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An oronasal mask is frequently used to treat OSA. In contrast to nasal CPAP, the effectiveness of oronasal CPAP varies by unknown mechanisms. We hypothesized that oral breathing and pressure transmission through the mouth compromises oronasal CPAP efficacy.Thirteen patients with OSA, well adapted to oronasal CPAP, were monitored by full polysomnography, pharyngeal pressure catheter, and nasoendoscope. Patients slept with low doses of midazolam, using an oronasal mask with sealed nasal and oral compartments. CPAP was titrated during administration by the oronasal and nasal routes, and was then reduced to induce stable flow limitation and abruptly switched to the alternate route. In addition, tape sealing the mouth was used to block pressure transmission to the oral cavity.Best titrated CPAP was significantly higher by the oronasal route rather than the nasal route (P = .005), and patients with25% oral breathing (n = 5) failed to achieve stable breathing during oronasal CPAP. During stable flow limitation, inspiratory peak flow was lower, driving pressure was higher, upper airway inspiratory resistance was higher, and retropalatal and retroglossal area were smaller by the oronasal rather than nasal route (P .05 for all comparisons). Differences were observed even among patients with no oral flow and were abolished when tape sealing the mouth was used (n = 6).Oral breathing and transmission of positive pressure through the mouth compromise oronasal CPAP.

OSA is associated with metabolic syndrome (MS), but it is unclear whether OSA treatment with CPAP can revert MS.Does OSA treatment with CPAP per se have effects on the MS reversibility and the associated metabolic, adiposity and vascular parameters?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.One hundred patients (79% men; mean age, 48 ± 9 years; BMI, 33 ± 4 kg/mDespite 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.ClinicalTrials.gov; No.: NCT02295202; URL: www.gov.

Background OSA and short sleep duration (SSD) are frequently associated with daytime symptoms and cardiometabolic deregulation. However, the vast majority of studies addressing OSA have not evaluated SSD, and vice versa. Our aim was to evaluate the association of OSA, SSD, and their interactions with sleepiness and cardiometabolic risk factors in a large cohort of adults. Methods Consecutive subjects from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) participated in clinical evaluations, sleep questionnaires, home sleep monitoring, and actigraphy. OSA was defined as an apnea-hypopnea index ≥ 15 events/hour. SSD was defined by a mean sleep duration Results Data from 2,064 participants were used in the final analysis (42.8% male; mean age, 49 ± 8 years). The overall frequency of OSA and SSD were 32.9% and 27.2%, respectively. Following an adjustment for multiple confounding factors, excessive daytime sleepiness was independently associated with SSD (OR, 1.448; 95% CI, 1.172-1.790) but not with OSA (OR, 1.107; 95% CI, 0.888-1.380). The SSD interaction with OSA was not significant. Prevalent obesity (OR, 3.894; 95% CI, 3.077-4.928), hypertension (OR, 1.314; 95% CI, 1.035-1.667), and dyslipidemia (OR, 1.251; 95% CI, 1.006-1.555) were independently associated with OSA but not with SSD. Similarly, the interactions of OSA with SSD were not significant. An additional analysis using Conclusions Objective SSD but not OSA was independently associated with daytime sleepiness. By contrast, OSA, but not SSD, was independently associated with obesity, hypertension, and dyslipidemia.

Background Although recent evidence suggests that OSA treatment may cause weight gain, the long-term effects of CPAP on weight are not well established. Methods This study was a post hoc analysis of the Sleep Apnea Cardiovascular Endpoints (SAVE) study, a multicenter, randomized trial of CPAP plus standard care vs standard care alone in adults with a history of cardiac or cerebrovascular events and moderate to severe OSA. Participants with weight, BMI, and neck and waist circumferences measured at baseline and during follow-up were included. Linear mixed models were used to examine sex-specific temporal differences, and a sensitivity analysis compared high CPAP adherers (≥ 4 h per night) with propensity-matched control participants. Results A total of 2,483 adults (1,248 in the CPAP group and 1,235 in the control group) were included (mean 6.1 ± 1.5 measures of weight available). After a mean follow-up of 3.78 years, there was no difference in weight change between the CPAP and control groups, for male subjects (mean [95% CI] between-group difference, 0.07 kg [–0.40 to 0.54]; P = .773) or female subjects (mean [95% CI] between-group difference, –0.14 kg [–0.37 to 0.09]; P = .233). Similarly, there were no significant differences in BMI or other anthropometric measures. Although male participants who used CPAP ≥ 4 h per night gained slightly more weight than matched male control subjects without CPAP (mean difference, 0.38 kg [95% CI, 0.04 to 0.73]; P = .031), there were no between-group differences in other anthropometric variables, nor were there any differences between female high CPAP adherers and matched control subjects. Conclusions Long-term CPAP use in patients with comorbid OSA and cardiovascular disease does not result in clinically significant weight change. Trial Registry ClinicalTrials.gov; No.: NCT00738179 ; URL: www.clinicaltrials.gov .

