Association between hydrogen sulfide and OSA-associated hypertension: a clinical study

Purpose

We sought to unravel the role of hydrogen sulfide (H₂S) in the development of hypertension in patients with obstructive sleep apnea (OSA).

Methods

The study sample included 80 patients with OSA and 45 healthy controls. All subjects underwent measurement of blood pressure (BP) and serum H₂S level in the morning. Twentynine of the 39 patients with OSA and concomitant hypertension and 23 of the 41 patients with OSA but no concomitant hypertension received continuous positive alveolar pressure (CPAP) therapy for 4 weeks. Twenty-four-hour ambulatory BP and serum H₂S were determined before and after CPAP. Respiratory indices including apnea hypopnea index (AHI), lowest oxygen saturation (SaO₂), and length of time < 90% saturated (T90) were determined by polysomnography.

Results

Associations between H₂S, BP, respiratory indices, and changes with CPAP were analyzed. OSA patients had significantly higher systolic BP (p = 0.003) and diastolic BP (p = 0.009) and lower H₂S levels (p = 0.02) compared to healthy controls. H₂S negatively correlated with AHI (p = 0.005), T90 (p = 0.009), morning systolic BP (p = 0.02), and morning diastolic BP (p = 0.03). All respiratory indices were significantly improved (p < 0.05) after CPAP in OSA patients with or without hypertension. BP was significantly reduced and H₂S significantly increased after CPAP in OSA patients with hypertension (p < 0.05) but not in OSA patients without hypertension (p > 0.05).

Conclusion

Multivariate linear regression analysis demonstrated that 24h systolic BP and 24h diastolic BP correlated with H₂S as well as their changes after CPAP treatment. Reduction in H₂S may play a role in the pathogenesis of hypertension in patients with OSA.

     

Effect of a 2 week CPAP treatment on mood states in patients with obstructive sleep apnea: a double-blind trial

Obstructive sleep apnea (OSA) is a common disease with significant medical and psychiatric comorbidities. The literature documenting the effects of continuous positive airway pressure (CPAP) treatment on mood in OSA patients is mixed. We previously observed that 1 week of CPAP treatment did not result in improvements in mood beyond those observed in a group treated with placebo–CPAP. This study examined the effect of a 2 week CPAP treatment on mood in a placebo-controlled design in OSA patients. Fifty patients with untreated sleep apnea were evaluated by polysomnography and completed the Profile of Mood States (POMS) pre-/post-treatment. The patients were randomized for 2 weeks to either therapeutic CPAP or placebo–CPAP (at insufficient pressure). Both the therapeutic CPAP and the placebo–CPAP groups showed significant improvements in POMS total score, tension, fatigue, and confusion. No significant time × treatment effect was observed for either group. We could not show a specific beneficial impact of CPAP treatment on mood in OSA patients.     

CPAP Does Not Reduce High-Sensitivity C-Reactive Protein in Patients With Coronary Artery Disease and Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is associated with an increase in high-sensitivity C-reactive protein (hs-CRP). Studies suggested that the degree of severity of OSA in obese patients with no known coronary artery disease correlates with higher levels of hs-CRP and that continuous positive airway pressure (CPAP) could reduce this inflammation marker. In this study we tested the hypothesis that CPAP therapy could also reduce hs-CRP in cardiac patients with multiple comorbidities and known OSA. Sixty-two consecutive patients were included in this study. All patients were referred for a sleep test because of clinical suspicion of OSA. Clinical variables, body mass index (BMI), hs-CRP, and lipid profile were obtained at the time of their referral and at 126.2 ± 33.7 days followup. Thirty-four patients (group A) underwent CPAP therapy and 28 patients did not (group B). The linear regression of hs-CRP level on the severity of the apnea–hypopnea index (AHI) was significant (p = 0.05), but this significance is lost when ln(hs-CRP) was used (p = 0.263). Through analysis of covariance, ln(hs-CRP) was predicted by BMI (p = 0.000) (R-Sq = 46.2%). In group A, and despite a significant drop in the AHI with CPAP [median difference = −29.7 (−41.8, −22.2)], there were no significant differences in patients’ BMI, lipid profile, or hs-CRP [median difference = −0.15 (−0.83, 0.64)] (p = 0.53) on followup. When both groups A and B were compared, they had matched BMI, lipids, ejection fraction, blood pressure, age, creatinine, awake O₂ saturations, alcohol consumption, coronary artery disease, and baseline and followup hs-CRP despite significant differences in baseline AHI (37.65 vs 14.30, respectively, p = 0.000). We conclude that the degree of OSA or CPAP treatment does not independently predict levels of ln(hs-CRP) in cardiac outpatients when other clinical variables, BMI, and lipids are adjusted for. BMI remains the strongest independent predictor of hs-CRP in this patient population. Supported by the Midwest Cardiovascular Research Foundation, Davenport, Iowa.     

