Vitamin D deficiency in patients evaluated for obstructive sleep apnea: is it associated with disease severity?

PURPOSE: The aim of the present study was to assess vitamin D levels in a large cohort of OSA patients and to investigate possible correlations with clinical and polysomnographic parameters. METHODS: In this cross-sectional study, 685 consecutive patients underwent type 1 polysomnography (PSG) for OSA diagnosis. They were grouped according to apnea-hypopnea index (AHI) as mild, moderate, and severe. Patients with AHI < 5 served as controls. Demographic, PSG data, and serum levels of vitamin D were measured and compared between groups. RESULTS: OSA was diagnosed in 617 of the patients (90%). Of those, 94 (15%) had mild OSA, 150 (24%) moderate OSA, and 373 (61%) severe OSA. The risk of vitamin D deficiency (< 20 ng/mL) was observed in 38% of the cohort. OSA patients had lower vitamin D levels compared to controls (23 ng/mL vs 26 ng/mL, p = 0.006). The lowest levels of vitamin D [mean 21] (p < 0.001 among all groups) and the higher prevalence for vitamin D deficiency (45%) were observed in severe OSA patients. After multiparametric adjustments for age, gender, obesity, and comorbidities, severe OSA showed significant independent associations with the risk of vitamin D deficiency [OR (95% CI) 2.002 (1.049-3.819), p = 0.035]. CONCLUSIONS: A large proportion of patients referred for OSA evaluation had vitamin D deficiency, which was independently associated with severe OSA. However, further research is needed in order to determine the role of vitamin D in OSA patients.

Long-term variations of arterial stiffness in patients with obesity and obstructive sleep apnea treated with continuous positive airway pressure.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with cardiovascular co-morbidities and mortality. Arterial stiffness is an independent predictor of cardiovascular risk and mortality, and is influenced by the presence of OSA and related comorbidities. There is a paucity of data regarding long-term evolution of arterial stiffness in CPAP-treated OSA patients. We aimed to prospectively study long term PWV variations and determinants of PWV deterioration. METHODS: In a prospective obese OSA cohort, at time of diagnosis and after several years of follow-up we collected arterial stiffness measured by carotid-femoral pulse wave velocity (PWV), clinical and metabolic parameters, and CPAP adherence. Univariate and multivariate analyses were performed in order to determine contributing factors. RESULTS: Seventy two OSA patients (men: 52.8%, median age: 55.8 years and median BMI of 38.5 kg/m2) with a prevalence of hypertension: 58.3%, type 2 diabetes: 20.8%, hypercholesterolemia: 33.3%, current or past smoking: 59.7%, were evaluated after a median follow-up of 7.4 [5.8; 8.3] years. Over the period of follow-up, the median increase in PWV was 1.34 [0.10; 2.37] m/s. In multivariate analysis, the increase in PWV was associated with older age (10 extra years was associated with a 5.24 [1.35; 9.12] % increase in PWV) and hypertension (a significant increase in PWV of 8.24 [1.02; 15.57] %). No impact of CPAP adherence on PWV evolution was found. CONCLUSION: PWV progression in CPAP-treated OSA patients is mainly related to pre-existing cardio-metabolic comorbidities and not influenced by CPAP adherence. In this high cardiovascular risk population, it is crucial to associated weight management and exercise with CPAP treatment.

Mild obstructive sleep apnea increases hypertension risk, challenging traditional severity classification.

STUDY OBJECTIVES: The association of mild obstructive sleep apnea (OSA) with important clinical outcomes remains unclear. We aimed to investigate the association between mild OSA and systemic arterial hypertension (SAH) in the European Sleep Apnea Database cohort. METHODS: In a multicenter sample of 4,732 participants, we analyzed the risk of mild OSA (subclassified into 2 groups: mildAHI 5-<11/h (apnea-hypopnea index [AHI], 5 to <11 events/h) and mildAHI 11-<15/h (AHI, ≥11 to <15 events/h) compared with nonapneic snorers for prevalent SAH after adjustment for relevant confounding factors including sex, age, smoking, obesity, daytime sleepiness, dyslipidemia, chronic obstructive pulmonary disease, type 2 diabetes, and sleep test methodology (polygraphy or polysomnography). RESULTS: SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and nonapneic snorers (52% vs 45% vs 30%; P < .001). Corresponding adjusted odds ratios for SAH were 1.789 (mildAHI 11-<15/h; 95% confidence interval [CI], 1.49-2.15) and 1.558 (mildAHI 5-<11/h; 95%, CI, 1.34-1.82), respectively (P < .001). In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in the polygraphy (odds ratio, 1.779; 95% CI, 1.403-2.256; P < .001) and polysomnography groups (odds ratio, 1.424; 95% CI, 1.047-1.939; P = .025). CONCLUSIONS: Our data suggest a dose-response relationship between mild OSA and SAH risk, starting from 5 events/h in polygraphy recordings and continuing with a further risk increase in the 11- to <150-events/h range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify participants with OSA according to cardiovascular risk.