Inhibition of awake sympathetic nerve activity of heart failure patients with obstructive sleep apnea by nocturnal continuous positive airway pressure

OBJECTIVES: This study was designed to determine whether reductions in morning systolic blood pressure (BP) elicited by treatment of moderate to severe obstructive sleep apnea (OSA) in heart failure (HF) patients are associated with a reduction in sympathetic vasoconstrictor tone. BACKGROUND: Daytime muscle sympathetic nerve activity (MSNA) is elevated in HF patients with coexisting OSA. In our recent randomized trial in HF, abolition of OSA by continuous positive airway pressure (CPAP) increased left ventricular ejection fraction (LVEF) and lowered morning systolic BP. METHODS: Muscle sympathetic nerve activity, BP, and heart rate (HR) of medically treated HF patients (EF <45%) and OSA (apnea-hypopnea index > or =20/h of sleep) were recorded on the morning after overnight polysomnography, and again one month after patients were randomly allocated nocturnal CPAP treatment or no CPAP (control). RESULTS: In nine control patients, there were no significant changes in the severity of OSA, MSNA, systolic BP, or HR. In contrast, in the 8 CPAP-treated patients, OSA was attenuated, and there were significant reductions in daytime MSNA (from 58 +/- 4 bursts/min to 48 +/- 5 bursts/min; 84 +/- 4 bursts/100 heart beats to 72 +/- 5 bursts/100 heart beats; p < 0.001 and p = 0.003, respectively), systolic BP (from 135 +/- 5 mm Hg to 120 +/- 6 mm Hg, p = 0.03), and HR (from 69 +/- 2 min(-1) to 66 +/- 2 min(-1); p = 0.013). CONCLUSIONS: Treatment of coexisting OSA by CPAP in HF patients lowers daytime MSNA, systolic BP, and HR. Inhibition of increased central sympathetic vasoconstrictor outflow is one mechanism by which nocturnal CPAP reduces awake BP in HF patients with moderate to severe OSA.     

Fixed and autoadjusting continuous positive airway pressure treatments are not similar in reducing cardiovascular risk factors in patients with obstructive sleep apnea

BACKGROUND: A strong association between obstructive sleep apnea (OSA) and the risk for cardiovascular and cerebrovascular diseases has been reported. Continuous positive airway pressure (CPAP) is the first-line therapy for OSA, able not only to reduce daytime sleepiness but also to improve cardiovascular and metabolic outcomes. Autoadjusting CPAP (APAP), an alternative treatment to CPAP, can reduce OSA symptoms while increasing long-term CPAP compliance without the high costs of CPAP titration. However, no data are available on the effects of APAP on cardiovascular risk factors METHODS: We performed standard full polysomnography; obtained plasma levels of glucose, insulin, and C-reactive protein (CRP); and measured systolic BP (SBP) and diastolic BP (DBP) in 31 patients with newly diagnosed, severe OSA. After standard CPAP titration, all subjects were randomized to CPAP or APAP treatment. Measurements were obtained at baseline and after 3 months of treatment. RESULTS: The two groups were similar in terms of age, sex, body mass index (BMI), and severity of OSA. SBP, DBP, heart rate (HR), homeostasis model assessment index (HOMA-IR), and CRP were similar in the two groups. After 3 months of treatment, BMI, HR, and compliance to therapy were also comparable. OSA indexes were significantly reduced in both groups. Significant reductions in SBP, DBP, and HOMA-IR were observed in the CPAP group but not in the APAP group, while CRP plasma levels were similarly reduced. CONCLUSIONS: Our results suggest that CPAP and APAP, despite significant effects on OSA indexes and symptoms, do not improve cardiovascular risk factors in the same fashion.     