Gender differences in Saudi patients with obstructive sleep apnea

Obstructive sleep apnea (OSA) remains under-recognized in women possibly due to differences in clinical presentation, difference in tolerance to symptoms, and rate of usage and referral to sleep services. No reports have addressed OSA in women in the Middle Eastern (Arab) population. Therefore, we conducted this study to assess the differences in demographics, clinical presentation, and polysomnographic (PSG) findings between Saudi women and men diagnosed to have (OSA). The study group comprised 191 consecutive Saudi women and 193 consecutive men who were referred to the Sleep Disorders Centre and were found by in-laboratory PSG to have OSA. Demographic and clinical data were obtained by personal interviews. Women were significantly older than men (53.9 and 43.0 years, respectively; p < 0.001). Similarly, their body mass index was significantly higher than men (p < 0.001). Insomnia was more common among women (39.8%) compared to men (25.9%; p = 0.005). Other sleep symptoms including witnessed apnea, and excessive daytime sleepiness did not show any statistical difference between the two groups. Women were more likely than men to be diagnosed with hypothyroidism, diabetes, hypertension, cardiac disease, and asthma. Apnea–hypopnea index (AHI) was statistically higher in men compared to women; however, most of apnea/hypopnea events in women occurred during rapid eye movement sleep, and the mean duration of hypopnea and apnea was significantly lower in women (p = 0.004). Sleep efficiency was lower in women (71.5% vs. 77.7%) in men (p < 0.001). The desaturation index was higher in men (p = 0.01), but no difference was found in lowest SaO₂ or time with SaO₂ less than 90%. The present study showed important clinical and PSG differences between Saudi women and men with OSA. Clinicians need to be aware of these differences when assessing women for the possibility of OSA as they may be symptomatic at a lower AHI and have significant comorbid conditions that can be adversely affected if their OSA was not timely managed.     

Lack of Benefit of Continuous Positive Airway Pressure on Lung Function in Patients with Overlap Syndrome

Obstructive sleep apnea (OSA) has been shown to be an inflammatory stimulus and may potentially result in a deterioration in the respiratory status of patients with coexistent chronic obstructive pulmonary disease (COPD) (overlap syndrome). We hypothesized that with treatment of OSA, there would be an improvement in coexistent COPD in overlap patients. We also sought to characterize overlap patients by comparing them with patients with either OSA or COPD alone. We performed a retrospective study of patients who attended a university-affiliated Veterans Affairs hospital. Demographic and clinical data were obtained from the medical charts and pharmacy records for the preceding two years and for the two years following the initiation of continuous positive airway pressure (CPAP) therapy. Overlap patients had moderately severe sleep apnea (AHI 28.6 ± 4.2) and moderately severe COPD (FEV₁= 1.94 ± 0.10 L). The prevalence of overlap syndrome in COPD patients was 11.9%, and 41% in OSA patients. Overlap patients who were compliant with CPAP therapy experienced a greater decrease in FEV₁, percent predicted FEV₁, percent decrease in FEV₁, FVC, percent predicted FVC, and percent decrease in FVC when compared with noncompliant patients. A very strong correlation was found between the average hours of CPAP use per day and the percent decrease in FEV₁ (r = 0.69, p = 0.003). There was a similar strong correlation for the decrease in FEV₁ and percent predicted FEV₁. OSA is common in COPD patients; similarly, COPD is common in OSA patients. Treatment of OSA with CPAP therapy in patients with overlap syndrome may not lead to an improvement in the coexistent COPD.     

Serum levels of magnesium and their relationship with CRP in patients with OSA

Background

Low levels of magnesium (Mg) are associated with chronic inflammatory stress. Some animal studies have reported that a moderate deficiency of Mg, similar to that which occurs in humans, may increase inflammatory or oxidative stress stimulated by other factors, such as disrupted sleep or sleep deficiency.

Purpose

This cross-sectional study evaluated the relationship between serum levels of Mg and the inflammatory response in patients with a new diagnosis of obstructive sleep apnea (OSA).