Background Nasal CPAP is the "gold standard" treatment for OSA. However, oronasal masks are frequently used in clinical practice. The aim of this study was to perform a meta-analysis of all randomized and nonrandomized trials that compared nasal vs oronasal masks on CPAP level, residual apnea-hypopnea index (AHI), and CPAP adherence to treat OSA. Methods The Cochrane Central Register of Controlled Trials, Medline, and Web of Science were searched for relevant studies in any language with the following terms: "sleep apnea" and "CPAP" or "sleep apnea" and "oronasal mask" or "OSA" and "oronasal CPAP" or "oronasal mask" and "adherence." Studies on CPAP treatment for OSA were included, based on the following criteria: (1) original article; (2) randomized or nonrandomized trials; and (3) comparison between nasal and oronasal CPAP including pressure level, and/or residual AHI, and/or CPAP adherence. Results We identified five randomized and eight nonrandomized trials (4,563 patients) that reported CPAP level and/or residual AHI and/or CPAP adherence. Overall, the random-effects meta-analysis revealed that as compared with nasal, oronasal masks were associated with a significantly higher CPAP level (Hedges' g, –0.59; 95% CI, –0.82 to –0.37; P Conclusions Oronasal masks are associated with a higher CPAP level, higher residual AHI, and poorer adherence than nasal masks. Trial Registry PROSPERO database; No.: CRD42017064584; URL: https://www.crd.york.ac.uk/prospero/.

Background Acute cardiogenic pulmonary edema (ACPE) is a life-threatening condition. OSA may be a modifiable risk factor for ACPE recurrence. This study was designed to evaluate the impact of OSA on the incidence of cardiovascular events following ACPE recovery. Methods Consecutive patients with confirmed ACPE from 3 centers underwent a sleep study following clinical stabilization. OSA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. The mean follow-up was 1 year, and the primary outcome was ACPE recurrence. Results A total of 104 patients were included in the final analysis; 61% of the patients had OSA. A higher rate of ACPE recurrence (25 vs 6 episodes; P = .01) and a higher incidence of myocardial infarction (15 vs 0 episodes; P = .0004) were observed in patients with OSA than in those without OSA. All 17 deaths occurred in the OSA group ( P = .0001). In a Cox proportional hazards regression analysis, OSA was independently associated with ACPE recurrence (hazard ratio [HR], 3.3 [95% CI, 1.2-8.8]; P = .01), incidence of myocardial infarction (HR, 2.3 [95% CI, 1.1-9.5]; P = .02), cardiovascular death (HR, 5.4 [95% CI, 1.4-48.4]; P = .004), and total death (HR, 6.5 [95% CI, 1.2-64.0]; P = .005). When the analysis was limited only to patients with OSA, levels of AHI and hypoxemic burden and rates of sleep-onset ACPE were significantly higher in those who presented with ACPE recurrence or who died than in those who did not experience these events. Conclusions OSA is independently associated with higher rates of ACPE recurrence and both fatal and nonfatal cardiovascular events.