Acute effects of autoadjusting and fixed continuous positive airway pressure treatments on cardiorespiratory coupling in obese patients with obstructive sleep apnea

BackgroundTreatment with positive airway pressure devices improved signs and symptoms of obstructive sleep apnea syndrome (OSA); however, auto-adjusting positive pressure (APAP) device was not as effective as continuous positive airway pressure (CPAP) in reducing arterial blood pressure and insulin resistance. The role played by autonomic cardiac regulation remains to be clarified.We aimed to test the effects of CPAP and APAP on autonomic regulation and cardiorespiratory coupling during sleep.MethodsWe retrospectively analyzed full-night polysomnographic studies. 19 patients newly diagnosed with severe OSA (AHI > 30) and 7 obese subjects without OSA (CON) were enrolled. Each OSA subject was assigned to CPAP or APAP treatment and underwent a sleep study after 1 week of treatment. Spectral and cross-spectral analyses of heart rate variability (HRV) and respiration were performed to assess autonomic profile and coherence (K²) between respiration and HF oscillation during sleep in CPAP, APAP and CON groups.ResultsIn CPAP and CON, LFnu and LF/HF, markers of sympathetic modulation, decreased from N2 to N3 and increased during REM sleep (p < 0.001), while in APAP group, sympathetic modulation was significantly higher compared with those of CPAP and CON during all sleep stages. K² values were lower in APAP compared with those in CPAP and CON.ConclusionAPAP treatment was characterized by a greater sympathetic activation and it was associated with a lower cardio-respiratory coupling compared with CPAP. This might account for the different effects on cardiovascular risk factors induced by the two treatments.     

Continuous Positive Airway Pressure in Patients With Obstructive Sleep Apnea and Resistant Hypertension: A Meta‐Analysis of Randomized Controlled Trials

This study aimed to analyze the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with obstructive sleep apnea (OSA) and resistant hypertension. Randomized controlled trials (RCTs) that evaluated the effect of CPAP on BP in patients with OSA and resistant hypertension, indexed in MEDLINE, Embase, and the Cochrane Library from inception until March 20, 2015, were included in the meta‐analysis. A total of five RCTs were identified to meet the inclusion criteria. The pooled changes after CPAP treatment for 24‐hour ambulatory systolic BP and diastolic BP (DBP) were −4.78 mm Hg (95% confidence interval [CI], −7.95 to −1.61) and −2.95 mm Hg (95% CI, −5.37 to −0.53) in favor of the CPAP group. CPAP was also associated with reduction in nocturnal DBP (mean difference, −1.53 mm Hg, 95% CI, −3.07 to 0). The results indicated a favorable reduction in BP with CPAP treatment in patients with OSA and resistant hypertension.     

Effect of obstructive sleep apnea on the response to hypertension therapy

Obstructive sleep apnea (OSA) often precedes cardiovascular disease, partly due to treatment resistant hypertension. The nocturnal apneas of OSA trigger increased sympathetic nervous discharge during both sleep and wakefulness. Apneas also trigger cardiac release of the endogenous diuretic atrial natriuretic peptide. We hypothesized that treatment of the excess sympathetic nervous activity of OSA with a β₁ blocker would lower 24 h blood pressure (BP) more than diuretic therapy. Subjects with OSA associated hypertension received 2 weeks of placebo followed by the β₁ blocker nebivolol or hydrochlorothiazide (HCTZ) for 6 weeks in a blinded crossover study. BP, baroreflex sensitivity (BRS), heart rate variability (HRV), arterial reactivity, and stiffness were measured after placebo and each treatment. The β₁ blocker lowered clinic BP by ?11/?8 mmHg, more than the ?3/?1 effect of HCTZ (P < 0.01). The β₁ blocker lowered 24 h diastolic blood pressure (DBP) more than HCTZ. Although given at bedtime, neither drug increased BP dipping. Nebivolol increased HRV in the high-frequency band. Nebivolol did not alter BRS while HCTZ significantly diminished BRS compared to nebivolol (P < 0.01). Nebivolol increased flow-mediated brachial artery dilation when compared to HCTZ and slowed pulse wave velocity, indicating a decrease in arterial stiffness.

Diuretic therapy failed to lower BP in OSA subjects and this might account for the frequent association of OSA with treatment resistant hypertension. However, blockade of the excess sympathetic nervous activity of OSA with a β₁ blocker lowered both clinic and 24 h DBP.     

Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex.