Methods

This clinical, retrospective study registered 68 patients with newly diagnosed mild to severe OSA and 30 without OSA. The Apnea–Hypopnea Index (AHI), oxygen desaturation index (ODI), time until blood hemoglobin oxygen saturation <90 % (SpO₂ <90 %), and mean blood hemoglobin SpO₂ were measured. Serum levels of Mg, plasma C-reactive protein (CRP), and total sleep time (TST) by polysomnography were also measured.

Results

Mg levels were lower in patients with OSA than those in controls matched for age, sex, and body mass index (BMI). Patients with OSA had substantially higher plasma CRP concentrations than controls. A negative correlation was observed between the AHI and ODI and Mg levels. Significant differences in Mg and CRP levels were observed between patients with AHI scores of 5–15 and scores ≥30 based on OSA severity but independent of BMI. Furthermore, the AHI, ODI, TST <90 %, and mean SpO₂ significantly correlated with CRP. A significant negative correlation was observed between Mg and CRP levels (p < 0.0001).

Conclusion

Our results show that Mg levels changed depending on the presence and severity of OSA. Low levels were associated with a higher CRP concentration in patients with OSA.

     

Association between polysomnographic measures of disrupted sleep and prothrombotic factors

BACKGROUND: Subjective sleep disturbances have been associated with increased risk of coronary artery disease (CAD). We hypothesized that disrupted sleep as verified by polysomnography is associated with increased levels of prothrombotic hemostasis factors previously shown to predict CAD risk. METHODS: Full-night polysomnography was performed in 135 unmedicated men and women (mean age +/- SD, 36.8 +/- 7.8 years) without a history of sleep disorders. Morning fasting plasma levels of von Willebrand Factor (VWF) antigen, soluble tissue factor (sTF) antigen, d-dimer, and plasminogen activator inhibitor (PAI)-1 antigen were determined. Statistical analyses were adjusted for age, gender, ethnicity, body mass index, BP, and smoking history. RESULTS: Higher total arousal index (ArI) was associated with higher levels of VWF (beta = 0.25, p = 0.011, DeltaR(2) = 0.045), and longer wake after sleep onset was associated with higher levels of sTF (beta = 0.23, p = 0.023, DeltaR(2) = 0.038). More nighttime spent at mean oxygen saturation < 90% (beta = 0.20, p = 0.020, DeltaR(2) = 0.029) and higher apnea-hypopnea index (AHI) [beta = 0.19, p = 0.034, DeltaR(2) = 0.024] were associated with higher PAI-1. There was a trend for a relationship between mean oxygen desaturation < 90% and PAI-1 (p = 0.053), even after controlling for AHI. Total ArI (beta = 0.28, p = 0.005, DeltaR(2) = 0.056) and WASO (beta = 0.25, p = 0.017, DeltaR(2) = 0.042) continued to predict VWF and sTF, respectively, even after controlling for AHI. CONCLUSIONS: Polysomnographically verified sleep disruptions were associated with prothrombotic changes. Measures of sleep fragmentation and sleep efficiency were related to VWF and sTF, respectively. Apnea-related measures were related to PAI-1. Our findings suggest that sleep disruptions, even in a relatively healthy population, are associated with potential markers of prothrombotic cardiovascular risk.     

Prevalence of masked and nocturnal hypertension in patients with obstructive sleep apnea syndrome

IntroductionObstructive sleep apnea (OSA) is considered as a risk factor for the development and worsening of compensation of arterial hypertension and other cardiovascular diseases. Prevalence of masked and nocturnal hypertension can have a significant negative impact on these patients and these prevalences are not well known.AimTo evaluate the prevalence of masked and nocturnal hypertension in patients with OSA.Materials and methodsIn this study, 97 (88 men) patients were enrolled, average age 53.9 ± 9.7 years. OSA was diagnosed with polysomnography and the continuous positive airway pressure therapy has been indicated according to current guidelines. Then were evaluated parameters of OSA (apnea-hypopnea index (AHI), oxygen desaturation index (ODI), % of sleep time <90% SpO₂, average night SpO₂). Patients also underwent physical examination including office blood pressure measurement, 24 h blood pressure monitoring (ABPM) and measurement of anthropometric parameters.ResultsFollowing average values were present in OSA patients (mean value and standard deviation): AHI 54.6 ± 22.7, ODI 58.3 ± 24, % of sleep time < 90% SpO₂ 35.4 ± 25.1, average night SpO₂ 88.8 ± 5. Masked hypertension was present in 55 (56.7%) patients, nocturnal hypertension in 79 (81.4%) patients. Arterial hypertension was appropriately compensated in only 15 (15.5%) patients. Results have not shown any statistically significant correlation between prevalence of nocturnal hypertension and AHI (p = 0.059), % of sleep time <90% SpO₂ (p = 0.516), average night SpO₂ (p = 0.167). ODI was significantly higher in patients with nocturnal hypertension (p = 0.002). No correlation between prevalence of masked hypertension and AHI (p = 0.841), ODI (p = 0.137), average night SpO₂ (p = 0.991) and % of sleep time <90% SpO₂ (p = 0.896) has been present.ConclusionThis study has demonstrated high prevalence of masked and nocturnal hypertension in patients with OSA, which can considerably increase risks of cardiovascular diseases in these patients.     

