfunction reversibility by CPAP was 6.8-fold (95% CI: 1.48-50.26, p = 0.025) compared with placebo. CONCLUSIONS: In patients with MS and OSA, 6 months of CPAP therapy prevented atrial remodeling and increased the chance of diastolic dysfunction reversibility.

Effects of CPAP on Metabolic Syndrome in Patients With OSA: A Randomized Trial.

BACKGROUND: OSA is associated with metabolic syndrome (MS), but it is unclear whether OSA treatment with CPAP can revert MS. RESEARCH QUESTION: Does OSA treatment with CPAP per se have effects on the MS reversibility and the associated metabolic, adiposity and vascular parameters? STUDY DESIGN AND METHODS: The TREATOSA-MS trial is a randomized placebo-controlled trial that enrolled adult patients with a recent diagnosis of MS and moderate or severe OSA (apnea-hypopnea index [AHI], ≥ 15 events/h) to undergo therapeutic CPAP or nasal dilator strips (placebo group) for 6 months. Before and after each intervention, we measured anthropometric variables, BP, glucose, and lipid profile. To control potential-related mechanisms and consequences, we also measured adiposity biomarkers (leptin and adiponectin), body composition, food intake, physical activity, subcutaneous and abdominal fat (visceral and hepatic fat), and endothelial function. RESULTS: One hundred patients (79% men; mean age, 48 ± 9 years; BMI, 33 ± 4 kg/m2; AHI, 58 ± 29 events/h) completed the study (n = 50 per group). The mean CPAP adherence was 5.5 ± 1.5 h/night. After 6 months, most patients with OSA randomized to CPAP retained the MS diagnosis, but the rate of MS reversibility was higher than observed in the placebo group (18% vs 4%; OR, 5.27; 95% CI, 1.27-35.86; P = .04). In the secondary analysis, CPAP did not promote significant reductions in the individual components of MS, weight, hepatic steatosis, lipid profile, adiponectin, and leptin, but did promote a very modest reduction in visceral fat and improved endothelial function (all analyses were adjusted for baseline values). INTERPRETATION: Despite the higher rate of MS reversibility after CPAP therapy as compared with placebo, most patients retained this diagnosis. The lack of significant or relevant effects on adiposity biomarkers and depots supports the modest role of OSA in modulating MS. TRIAL REGISTRATION: ClinicalTrials.gov; No.: NCT02295202; URL: www. CLINICALTRIALS: gov.

Performance of NoSAS score versus Berlin questionnaire for screening obstructive sleep apnoea in patients with resistant hypertension

ABSTRACT: Obstructive sleep apnoea (OSA) is the main secondary form associated with resistant hypertension (RH), but it is largely underdiagnosed and consequently undertreated in clinical practice. The Berlin questionnaire (BQ) is a useful tool among general population, but seems to not perform well among patients with RH. Recently, NoSAS score was validated in a large population, however, has not been tested in the cardiovascular scenario. Thus, we aimed to compare BQ versus the NoSAS score as screening tools for OSA in RH. In the present study, patients with confirmed diagnosis of RH were invited to perform polysomnography. OSA was diagnosed by an apnoea-hypopnoea index (AHI) ≥15 events/h. BQ and NoSAS were applied in a blinded way. We calculated the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and area under the curve (AUC) of the two sleep questionnaires to detect OSA in RH. The frequency of OSA was 64%. The BQ presented a better sensitivity (91 vs. 72%) and higher values of NPV (67 vs. 54%) than NoSAS score. In contrast, the NoSAS score had higher specificity for excluding OSA (58 vs. 33%) and higher PPV (75 vs. 70%). Compared to the BQ, NoSAS score had a better AUC (0.55 vs. 0.64) but these values are in the fail to poor accuracy range. In conclusion, both BQ and NoSAS score had low accuracy for detecting OSA in RH. Considering the high frequency of OSA, objective sleep study may be considered in these patients.

Performance of NoSAS score versus Berlin questionnaire for screening obstructive sleep apnoea in patients with resistant hypertension.

Obstructive sleep apnoea (OSA) is the main secondary form associated with resistant hypertension (RH), but it is largely underdiagnosed and consequently undertreated in clinical practice. The Berlin questionnaire (BQ) is a useful tool among general population, but seems to not perform well among patients with RH. Recently, NoSAS score was validated in a large population, however, has not been tested in the cardiovascular scenario. Thus, we aimed to compare BQ versus the NoSAS score as screening tools for OSA in RH. In the present study, patients with confirmed diagnosis of RH were invited to perform polysomnography. OSA was diagnosed by an apnoea-hypopnoea index (AHI) ≥15 events/h. BQ and NoSAS were applied in a blinded way. We calculated the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and area under the curve (AUC) of the two sleep questionnaires to detect OSA in RH. The frequency of OSA was 64%. The BQ presented a better sensitivity (91 vs. 72%) and higher values of NPV (67 vs. 54%) than NoSAS score. In contrast, the NoSAS score had higher specificity for excluding OSA (58 vs. 33%) and higher PPV (75 vs. 70%). Compared to the BQ, NoSAS score had a better AUC (0.55 vs. 0.64) but these values are in the fail to poor accuracy range. In conclusion, both BQ and NoSAS score had low accuracy for detecting OSA in RH. Considering the high frequency of OSA, objective sleep study may be considered in these patients.