This study was undertaken to determine whether abolition of obstructive sleep apnoea (OSA) by continuous positive airway pressure (CPAP) could reduce blood pressure (BP) in patients with refractory hypertension. In 11 refractory hypertensive patients with OSA, the acute effects of CPAP on nocturnal BP were studied during sleep and its longer term effects on 24-h ambulatory BP after 2 months. During a single night's application, CPAP abolished OSA and reduced systolic BP in stage 2 sleep from 138.3 +/- 6.8 to 126.0 +/- 6.3 mmHg. There was also a trend towards a reduction in average diastolic BP (from 77.7 +/- 4.5 to 72.9 +/- 4.5). CPAP usage for 2 months was accompanied by an 11.0 +/- 4.4 mmHg reduction in 24-h systolic BP. In addition, both the nocturnal and daytime components of systolic BP fell significantly by 14.4 +/- 4.4 and 9.3 +/- 3.9 mmHg, respectively. Diastolic BP was reduced significantly at night by 7.8 +/- 3.0 mmHg. In patients with refractory hypertension, acute abolition of obstructive sleep apnoea by continuous positive airway pressure reduces nocturnal blood pressure. These data also suggest that continuous positive airway pressure may reduce nocturnal and daytime systolic blood pressure chronically. Randomised trials are needed to confirm the latter results.     

阻塞性睡眠呼吸暂停患者持续正压通气治疗前后自主神经 …

目的 研究阻塞性睡眠呼吸暂停（ＯＳＡ）患者夜间睡眠时自主神经功能的状态，以及有效的持续正压通气治疗对自主神经张力的影响。方法 对５６例重度ＯＳＡ患者持续正压通气（ＣＰＡＰ）治疗前和治疗中进行夜间７小时多导睡眠图（ＰＳＧ）及动态心电图监测，另择３０名正常受试者作为对照。采用心率功率谱分析法（ＨＲＰＳＡ）定量分析ＯＳＡ患者治疗前后夜间自主神经功能的变化。结果 ＯＳＡ组夜间睡眠时伴随着反复的呼吸暂停和低     

The acute effects of continuous positive airway pressure and oxygen administration on blood pressure during obstructive sleep apnea.

We have measured blood pressure continuously with a digital artery blood pressure monitor in eight patients with severe obstructive sleep apnea (OSA) during 30 min each of wakefulness, OSA, OSA with added oxygen to keep saturation above 96 percent at all times (OSA+O2), and nasal continuous positive airway pressure (CPAP) therapy. Mean blood pressures were not different between wakefulness, OSA, OSA+O2, and CPAP, although the variability in blood pressure was significantly greater during OSA and OSA+O2 than during wakefulness and CPAP. The addition of oxygen did not attenuate the variability in blood pressure. Using multiple linear regression modeling to further dissect out the principal variables determining the postapneic blood pressure rise, we found that only apnea length (r2 = 0.28, p less than 0.0001) and pulse rate changes (r2 = 0.15, p less than 0.0001) remained significantly related to SBPmax, while hypoxemia did not. We found the same trends in the other variables SBPten, DBPmax, and DBPten. Hypoxemia made a small contribution to the size of DBPmax, although this was small by comparison with apnea length. We conclude that CPAP treatment of OSA does not lower mean blood pressure acutely, although it significantly reduces the large oscillations in blood pressure seen in patients with untreated OSA. The rise in blood pressure following each apnea is not primarily due to arterial desaturation but is related to apnea length and may be caused by increased sympathetic activity secondary to arousal.     

Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure

Obstructive sleep apnea (OSA) is highly prevalent among patients with congestive heart failure (CHF) and may contribute to progression of cardiac dysfunction via hypoxia, elevated sympathetic nervous system activity, and systemic hypertension. Our aim was to assess the long-term effect of OSA treatment with nocturnal continuous positive airway pressure (CPAP) on systolic heart function, sympathetic activity, blood pressure, and quality of life in patients with CHF. Fifty-five patients with CHF and OSA were randomized to 3 months of CPAP or control groups. End points were changes in left ventricular ejection fraction, overnight urinary norepinephrine excretion, blood pressure, and quality of life. Nineteen patients in the CPAP group and 21 control subjects completed the study. Compared with the control group, CPAP treatment was associated with significant improvements in left ventricular ejection fraction (delta 1.5 +/- 1.4% vs. 5.0 +/- 1.0%, respectively, p = 0.04), reductions in overnight urinary norepinephrine excretion (delta 1.6 +/- 3.7 vs. -9.9 +/- 3.6 nmol/mmol creatinine, p = 0.036), and improvements in quality of life. There were no significant changes in systemic blood pressure. In conclusion, treatment of OSA among patients with CHF leads to improvement in cardiac function, sympathetic activity, and quality of life.     