The effects of continuous positive airway pressure therapy on mean platelet volume in patients with obstructive sleep apnea

Previous studies have reported increased platelet activation and aggregation in patients with obstructive sleep apnea (OSA). Continuous positive airway pressure (CPAP) treatment has been shown to decrease platelet activation. We aimed to study the effects of nasal CPAP therapy has on MPV values in patients with severe OSA. Thirty-one patients (21 men; mean age 53.8?±?9.2 years) with severe OSA (AHI?>?30 events/hour) constituted the study group. An age, gender and body mass index (BMI) matched control group was composed 25 subjects (14 men; mean age 49.6?±?8.5 years) without OSA (AHI?<?5 events/hour). We measured MPV values in patients with severe OSA and control subjects and we measured MPV values after 6 months of CPAP therapy in severe OS patients. The median (IQR) MPV values were significantly higher in patients with severe OSA than in control group (8.5 [8.3–9.1] vs. 8.3 [7.5–8.8] fL; p?=?0.03). The platelet counts were significantly lower in patients with severe OSA than in control group (217.8?±?45.9 vs. 265.4?±?64.0?×?10⁹/L; p?=?0.002). The six months of CPAP therapy caused significant reductions in median (IQR) MPV values in patients with severe OSA (8.5 [8.3–9.1] to 7.9 [7.4–8.2] fL; p?<?0.001). Six months of CPAP therapy caused significant increase in platelet counts when compared with baseline values (217.8?±?45.9 to 233.7?±?60.6?×?10⁹/L; p?<?0.001). We have found that the MPV values of patients with severe OSA were significantly higher than those of the control subjects and 6 months CPAP therapy caused significant reductions in the MPV values in patients with severe OSA.     

Continuous positive airway pressure device-based automated detection of obstructive sleep apnea compared to standard laboratory polysomnography

Purpose

Obstructive sleep apnea (OSA) is a common health problem that affects more than 2–4% of the US population. Polysomnography (PSG) is the gold standard for diagnosing OSA. PSG is, however, expensive, time-consuming, and not always readily accessible. Hence, alternative diagnostic methods such as home-based testing have been evaluated. We studied the ability of the REMstar Pro (RSP2, a brand of continuous positive airway pressure (CPAP) device) to identify abnormal breathing events in subjects with OSA and compared this with breathing events simultaneously determined by laboratory-based PSG.

Methods

We evaluated 10 subjects previously diagnosed with OSA (apnea hypopnea index (AHI)?>?15, known therapeutic level of CPAP). Subjects underwent attended PSG using the REMstar Pro M series machine and their prescribed interface/mask type. The first 3 h of the study were conducted using a subtherapeutic CPAP (4 cm H2O). The last 3 h or remaining portion of the PSG was completed using the previously determined therapeutic CPAP. Comparison of respiratory events detected by PSG vs the RSP2 was performed.

Results

Subjects included four men and six women, aged 32 to 57 years and with a body mass index ranging from 29.5–66.4. The baseline AHI ranged from 18.3–93.1, with the AHI at therapeutic CPAP ranging from 0–3. Apnea counts at baseline and at therapeutic CPAP by manually scored PSG and REMstar were not significantly different (mean at subtherapeutic 11.7 vs 12.5, p?=?0.76; median at therapeutic CPAP 2.0 vs 4.5, p?=?0.15). Hypopnea counts at baseline and at effective CPAP by PSG and REMstar were not significantly different (mean at subtherapeutic 38.1 vs. 40.9, p?=?0.72; median at therapeutic CPAP 5.0 vs. 2.5, p?=?0.34). The correlation coefficient of REMstar and PSG for apnea and hypopnea was significant in subtherapeutic phase only (apnea r?=?0.78, p?=?0.007; hypopnea r?=?0.76, p?=?0.01). Agreement between the two methods declined for hypopnea detection at therapeutic CPAP.