Background CPAP is the gold standard treatment for OSA and was conceived to be applied through a nasal interface. This study was designed to determine the acute effects of changing the nasal CPAP route to oronasal and oral in upper airway patency during sleep in patients with OSA. We hypothesized that the oronasal route may compromise CPAP’s effectiveness in treating OSA. Methods Eighteen patients (mean ± SD age, 44 ± 9 years; BMI, 33.8 ± 4.7 kg/m 2 ; apnea-hypopnea index, 49.0 ± 39.1 events/hour) slept with a customized oronasal mask with nasal and oral sealed compartments connected to a multidirectional valve. Sleep was monitored by using full polysomnography and induced by low doses of midazolam. Nasal CPAP was titrated up to holding pressure. Flow route was acutely changed to the oronasal (n = 18) and oral route (n = 16) during sleep. Retroglossal area was continuously observed by using nasoendoscopy. Results Nasal CPAP (14.8 ± 4.1 cm H 2 O) was able to stabilize breathing in all patients. In contrast, CPAP delivered by the oronasal and oral routes promoted obstructive events in 12 (66.7%) and 14 (87.5%) patients, respectively. Compared with stable breathing during the nasal route, there was a significant and progressive reduction in the distance between the epiglottis and tongue base and the retroglossal area when CPAP was delivered by the oronasal and oral routes. Conclusions CPAP delivered through the oronasal route may compromise CPAP’s effectiveness in treating OSA.

Background Hypertrophic cardiomyopathy (HCM) is a common genetic disease that may cause left ventricular outflow tract (LVOT) obstruction, heart failure, and sudden death. Recent studies have shown a high prevalence of OSA among patients with HCM. Because the hemodynamics in patients with LVOT obstruction are unstable and depend on the loading conditions of the heart, we evaluated the acute effects of CPAP on hemodynamics and cardiac performance in patients with HCM. Methods We studied 26 stable patients with HCM divided into nonobstructive HCM (n = 12) and obstructive HCM (n = 14) groups (LVOT gradient pressure lower or higher than 30 mm Hg, respectively). Patients in the supine position while awake were continuously monitored with beat-to-beat BP measurements and electrocardiography. Two-dimensional echocardiography was performed at rest (baseline) and after 20 min of nasal CPAP at 1.5 cm H 2 O and 10 cm H 2 O, which was applied in a random order interposed by 10 min without CPAP. Results BP, cardiac output, stroke volume, heart rate, left ventricular ejection fraction, and LVOT gradient did not change during the study period in either group. CPAP at 10 cm H 2 O decreased right atrial size and right ventricular relaxation in all patients. It also decreased left atrial volume significantly and decreased right ventricular outflow acceleration time, suggesting an increase in pulmonary artery pressure in patients with obstructive HCM. Conclusions The acute application of CPAP is apparently safe in patients with HCM, because CPAP does not lead to hemodynamic compromise. Long-term studies in patients with HCM and sleep apnea and nocturnal CPAP are warranted. Trial Registry ClinicalTrials.gov; No. NCT01631006 ; URL: www.clinicaltrials.gov

Background Little is known about the effects of long-term nasal low-flow oxygen (NLFO) on mucus and symptoms and how this variable is affected by dry or cold humidified gas. The aim of this study was to investigate the effects of dry-NLFO and cold bubble humidified-NLFO on nasal mucociliary clearance (MCC), mucus properties, inflammation, and symptoms in subjects with chronic hypoxemia requiring long-term domiciliary oxygen therapy. Methods Eighteen subjects (mean age, 68 years; 7 male; 66% with COPD) initiating NLFO were randomized to receive dry-NLFO (n = 10) or humidified-NLFO (n = 8). Subjects were assessed at baseline, 12 h, 7 days, 30 days, 12 months, and 24 months by measuring nasal MCC using the saccharin transit test, mucus contact angle (surface tension), inflammation (cells and cytokine concentration in nasal lavage), and symptoms according to the Sino-Nasal Outcome Test–20. Results Nasal MCC decreased significantly (40% longer saccharin transit times) and similarly in both groups over the study period. There was a significant association between impaired nasal MCC and decline in lung function. Nasal lavage revealed an increased proportion of macrophages, interleukin-8, and epidermal growth factor concentrations with decreased interleukin-10 during the study. No changes in the proportion of ciliated cells or contact angle were observed. Coughing and sleep symptoms decreased similarly in both groups. There were no outcome differences comparing dry vs cold bubble humidified NLFO. Conclusions In subjects receiving chronic NLFO, cold bubble humidification does not adequately humidify inspired oxygen to prevent deterioration of MCC, mucus hydration, and pulmonary function. The unheated bubble humidification performed no better than no humidification. Trial Registry ClinicalTrials.gov; No.: NCT02515786 ; URL: www.clinicaltrials.gov .