Renal function in patients with obstructive sleep apnea. Effects of nasal continuous positive airway pressure

Patients with obstructive sleep apnea (OSA) often exhibit nocturnal polyuria, which disappears with nasal continuous positive airway pressure (CPAP) treatment. We measured water and electrolyte urinary excretion, creatinine and osmolal clearances, and water transport during sleep in 13 polygraphically monitored patients with OSA during two consecutive nights, either untreated or treated with nasal CPAP, and in eight normal subjects. Untreated patients with OSA had greater urinary flows and greater urinary sodium, chloride, and potassium excretions than did controls. Nasal CPAP treatment in patients with OSA resulted in a reduction in urinary flow and in sodium and chloride excretion, with a concomitant increase in sodium resorption. None of these effects was observed in CPAP-treated normal subjects. The only effect of nasal CPAP common to normal subjects and patients was a trend toward decreased glomerular filtration rate.     

Blood pressure effects of CPAP in nonresistant and resistant hypertension associated with OSA: A systematic review of randomized clinical trials

Obstructive sleep apnea (OSA) is a rather common chronic disorder, associated with increased prevalence of hypertension. The pathophysiological mechanisms for hypertension in OSA are at least in part linked to intermittent hypoxia developed during nightly hypopneas and apneas. Hypoxemia stimulates sympathetic overactivity, systemic inflammation, oxidative stress, and endothelial dysfunction. However, it appears that intermittent hypoxemia is not the only factor in the development of hypertension in OSA. Supplemental oxygen therapy that improved oxyhemoglobin saturation to similar levels to those achieved with CPAP treatment did not reduce BP. In this scenario, it could be proposed that hypoxemia acts as a trigger of sympathetic overdrive, which when set is the main factor in the development of hypertension in OSA. This review appraises evidence provided by randomized controlled trials on the BP-lowering effectiveness of continuous positive airway pressure (CPAP) treatment of OSA patients with nonresistant and resistant hypertension. It suggests that CPAP treatment is more effective in treating resistant hypertension than nonresistant hypertension. A possible explanation is that sympathetic overactivity and altered vascular reactivity in OSA could be more severe in resistant hypertension than in nonresistant hypertension. An intricate interaction among compliance, adherence, and their interaction with demographic characteristics, genetic factors, and comorbidities of the population included might explain the differences found between trials on their influence over the antihypertensive effectiveness of CPAP. Further long-term trials are needed in hypertensive OSA patients to assess whether CPAP treatment in OSA patients consistently restores physiological nocturnal BP fall and adjusts resting and circadian heart rate.     

Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea

BACKGROUND: Patients with obstructive sleep apnea (OSA) are at increased risk for hypertension. The mechanisms responsible for the development of hypertension are controversial. We hypothesized that patients with OSA had an abnormal 24-h blood pressure (BP) and an abnormal activity in vasoactive hormones, and that both BP and hormones were normalized during treatment with long-term nasal continuous positive airway pressure (CPAP). METHODS: The 24-h BP and plasma levels of the vasoactive hormones (renin, angiotensin II, aldosterone, atrial natriuretic peptide, brain natriuretic peptide, vasopressin, and endothelin-1) were measured in 24 patients with OSA and in 18 control subjects. Thirteen patients with OSA were reexamined after 14 months of CPAP therapy. RESULTS: Patients with OSA had significantly increased BP and heart rate and a reduced nocturnal BP drop. Both angiotensin II (13.3 +/- 1.6 v 7.8 +/- 1.0 pmol/L) and aldosterone (94.0 +/- 9.4 v 62.2 +/- 4.5 pmol/L) were significantly higher in OSA than in control subjects. Positive correlations were found between angiotensin II and daytime BP (systolic: r = 0.49, P <.01; diastolic: r = 0.52, P <.01). The CPAP therapy resulted in a decrease in BP, and this CPAP-induced reduction in BP was correlated with a decrease in both plasma renin (r = 0.76 to 0.92, all P <.01) and plasma angiotensin II concentration (r = 0.58 to 0.81, all P <.05). CONCLUSIONS: Plasma angiotensin II and aldosterone were elevated in OSA, and plasma angiotensin II was correlated with BP. Long-term CPAP reduced BP, and this decrease in BP was correlated with the reductions in plasma renin and angiotensin II levels. We suggest that OSA mediates hypertension, at least in part, via a stimulation of angiotensin II production.     