Conclusions

The monitoring of residual sleep-disordered breathing on treatment, in addition to adherence, is an important objective therapeutic target in OSA. The REMstar Pro detects sleep-disordered breathing events similar to that of a manually scored PSG—for apnea but not for hypopnea—and merits further investigation as a device to determine disease severity and treatment efficacy.     

Effects of CPAP and mandibular advancement device treatment in obstructive sleep apnea patients: a systematic review and meta-analysis

The purpose of this review is to conduct a systematic review and meta-analysis comparing the effects of continuous positive airway pressure (CPAP) with a mandibular advancement device (MAD) in improving the quality of life (sleepiness, cognitive, and functional outcomes) in patients diagnosed with obstructive sleep apnea (OSA). Authors identified randomized, placebo-controlled studies from MEDLINE through PubMed, Web of Science, and the Cochrane Library. Studies were assessed for inclusion and exclusion criteria, as well as risk of bias. Initial search yielded 240 unduplicated references, which the authors reduced to 12 relevant studies. Patients with CPAP therapy showed no statistically significant difference in the post-treatment quality of life measured with the SF-36 mental health component (p = .994), or the SF-36 physical functioning component (p = .827). There was no significant improvement in neither Functional Outcomes of Sleep Questionnaire (p = .788) nor cognitive performance (p = .395) compared to patients treated with oral appliances. However, the meta-analyses’ overall results showed a significant improvement in the post-treatment apnea–hypopnea index (AHI) in favor of CPAP therapy as compared with the oral appliance group (p < .001). Meta-analyses showed unclear results for sleepiness with no significant differences in average post-treatment Epworth Sleepiness Scale [ESS] (p = .203), but significant differences in change in ESS from baseline favorable to CPAP treatment (p = .047). Further studies are needed. Compliance with treatment was 1.1 h per night significantly lower with CPAP than MAD (p = .004), which could explain why though efficacy (AHI) is better with CPAP, no significant results are shown for quality of life, cognitive, and functional outcomes. Though CPAP is significantly more efficient in reducing AHI (moderate quality of evidence), it has a significantly lower compliance resulting in no differences with MAD in quality of life, cognitive, or functional outcomes. Sleep medicine professionals should monitor treatment compliance and offer patients non-compliant with CPAP an oral appliance for treatment of OSA.     

Effects of obstructive sleep apnea treatment on left atrial volume and left atrial volume index

Obstructive sleep apnea (OSA) and increased left atrial volume (LAV) both independently increase cardiovascular mortality. We hypothesized that treatment of OSA with continuous positive airway pressure (CPAP) may decrease LAV. We retrospectively identified 47 OSA patients receiving CPAP who had echocardiograms done before and after polysomnography. Compliance was defined as CPAP use at-least five nights weekly and 5 h per night. The compliant group (n = 23) had a significant decrease in diastolic blood pressure (DBP; 4.4 ± 8.9 mmHg, p < 0.05) and mean arterial pressure (MAP; 4.7 ± 10.3 mmHg, p < 0.05), while no significant changes were observed in the noncompliant group (n = 24). LAV data were available in 13 compliant and 20 noncompliant patients. LAV decreased nonsignificantly (3.54 ± 16.6 mL, n = 13, p = 0.65) in CPAP-compliant patients, while it increased (15.47 ± 22.3 mL, n = 20, p < 0.006) in noncompliant patients. Similar changes were seen in the LAV index. Untreated OSA was associated with an increase in LAV and LAV index without significant changes in blood pressure. Treatment of OSA was associated with a decrease in DBP and MAP with a nonsignificant decrease in LAV. Treatment of OSA may prevent adverse left atrial remodeling. There are no conflicts of interest or financial disclosures for any of the authors.     