The aim of this study was to compare the effects of CPAP treatment and placebo intervention on the facial appearance of patients with OSA.Patients with severe OSA were randomized to receive either CPAP treatment or nasal dilator (placebo) intervention for 1 month. The sequence was interposed by 15 days of washout with no treatment. Patients were evaluated by using questionnaires, polysomnography, and facial photographs at baseline and at the end of both interventions. In an electronic survey, the photographs were presented in a randomized order to 704 observers who rated the perceived age, health, attractiveness, and tiredness of the patients. Observers were unaware of the patients' conditions.Thirty patients (age, 46 ± 9 years; 21 men; apnea-hypopnea index, 61.8 ± 26.2) were evaluated. During each intervention period, patients used CPAP 6.0 ± 1.7 h per night on 94% of the nights and the placebo intervention on 98% of the nights. After CPAP treatment, patients were rated younger (47.9 ± 3.5 years) than they appeared at baseline (53.9 ± 4.0 years) and following the placebo treatment (49.8 ± 3.7 years) (P .001). Linear regression analysis identified that CPAP adherence, total sleep time, and percentage of total sleep time with oxyhemoglobin saturation 90% were predictors of a decreased age rating following CPAP treatment.Patients with severe OSA had a younger appearance following 1 month of CPAP treatment. This benefit can serve as an additional source of motivation for patients with OSA to comply with CPAP treatment and may facilitate OSA management.ClinicalTrials.gov; No.: NCT02117271; URL: www.clinicaltrials.gov.

Although recent evidence suggests that OSA treatment may cause weight gain, the long-term effects of CPAP on weight are not well established.This study was a post hoc analysis of the Sleep Apnea Cardiovascular Endpoints (SAVE) study, a multicenter, randomized trial of CPAP plus standard care vs standard care alone in adults with a history of cardiac or cerebrovascular events and moderate to severe OSA. Participants with weight, BMI, and neck and waist circumferences measured at baseline and during follow-up were included. Linear mixed models were used to examine sex-specific temporal differences, and a sensitivity analysis compared high CPAP adherers (≥ 4 h per night) with propensity-matched control participants.A total of 2,483 adults (1,248 in the CPAP group and 1,235 in the control group) were included (mean 6.1 ± 1.5 measures of weight available). After a mean follow-up of 3.78 years, there was no difference in weight change between the CPAP and control groups, for male subjects (mean [95% CI] between-group difference, 0.07 kg [-0.40 to 0.54]; P = .773) or female subjects (mean [95% CI] between-group difference, -0.14 kg [-0.37 to 0.09]; P = .233). Similarly, there were no significant differences in BMI or other anthropometric measures. Although male participants who used CPAP ≥ 4 h per night gained slightly more weight than matched male control subjects without CPAP (mean difference, 0.38 kg [95% CI, 0.04 to 0.73]; P = .031), there were no between-group differences in other anthropometric variables, nor were there any differences between female high CPAP adherers and matched control subjects.Long-term CPAP use in patients with comorbid OSA and cardiovascular disease does not result in clinically significant weight change.ClinicalTrials.gov; No.: NCT00738179; URL: www.clinicaltrials.gov.