Continuous positive airway pressure: new generations

Automatic positive airway pressure devices are the most technologically advanced positive airway pressure devices available for use in OSA. Although heterogeneous, they have in common the ability to detect and respond to changes in upper airway resistance. Data cannot necessarily be extrapolated from one device to another, and the field is rapidly advancing. Most studies of APAP have been performed in a supervised setting, or patients have been carefully selected to have a high likelihood of OSA uncomplicated by disorders such as alveolar hypoventilation or central apnea or technical problems such as mask leaks. Studies of APAP for the diagnosis of OSA have shown that APAP can diagnose severe OSA effectively, but the diagnosis of mild-moderate OSA is less reliable. APAP devices also can be effective therapy for selected patients with OSA, with overall similar results to conventional fixed CPAP in terms of respiratory disturbances, sleep quality, nocturnal oxygenation, and daytime sleepiness and performance, with less known or other long-term outcomes. In most studies, mean treatment pressures are lower, without change in side effect profile. Compliance and preference with APAP are similar to or somewhat better than CPAP in most studies. APAP also can be used in an attended setting to titrate an effective pressure for use in long-term conventional CPAP therapy, also with similar results to CPAP in many patients. APAP devices are more expensive than CPAP devices, but the cost may be outweighed if a group of patients who can be diagnosed, treated, or titrated safely in the unattended setting can be identified. Although diagnostic and therapeutic algorithms for APAP have been proposed, the best candidates for this modality must be defined better.     

24-hour BP in children with congenital central hypoventilation syndrome

OBJECTIVE: To study circadian BP patterns in patients with congenital central hypoventilation syndrome (CCHS). DESIGN: Case-control study. SETTING: Teaching hospital in Paris, France. PATIENTS: Eleven patients with CCHS (median age, 13 years; range, 6 to 18 years) and 11 sex- and height-matched control subjects. INTERVENTION: None. METHODS: Each subject underwent 24-h ambulatory BP monitoring. Oxygen saturation and end-tidal PCO(2) were monitored noninvasively. Polysomnography was performed to determine sleep times. All patients with CCHS received mechanical ventilation during sleep. Mean values for systolic BP (SBP) and diastolic BP (DBP) during wakefulness and sleep were analyzed. Nocturnal BP "dipping" was defined as the difference in mean SBP (and/or DBP) between wakefulness and sleep, divided by individual waking mean values. BP "dippers" were defined as subjects showing at least 10% nocturnal dipping. RESULTS: Patients with CCHS had BPs in the low normal range of normative data. As compared to control subjects, patients with CCHS had lower BP during wakefulness (p = 0.003 and p = 0.016 for SBP and DBP, respectively), and higher BP during sleep (p = 0.016 and p = 0.002). Nocturnal BP dipping was abnormally reduced in patients with CCHS (p = 0.000). Ten of the 11 patients with CCHS were BP nondippers, compared to none of the control subjects. CONCLUSION: The abnormal circadian BP pattern observed in children and adolescents with CCHS may be related to autonomic nervous dysfunction. Lifelong cardiovascular follow-up is recommended for patients with CCHS.     