Natural course of complex sleep apnea—a retrospective study

Patients with complex sleep apnea syndrome (CompSAS) have obstructive sleep apnea but develop troublesome central sleep apnea activity or Cheyne–Stokes breathing when provided continuous positive airway pressure (CPAP) therapy. We examined whether CompSAS activity persists with long-term CPAP treatment. We retrospectively identified all patients with CompSAS who underwent two therapeutic polysomnograms (PSGs) separated by at least 1 month during 2003–2005. We compared PSG findings between the initial and follow-up study and noted clinical responses to therapy. We identified 13 CompSAS patients meeting criteria. Most follow-up PSGs were ordered after an abnormal overnight oximetry on CPAP or because of CPAP intolerance after 195 (49–562) days. The residual apnea–hypopnea index (AHI) on CPAP decreased from 26 (23–40) on the first PSG to 7 (3–21.5) on the follow-up PSG. Only seven patients reached AHI < 10 and 6 had AHI ≥ 10 (“CPAP nonresponders”) at follow-up. “CPAP nonresponders” were sleepier (Epworth Sleepiness Score 13 [12.5–14] vs 9 [6–9.5], p = 0.03) and trended toward lower body mass index (29.7 [28.6–31.6] vs 34.3 [32.5–35.1], p = 0.06). Both groups were equally compliant with CPAP therapy. Although the AHI tends to improve over time in CompSAS patients treated with CPAP, in this retrospective study nearly half-maintained a persistently elevated AHI. A prospective trial is merited to determine the optimal treatment for these patients.     

An electrocardiogram-based analysis evaluating sleep quality in patients with obstructive sleep apnea

Objective

The study compares polysomnography (PSG) and cardiopulmonary coupling (CPC) sleep quality variables in patients with (1) obstructive sleep apnea (OSA) and (2) successful and unsuccessful continuous positive airway pressure (CPAP) response.

Patients/methods

PSGs from 50 subjects (32 F/18 M; mean age 48.4?±?12.29 years; BMI 34.28?±?9.33) were evaluated. OSA patients were grouped by no (n?=?16), mild (n?=?13), and moderate to severe (n?=?20) OSA (apnea–hypopnea index (AHI)?≤?5, >5–15, >15 events/h, respectively). Outcome sleep quality variables were sleep stages in non-rapid eye movement, rapid eye movement sleep, and high (HFC), low (LFC), very low-frequency coupling (VLFC), and elevated LFC broad band (e-LFC_BB). An AHI?≤?5 events/h and HFC?≥?50 % indicated a successful CPAP response. CPC analysis extracts heart rate variability and QRS amplitude change that corresponds to respiration. CPC-generated spectrograms represent sleep dynamics from calculated coherence product and cross-power of both time series datasets.

Results

T tests differentiated no and moderate to severe OSA groups by REM % (p?=?0.003), HFC (p?=?0.007), VLFC (p?=?0.007), and LFC/HFC ratio (p?=?0.038) variables. The successful CPAP therapy group (n?=?16) had more HFC (p?=?0.003), less LFC (p?=?0.003), and e-LFC_BB (p?=?0.029) compared to the unsuccessful CPAP therapy group (n?=?8). PSG sleep quality measures, except the higher arousal index (p?=?0.038) in the unsuccessful CPAP group, did not differ between the successful and unsuccessful CPAP groups. HFC?≥?50 % showed high sensitivity (77.8 %) and specificity (88.9 %) in identifying successful CPAP therapy.

Conclusions

PSG and CPC measures differentiated no from moderate to severe OSA groups and HFC?≥?50 % discriminated successful from unsuccessful CPAP therapy. The HFC?≥?50 % cutoff showed clinical value in identifying sleep quality disturbance among CPAP users.     

Long-term nasal CPAP does not ameliorate obstructive sleep apnoea

Fifty-seven patients with obstructive sleep apnoea (OSA) were treated for at least six months with nasal continuous positive airway pressure (CPAP). At follow-up, sleep studies were performed in which CPAP was not used for the first half of the night. We compared the severity of OSA at follow-up without CPAP to the severity of OSA during the patient's initial diagnostic study. Apnoea and hypopnoea index (AHI) fell from 41.4 ± 7.5 (mean ±95% CI) to 34.8 ± 7.9 (p= 0.06 by Wilcoxon test) and minimum oxygen saturation rose from 71.6 ± 3.2 to 78.5 ± 2.6 (p<0.001). Some of this change may have been due to reduced REM sleep in the follow-up study (10.5±2.1% Total Sleep Time vs 7.4±2.4% TST, p<0.05). Long-term nasal CPAP was not associated with any reduction of obesity (BMI before CPAP 31.9 ± 1.0, after CPAP 31.7 ± 1.0 (p= 0.39). Systolic arterial pressure fell (before CPAP 143.0 ±4.5 mmHg, after CPAP 136.3 ± 4.6, p < 0.05) but diastolic pressure did not (before CPAP 88.5 ± 3.0 mmHg, after CPAP 85.6 ±2.9 mmHg, p = 0.11). We concluded that the effect of CPAP treatment for six or more months was a small fall in AHI and a small rise in minimum Sa0₂, but that this would be of marginal clinical significance, and may be artefactual. (Aust NZ J Med 1991; 21: 235–238.)     