BACKGROUND Snoring is extremely common in the general population and may indicate OSA. However, snoring is not objectively measured during polysomnography, and no standard treatment is available for primary snoring or when snoring is associated with mild forms of OSA. This study determined the effects of oropharyngeal exercises on snoring in minimally symptomatic patients with a primary complaint of snoring and diagnosis of primary snoring or mild to moderate OSA. METHODS Patients were randomized for 3 months of treatment with nasal dilator strips plus respiratory exercises (control) or daily oropharyngeal exercises (therapy). Patients were evaluated at study entry and end by sleep questionnaires (Epworth Sleepiness Scale, Pittsburgh Sleep Quality Index) and full polysomnography with objective measurements of snoring. RESULTS We studied 39 patients (age, 46 ± 13 years; BMI, 28.2 ± 3.1 kg/m2; apnea-hypopnea index (AHI), 15.3 ± 9.3 events/h; Epworth Sleepiness Scale, 9.2 ± 4.9; Pittsburgh Sleep Quality Index, 6.4 ± 3.3). Control (n = 20) and therapy (n = 19) groups were similar at study entry. One patient from each group dropped out. Intention-to-treat analysis was used. No significant changes occurred in the control group. In contrast, patients randomized to therapy experienced a significant decrease in the snore index (snores > 36 dB/h), 99.5 (49.6-221.3) vs 48.2 (25.5-219.2); P = .017 and total snore index (total power of snore/h), 60.4 (21.8-220.6) vs 31.0 (10.1-146.5); P = .033. CONCLUSIONS Oropharyngeal exercises are effective in reducing objectively measured snoring and are a possible treatment of a large population suffering from snoring. TRIAL REGISTRY ClinicalTrials.gov; No.: NCT01636856; URL: www.clinicaltrials.gov

BACKGROUND The impact of OSA on new cardiovascular events in patients undergoing coronary artery bypass graft (CABG) surgery is poorly explored. METHODS Consecutive patients referred for CABG underwent clinical evaluation and standard polysomnography in the preoperative period. CABG surgery data, including percentage of off-pump and on-pump CABG, number of grafts, and intraoperative complications, were collected. The primary end point was major adverse cardiac or cerebrovascular events (MACCEs) (combined events of all-cause death, myocardial infarction, repeated revascularization, and cerebrovascular events). Secondary end points included individual MACCEs, typical angina, and arrhythmias. Patients were evaluated at 30 days (short-term) and up to 6.1 years (long term) after CABG. RESULTS We studied 67 patients (50 men; mean age, 58 ± 8 years; mean BMI, 28.5 ± 4.1 kg/m 2 ). OSA (apnea-hypopnea index ≥ 15 events/h) was present in 56% of the population. The patients were followed for a mean of 4.5 years (range, 3.2-6.1 years). No differences were observed in the short-term follow-up. In contrast, MACCE (35% vs 16%, P = .02), new revascularization (19% vs 0%, P = .01), episodes of typical angina (30% vs 7%, P = .02), and atrial fibrillation (22% vs 0%, P = .0068) were more common in patients with than without OSA in the long-term follow-up. OSA was an independent factor associated with the occurrence of MACCE, repeated revascularization, typical angina, and atrial fibrillation in the multivariate analysis. CONCLUSIONS OSA is independently associated with a higher rate of long-term cardiovascular events after CABG and may have prognostic and economic significance in CABG surgery.

Nasal CPAP is the "gold standard" treatment for OSA. However, oronasal masks are frequently used in clinical practice. The aim of this study was to perform a meta-analysis of all randomized and nonrandomized trials that compared nasal vs oronasal masks on CPAP level, residual apnea-hypopnea index (AHI), and CPAP adherence to treat OSA.The Cochrane Central Register of Controlled Trials, Medline, and Web of Science were searched for relevant studies in any language with the following terms: "sleep apnea" and "CPAP" or "sleep apnea" and "oronasal mask" or "OSA" and "oronasal CPAP" or "oronasal mask" and "adherence." Studies on CPAP treatment for OSA were included, based on the following criteria: (1) original article; (2) randomized or nonrandomized trials; and (3) comparison between nasal and oronasal CPAP including pressure level, and/or residual AHI, and/or CPAP adherence.We identified five randomized and eight nonrandomized trials (4,563 patients) that reported CPAP level and/or residual AHI and/or CPAP adherence. Overall, the random-effects meta-analysis revealed that as compared with nasal, oronasal masks were associated with a significantly higher CPAP level (Hedges' g, -0.59; 95% CI, -0.82 to -0.37; P .001) (on average, +1.5 cm HOronasal masks are associated with a higher CPAP level, higher residual AHI, and poorer adherence than nasal masks.PROSPERO database; No.: CRD42017064584; URL: https://www.crd.york.ac.uk/prospero/.