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Stress from obstructive sleep apnea (OSA) stimulates catecholamine release consequently exacerbating hypertension. However, different studies have shown a conflicting impact of continuous positive airway pressure (CPAP) treatment in patients with OSA on catecholamine levels and blood pressure. We aimed to examine changes to catecholamine levels and blood pressure in response to CPAP treatment. We conducted a meta‐analysis of data published up to May 2020. The quality of the studies was evaluated using standard tools for assessing the risk of bias. Meta‐analysis was conducted using RevMan (v5.3) and expressed in standardized mean difference (SMD) for catecholamines and mean difference (MD) for systolic (SBP) and diastolic blood pressure (DBP). A total of 38 studies met our search criteria; they consisted of 14 randomized control trials (RCT) totaling 576 participants and 24 prospective cohort studies (PCS) of 547 participants. Mean age ranged between 41 and 62 year and body mass index between 27.2 and 35.1 kg/m². CPAP treatment reduced 24‐hour urinary noradrenaline levels both in RCT (SMD = −1.1; 95% confidence interval (CI): −1.63 to − 0.56) and in PCS (SMD = 0.38 (CI: 0.24 to 0.53). SBP was also reduced by CPAP treatment in RCT (4.8 mmHg; CI: 2.0‐7.7) and in PCS (7.5 mmHg; CI: 3.3‐11.7). DBP was similarly reduced (3.0 mmHg; CI: 1.4‐4.6) and in PCS (5.1 mmHg; CI: 2.3‐8.0). In conclusion, CPAP treatment in patients with OSA reduces catecholamine levels and blood pressure. This suggests that sympathetic activity plays an intermediary role in hypertension associated with OSA‐related stress.     

Continuous positive airway pressure treatment improves baroreflex control of heart rate during sleep in severe obstructive sleep apnea syndrome

The role of the arterial baroreflex in the cardiovascular changes associated with the obstructive sleep apnea syndrome (OSAS), and the effect of nasal continuous positive airway pressure (CPAP) treatment on baroreflex function during sleep are unknown. Baroreflex control of heart rate was studied in 29 normotensive patients with OSAS under no treatment, in 11 age-matched control subjects, and in 10 patients at CPAP withdrawal after 5.5 +/- 3.7 (range 3-14) months of treatment. Baroreflex control of heart rate was assessed by "sequence method" analysis of continuous blood pressure recordings (Finapres) obtained during nocturnal polysomnography. In untreated OSAS, baroreflex sensitivity (BRS) was low during wakefulness and non-rapid eye movement (REM) stage 2 sleep compared with control subjects, and correlated inversely with mean lowest Sa(O(2)) and the blood pressure increase after apneas. After CPAP treatment, the apnea-hypopnea index was lower, and mean lowest Sa(O(2)) higher than before treatment. After CPAP, patients were more bradycardic, blood pressure and its standard deviation decreased as Sa(O(2)) improved in non-REM stage 2 sleep, and BRS increased (nocturnal wakefulness: +59%; non-REM stage 2 sleep: +68% over pretreatment values). Our data suggest that baroreflex dysfunction in OSAS may be at least partly accounted for by nocturnal intermittent hypoxemia, and can be reversed by long-term CPAP treatment.     

Blood pressure variability in obstructive sleep apnea: role of sympathetic nervous activity and effect of continuous positive airway pressure

BACKGROUND: Many studies support a link between obstructive sleep apnea (OSA), increased blood pressure (BP) and/or BP variability, and sympathetic nervous system (SNS) activity. We assessed the relationship between SNS activity and 24-h BP variability in patients with OSA, and the effect of continuous positive airway pressure (CPAP) on BP variability. DESIGN: Forty-one patients with a respiratory disturbance index (RDI) > 15 were randomized into CPAP or CPAP placebo groups for a 1-week trial. METHODS: Ambulatory BP, 24-h urine norepinephrine (NE) and polysomnography were measured prior to treatment and after 1 and 7 days of treatment. RESULTS: Neither RDI nor 24-h urine NE levels were related to 24-h mean BP levels. While RDI was associated only with night-time BP variability, daytime urine NE levels were associated with both night-time and daytime BP variability. After treatment, the BP variability decreased significantly but equally in both active and placebo CPAP groups. CONCLUSIONS: Obstructive sleep apnea is more related to BP variability than BP. Sympathetic nervous activity, as inferred from daytime urine NE, is related to changes in BP variability in OSA patients. BP variability is not specifically affected by CPAP.     