The effects of long‐term continuous positive airway pressure on apnea–hypopnea index change following short‐term that withdrawal in patients with obstructive sleep apnea

The effect of long‐term continuous positive airway pressure (CPAP) treatment on apnea–hypopnea index (AHI) after CPAP withdrawal remains unclear, especially in obstructive sleep apnea (OSA) patients screened from the population. To examine that, 1241 civil servants who participated in the annual physical examination were screened for OSA between September and December 2017. Screened OSA firstly underwent 1‐week CPAP adherence assessment. Then, patients with good CPAP adherence would be freely provided CPAP to continued treatment. All OSA patients were followed for 2 years. At study end, all OSA patients underwent home sleep testing (HST) again within 1 week of CPAP withdrawal. The effect of 2‐year CPAP treatment on OSA severity was investigated by using linear regression and multinominal logistic regression. In total, 103 OSA patients were screened, including 41 cases (39.8%) in CPAP treatment group and 62 cases (60.2%) in non‐CPAP treatment group. At 2‐year follow‐up, compared with baseline, in CPAP treatment group, following CPAP withdrawal, a significant decrease in AHI was observed in patients with severe OSA (P = 0.014); in non‐CPAP treatment group, a significant increase in AHI was observed in patients with moderate OSA (P = 0.028). After adjustment for confounding factors, multivariate linear regression showed that △AHI was negatively associated with CPAP treatment (β = −4.930, 95% confidence interval [CI] [−9.361, −0.500], P = 0.030). Multinominal logistic regression showed that the AHI of patients not treated with CPAP tended to be unchanged or worsened with the AHI improvement group as a reference (OR [odds ration] [95% CI], 4.555 [1.307, 15.875], P = 0.017; 6.536 [1.171, 36.478], P = 0.032). In conclusion, active OSA screening and long‐term CPAP intervention may improve the severity of severe OSA patients following short‐term CPAP withdrawal in the general population.     

Pressure adjustment is the most useful intervention for improving compliance in telemonitored patients treated with CPAP in the first 6 months of treatment

Purpose

Telemonitoring (TMg) for patients treated with continuous positive airway pressure (CPAP) is now routine care in some sleep labs. The purpose of the present study was to identify technical interventions associated with improved CPAP compliance in a real-life cohort of newly telemonitored patients with obstructive sleep apnea (OSA) during the first 6 months of treatment.

Methods

All patients with moderate-to-severe OSA (apnea-hypopnea index (AHI) ≥ 15/h) who were newly treated with CPAP were included in the study and telemonitored. A group educational session was scheduled after 1 month. Technical interventions were performed at the patient’s request and during scheduled visits and the impact of each intervention on CPAP therapy compliance was collected.

Results

Between May 2018 and Dec 2019, 349 patients newly diagnosed with OSA were hospitalized in the sleep lab for CPAP titration and 212 patients were included (mean age 54.6 ± 13.1 years, mean BMI 31.7 ± 5.8 kg/m², mean AHI 42.8 ± 22.0). TMg acceptance rate was 87%. Mean 6-month compliance was 275 ± 154 min, 13% stopped CPAP, and 17% were non-compliant. Correlations were observed between BMI (r = 0.15, p = 0.029), median and 95th percentile leaks (r = ?0.23 and ?0.18, p = 0.016 and 0.002), and CPAP compliance.

During follow-up, 92 interventions were required, mainly for mask change (n = 80). Pressure modification (n = 16) was the only intervention that increased CPAP use > 30 min/night, p = 0.021.

Conclusion

Pressure modification was the only adaptation that significantly increased CPAP compliance during the first 6 months. Remote TMg allows providing daily, accurate, and immediate feedback that could help clinicians to confirm that the CPAP treatment is effective.

