Obstructive sleep apnea and objective short sleep duration are independently associated with the risk of serum vitamin D deficiency.

BACKGROUND: Studies demonstrate an association between vitamin D (25(OH)D) deficiency and sleep disturbances, such as obstructive sleep apnea (OSA) and short sleep duration. However, to date, no studies have concurrently and objectively evaluated the effect of these factors on 25(OH)D. OBJECTIVES: To evaluate whether OSA and objective short sleep duration are independently associated with reduced 25(OH)D in an adult population sample. METHODS: A cross-sectional study included 657 individuals from the city of Sao Paulo, Brazil, as part of the ERA project. Participants fulfilled questionnaires and underwent clinical evaluation, polysomnography and blood sample collection for 25(OH)D quantification. OSA was classified into three categories (mild, moderate and severe). The risk of 25(OH)D deficiency was considered as levels<30 ng/mL. Short sleep duration was defined as total sleep time<6 hours. RESULTS: The risk of 25(OH)D deficiency was observed in 59.5% of the sample, affecting more individuals of the female gender, obese, with African American ethnicity, and those that were smokers, sedentary and presented hypertension and diabetes. In the final logistic model adjusted for age, gender, ethnicity, obesity, smoking, hypertension, diabetes, sedentary lifestyle, seasonality and creatinine serum levels, both OSA and short sleep duration showed significant independent associations with the risk of 25(OH)D deficiency (moderate OSA: OR for 25(OH)D<30 = 2.21, 95% CI: 1.35-3.64, p<0.01; severe OSA: OR for 25(OH)D<30 = 1.78, 95% CI: 1.06-3.00, p = 0.03; short sleep duration: OR for 25(OH)D<30 = 1.61, 95% CI: 1.15-2.26, p = 0.01). After a subgroup analysis, similar results were observed only in participants ≥50 years. CONCLUSION: OSA and short sleep duration are independently associated with the risk of 25(OH)D deficiency in an adult population. Age-related changes in vitamin D metabolism and the frequency of sleep disorders may be involved in these associations. Future studies exploring whether 25(OH)D levels may modulate OSA and sleep curtailment-related outcomes are needed.

An assessment of oxidized LDL in the lipid profiles of patients with obstructive sleep apnea and its association with both hypertension and dyslipidemia, and the impact of treatment with CPAP.

OBJECTIVE: Obstructive sleep apnea (OSA) has been linked to increased oxidative stress, lipid peroxidation and worsening atherosclerosis. This study investigated oxidized low-density lipoprotein (oxLDL) as a marker of lipid peroxidation, and total LDL cholesterol (direct LDL-C), as a marker of the lipid profile among individuals with OSA, and its association with hypertension (HYP) and dyslipidemia (DYS). The impact of one year of continuous positive airway pressure (CPAP) was also assessed. METHODS: Blood was collected after 12 h of fasting from 99 consecutive patients who were diagnosed with OSA via polysomnography, and were also diagnosed with both HYP and DYS via clinical and laboratory studies. The patients were classified into the following three groups: GI [OSA with comorbidities (HYP or DYS)], GII [OSA without comorbidities], and GIII [control]. Thirty-five patients with an apnea/hypopnea index >20 per hour of sleep were randomized to groups that received either Sham-CPAP or CPAP treatments over 12 months. RESULTS: In a binary regression controlled for sex, age, body mass index, and glycemia, model 1 which analyzed direct LDL-C, demonstrated significant levels of risk in the setting of DYS but not in the settings of HYP and OSA. In model 2, which analyzed oxLDL, DYS (p = 0.01), HYP (p = 0.032), and OSA (p = 0.039) were statistically significant. Significant alterations were observed in only the sleep parameters following one year of CPAP. CONCLUSIONS: Based on the statistical regression model, only the presence of DYS (p = 0.001) was associated with the levels of direct LDL-C. The remaining comorbidities (OSA and HYP) were not significantly related to the levels of direct LDL-C. Regarding oxLDL, OSA, HYP and DYS each added significant score values to the levels of oxLDL. These findings are suggestive of the importance of assessing oxLDL among patients presenting with OSA, both with and without comorbidities.

Validation of a novel sleep-quality questionnaire to assess sleep in the coronary care unit: a polysomnography study.

INTRODUCTION: The sleep of patients admitted to coronary care unit (CCU) may be compromised. A feasible and cost-effective tool to evaluate sleep in this scenario could provide important data. The aim of this study was to evaluate sleep with a questionnaire developed specifically for the CCU and to validate it with polysomnography (PSG). METHODS: Ninety-nine patients (68% male; 56 ± 10 years old) with acute coronary syndrome were included. PSG was performed within 36 h of admission. A specific 18-question questionnaire (CCU questionnaire) was developed and applied after the PSG. Cronbach's alpha test was used to validate the questionnaire. The Spearman test was used to analyze the correlation between the PSG variables and the questionnaire, and the Kruskal-Wallis test was used to compare the PSG variables among patients with good, regular, or poor sleep. RESULTS: The total sleep time was 265 ± 81 min, sleep efficiency 62 ± 18%, REM sleep 10 ± 7%, apnea/hypopnea index 15 ± 23, and the arousal index 24 ± 15. Cronbach's alpha test was 0.69. The CCU questionnaire showed correlation with the sleep efficiency evaluated by PSG (r: 0.52; p < 0.001). Sleep quality was divided into three categories according to the CCU questionnaire: patients with good sleep had a sleep efficiency of 72 ± 9%, better than those with a regular or poor sleep (60 ± 16% and 53 ± 20%, respectively; p < 0.01). CONCLUSION: The CCU questionnaire is a feasible and reliable tool to evaluate sleep in the CCU, showing correlation with the PSG sleep efficiency.