Pulse wave analysis in a pilot randomised controlled trial of auto-adjusting and continuous positive airway pressure for obstructive sleep apnoea

Purpose  

Non-invasive measurements of arterial stiffness including the augmentation index (AIx) and central blood pressure (BP) have been used to assess the cardiovascular health of patients with obstructive sleep apnoea (OSA), a well-established independent risk factor of cardiovascular disease. Continuous positive airway pressure (CPAP) can significantly reduce the AIx, but no studies have analysed the effect of auto-adjusting PAP (APAP) or studied morbidly obese patients with severe OSA at higher risk of cardiovascular disease. In this randomised, single-blinded crossover pilot trial, we aimed to compare the efficacy of CPAP with APAP (ResMed S8 Autoset II) in improving peripheral BP, central BP and the AIx, using SphygmoCor technology.     

Optimal high-frequency oscillatory ventilation settings by nonlinear lung mechanics analysis

Obstructive sleep apnea causes cardiovascular morbidity and premature death. Potential links between sleep apnea and cardiovascular complications are chronically elevated activity of the sympathetic nervous system and abnormal vascular function. To explore vascular function, we determined the reactive hyperemic blood flow (RHBF) responses to 10 minutes of forearm arterial occlusion (plethysmography), blood pressure, and muscle sympathetic nerve activity (MSNA, microneurography) in eight patients with sleep apnea and in nine nonapneic control subjects. Peak RHBF and vascular conductance were markedly attenuated in sleep apnea compared with control subjects (p < 0.05). Seven sleep apnea patients were retested after at least two weeks of continuous positive airway pressure (CPAP) therapy. MSNA decreased after CPAP therapy (p < 0.05, n = 6), whereas blood pressure did not change. After CPAP therapy, peak RHBF and vascular conductance were increased compared with before treatment (p < 0.05; n = 7). Thus, vascular function is abnormal in sleep apnea and is improved by CPAP therapy. Furthermore, effective CPAP therapy decreases sympathetic activity in sleep apnea. Thus, sympathoexcitation and abnormal vascular function in patients with sleep apnea appear to be linked to the repetitive nocturnal apneic events.     

Obesity hypoventilation syndrome: hypoxemia during continuous positive airway pressure

BACKGROUND: Polysomnography findings between matched groups with obstructive sleep apnea (OSA) and OSA plus obesity-hypoventilation syndrome (OHS) before and after continuous positive airway pressure (CPAP), particularly in the extremely severe obese (body mass index [BMI] >or= 50 kg/m2), are unclear. DESIGN: Prospective study of subjects (BMI >or= 50 kg/m2) undergoing diagnostic polysomnography. Subjects with an apnea-hypopnea index (AHI) >or= 15/h underwent a second polysomnography with CPAP. The effect of 1 night of CPAP on sleep architecture, AHI, arousal indexes, and nocturnal oxygenation was assessed. OHS was defined as those subjects with obesity, PaCo2 > 45 mm Hg, and PaO2 < 70 mm Hg in the absence of lung disease. RESULTS: Twenty-three subjects with moderate-to-severe OSA and 23 subjects with moderate-to-severe OSA plus OHS underwent a 1-night trial of CPAP. Both groups were matched for spirometry, BMI, and AHI, but oxygen desaturation was worse in the OSA-plus-OHS group. CPAP significantly improved rapid eye movement (REM) duration (p < 0.005), AHI (p < 0.005), arousal indexes (p < 0.005), and percentage of total sleep time (TST) with oxygen saturation (SpO2) < 90% (p < 0.005) in both groups. In subjects with OSA plus OHS, 43% continued to spend > 20% of TST with SpO2 < 90%, compared to 9% of the OSA group, despite the adequate relief of upper airway obstruction. CONCLUSIONS: Extremely severe obese subjects (BMI >or= 50 kg/m2) with moderate-to-severe OSA plus OHS exhibit severe oxygen desaturation but similar severities of AHI, arousal indexes, and sleep architecture abnormalities when compared to matched subjects without OHS. CPAP significantly improves AHI, REM duration, arousal indexes, and nocturnal oxygen desaturation. Some subjects with OHS continued to have nocturnal desaturation despite the control of upper airway obstruction; other mechanisms may contribute. Further long-term studies assessing the comparative role of CPAP and bilevel ventilatory support in such subjects with OHS is warranted.