     

The effect of modafinil following acute CPAP withdrawal: a preliminary study

Daytime symptoms resulting from obstructive sleep apnea (OSA) include impaired neurobehavioural performance and increased sleepiness. Continuous positive airway pressure (CPAP) reduces these symptoms. However, even compliant users may temporarily withdraw from CPAP treatment resulting in an immediate return of OSA. It has been hypothesised that these treatment “holidays” may be associated with neurobehavioural decline. Acute administration of a wakefulness promoter during such treatment “holidays” may help maintain neurobehavioural functioning. We examined the effects of 200 mg modafinil on neurobehavioural performance in a placebo-controlled crossover trial including N = 12 OSA patients acutely removed from CPAP. Sleep–wake activity was assessed for four consecutive days on CPAP and one night off CPAP using actigraphy. During the night off, CPAP patients wore a single channel nasal airflow diagnostic device. On the morning after CPAP withdrawal, patients reported to the laboratory and were administered either modafinil (200 mg) or placebo. At 2 h post-administration, patients completed a single simulated drive of approximately 30 min with simultaneous administration of a divided attention task (STISIM™), critical flicker fusion (CFF) test and subjective sleepiness scales. After a 14-day washout, participants repeated the protocol. CPAP withdrawal was associated with a worsening of sleep efficiency and the movement and fragmentation index (MFI), compared to the on-CPAP nights (all p ≤ 0.02). Modafinil did not result in a superior driving simulator performance or CFF responses the morning after CPAP withdrawal but did result in better subjective sleepiness (both p ≤ 0.04) compared to placebo. These data do not support the use of modafinil for the maintenance of daytime functioning in patients with OSA who are acutely withdrawn from CPAP.     

Effect of continuous positive airway pressure on albuminuria in patients with obstructive sleep apnea: a meta-analysis

Purpose

A relationship between albuminuria and obstructive sleep apnea (OSA) has been documented in previous studies. Nevertheless, the impact of continuous positive airway pressure (CPAP) treatment on albuminuria in subjects with OSA is debated. This meta-analysis was carried out to investigate whether or not CPAP treatment affected urinary albumin-to-creatinine ratio (UACR) in subjects with OSA.

Methods

A comprehensive literature search was conducted on Web of Science, Embase, and PubMed from January 1990 to December 2020. Information on patients’ characteristics, features of the studies, and UACR of pre- and post-CPAP treatment was collected. For estimation of the pooled effects, standardized mean difference (SMD) was applied.

Results

This meta-analysis included 6 articles and 211 subjects. The pooled analysis suggested that CPAP therapy exerted a favorable effect on the decrease of UACR in subjects with OSA (SMD?=?0.415, 95% CI?=?0.026 to 0.804, z?=?2.09, p?=?0.037). Subgroup analyses revealed that the CPAP treatment effect was not influenced by sample size, BMI, age, or AHI.

Conclusion

The present meta-analysis indicated that UACR was significantly reduced by CPAP therapy in subjects with OSA. Further well-designed randomized controlled trials with large sample size are required to confirm the benefits.

     

Clinical,polysomnographic, and cephalometric features of obstructive sleep apnea with AHI over 100

Purpose

Obstructive sleep apnea (OSA) is induced by a sleep-related collapse of the upper airway in association with multiple factors. The severity of OSA is determined by the apnea-hypopnea index (AHI). Although obesity and sex differences are common factors in OSA, the level of the AHI varies to the same degree according to the age and sex and degree of obesity. However, only a few studies have evaluated AHI over 100/h, those reports did not describe why they set the AHI cutoff at 100/h. The purpose of this study was to elucidate the pathogenesis of “very” severe OSA, defined as having an AHI >?100/h.

Methods

AHI?>?100/h was set as very severe OSA (VS-OSA) in this study. As controls, moderate to severe OSA patients, matched with VS-OSA for age, sex, and body mass index (BMI), were enrolled. The findings of polysomnography and cephalography between VS-OSA and controls were compared.

Results

Eleven patients in the VS-OSA group (mean AHI 110.2/h) and 22 patients in the control group (mean AHI 41.6/h) were compared (mean age 50.2 vs 50.6, male:female 5:6 vs 10:12, mean BMI 35.4 kg/m² vs 34.5 kg/m²). There were no significant differences in the clinical characteristics. In the polysomnographic parameters, the VS-OSA group showed apnea predominance, the mean percutaneous oxygen saturation (SO₂) was significantly lower in all sleep stages, and the minimum SO₂ was significantly lower (49.0% vs 77.5%, p?=?0.002). A similar apnea duration and rather shorter hypopnea duration were shown. The time of apnea-to-arousal was significantly earlier (??0.1 s vs 0.9 s, p?=?0.003). Lung-to-finger circulation time showed no differences. The cephalometric findings showed no significant differences.

Conclusions

VS-OSA patients were more likely to have apnea predominance, desaturation when sleeping despite a similar apnea duration, and rather shorter hypopnea duration, and arousals were evoked significantly earlier.