Evaluation and validation of a method for determining platelet catecholamine in patients with obstructive sleep apnea and arterial hypertension.

BACKGROUND: Measurements of plasma and urinary catecholamine are susceptible to confounding factors that influence the results, complicating the interpretation of sympathetic nervous system (SNS) activity in the Obstructive sleep apnea (OSA) and arterial hypertension (HYP) conditions. OBJECTIVE: In this study, we validated a test for platelet catecholamine and compared the catecholamine levels (adrenaline and noradrenaline) in urine, plasma and platelets in patients with OSA and HYP compared with controls. METHODS: In the validation, 30 healthy, nonsmoking volunteers who were not currently undergoing treatment or medication were selected as the control group. One hundred fifty-four individuals (114 OSA, 40 non-OSA) were consecutively selected from the outpatient clinic of the Sleep Institute and underwent clinical, polysomnographic and laboratory evaluation, including the urinary, plasma and platelet levels of adrenaline (AD) and noradrenaline (NA). Patients were then allocated to groups according to the presence of OSA and/or hypertension. RESULTS: A logistic regression model, controlled for age and BMI, showed that urinary AD and urinary NA were risk factors in the OSA+HYP group and the HYP group; however, the model showed higher levels of platelet NA for OSA without HYP. After 1 year of CPAP (continuous upper airway pressure) treatment, patients (n = 9) presented lower levels of urinary NA (p = 0.04) and platelet NA (p = 0.05). CONCLUSION: Urinary NA and AD levels were significantly associated with the condition of hypertension with and without OSA, whereas platelet NA with OSA without comorbidity. These findings suggest that platelet catecholamine levels might reflect nocturnal sympathetic activation in OSA patients without hypertension.

Mandibular advancement device and CPAP upon cardiovascular parameters in OSA.

PURPOSE: This study aims to compare the effects of a mandibular advancement device (MAD) with continuous positive airway pressure (CPAP) treatment for obstructive sleep apnea (OSA) on blood pressure (BP), oxidative stress, and heart rate variability (HRV) in a randomized, crossed-over, single-blind, and controlled trial. METHODS: Twenty-nine moderate-to-severe adult OSA patients underwent MAD, CPAP, and placebo oral appliance treatment. Polysomnography, Epworth sleepiness scale, 24-h ambulatory BP monitoring, oxidative stress parameters (malondialdehyde, catalase, superoxide dismutase, vitamins C, E, B6, B12, folate, homocysteine, uric acid), and HRV were assessed at baseline and after 1 month of each treatment. Diaries were used to evaluate compliance for devices and a pressure-time meter for CPAP. RESULTS: Both active treatments resulted in decreases in apnea and hypopnea index and Epworth sleepiness scale; CPAP showed a greater effect. Frequency of diastolic BP dipping was higher in the MAD group compared with the CPAP group. A significant drop from baseline levels for catalase activity was observed after MAD. For HRV, there was a significant decrease in total power at night with CPAP and MAD compared with POA, and a decrease in index of sleep autonomic variation with MAD compared with baseline levels. Compliance rates were higher with MAD rather than CPAP. CONCLUSIONS: Even though CPAP proved to be more effective at attenuating OSA, better compliance with MAD favored the reduction of one of the enzymes which participates in oxidative stress and better autonomic modulation during sleep.

Reciprocal interactions of obstructive sleep apnea and hypertension associated with ACE I/D polymorphism in males.

BACKGROUND: The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism gene contributes to the genesis of hypertension (HTN) and may help explain the relationship between obstructive sleep apnea (OSA) and HTN. However, ACE is a pleiotropic gene that has several influences, including skeletal muscle and control of ventilation. We therefore tested the hypothesis that ACE polymorphism influences OSA severity. METHODS: Male OSA patients (apnea-hypopnea index [AHI]>5 events/h) from 2 university sleep centers were evaluated by polysomnography and ACE I/D polymorphism genotyping. RESULTS: We studied 266 males with OSA (age=48+/-13 y, body mass index=29+/-5 kg/m(2), AHI=34+/-25 events/h). HTN was present in 114 patients (43%) who were older (p<0.01), heavier (p<0.05) and had more severe OSA (p<0.01). The I allele was associated with HTN in patients with mild to moderate OSA (p<0.01), but not in those with severe OSA. ACE I/D polymorphism was not associated with apnea severity among normotensive patients. In contrast, the only variables independently associated with OSA severity among patients with hypertension in multivariate analysis were BMI (OR=1.12) and II genotype (OR=0.27). CONCLUSIONS: Our results indicate reciprocal interactions between OSA and HTN with ACE I/D polymorphism, suggesting that among hypertensive OSA males, the homozygous ACE I allele protects from severe OSA.