Acute cardiogenic pulmonary edema (ACPE) is a life-threatening condition. OSA may be a modifiable risk factor for ACPE recurrence. This study was designed to evaluate the impact of OSA on the incidence of cardiovascular events following ACPE recovery.Consecutive patients with confirmed ACPE from 3 centers underwent a sleep study following clinical stabilization. OSA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. The mean follow-up was 1 year, and the primary outcome was ACPE recurrence.A total of 104 patients were included in the final analysis; 61% of the patients had OSA. A higher rate of ACPE recurrence (25 vs 6 episodes; P = .01) and a higher incidence of myocardial infarction (15 vs 0 episodes; P = .0004) were observed in patients with OSA than in those without OSA. All 17 deaths occurred in the OSA group (P = .0001). In a Cox proportional hazards regression analysis, OSA was independently associated with ACPE recurrence (hazard ratio [HR], 3.3 [95% CI, 1.2-8.8]; P = .01), incidence of myocardial infarction (HR, 2.3 [95% CI, 1.1-9.5]; P = .02), cardiovascular death (HR, 5.4 [95% CI, 1.4-48.4]; P = .004), and total death (HR, 6.5 [95% CI, 1.2-64.0]; P = .005). When the analysis was limited only to patients with OSA, levels of AHI and hypoxemic burden and rates of sleep-onset ACPE were significantly higher in those who presented with ACPE recurrence or who died than in those who did not experience these events.OSA is independently associated with higher rates of ACPE recurrence and both fatal and nonfatal cardiovascular events.

Perimenopause is associated with increased cardiovascular risk. OSA is an emerging risk factor for cardiovascular disease, particularly among men, but the independent contribution of OSA to cardiovascular risk in climacteric women is not clear.We evaluated 277 consecutive women (age, 56 [52-61] years; BMI, 28 [25-32] kg/m2) without manifest cardiovascular disease (heart failure, coronary disease, or stroke). All women underwent 24-h ambulatory BP monitoring, arterial stiffness evaluation (pulse wave velocity), and portable sleep study.OSA (apnea-hypopnea index ≥ 5 events/h) and moderate to severe OSA (apnea-hypopnea index ≥ 15 events/h) were diagnosed in 111 (40.1%) and 31 (11.1%) women, respectively. None of the participants had received a previous diagnosis of OSA. Women with moderate to severe OSA vs those without OSA had a higher prevalence of hypertension, were prescribed more medications for hypertension, had higher awake BP (systolic, 133 [125-142] vs 126 [119-134] mm Hg [P.01]; diastolic, 82 [78-88] vs 79 [74-85] mm Hg [P = .07]), higher nocturnal BP (systolic, 125 [118-135] vs 115 [109-124] mm Hg [P.01]; diastolic, 73 [69-79] vs 69 [62-75] mm Hg [P.01]), and more arterial stiffness (pulse wave velocity, 11.5 [10.1-12.3] m/s vs 9.5 [8.6-10.8] m/s, P.001). Oxygen desaturation index during the night was independently associated with 24-h arterial BP and arterial stiffness (per five-unit increase in oxygen desaturation index, β = 1.30 [95% CI, 0.02-2.54; P = .04] vs 0.22 [95% CI, 0.03-0.40; P = .02] in women with vs without OSA, respectively).OSA is common, underdiagnosed, and independently associated with high BP and increased arterial stiffness in perimenopausal women.

Obstructive sleep apnea (OSA) is independently associated with death from cardiovascular diseases, including myocardial infarction and stroke. Myocardial infarction and stroke are complications of atherosclerosis; therefore, over the last decade investigators have tried to unravel relationships between OSA and atherosclerosis. OSA may accelerate atherosclerosis by exacerbating key atherogenic risk factors. For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. In addition, clinical data and experimental evidence in animal models suggest that OSA can have direct proatherogenic effects inducing systemic inflammation, oxidative stress, vascular smooth cell activation, increased adhesion molecule expression, monocyte/lymphocyte activation, increased lipid loading in macrophages, lipid peroxidation, and endothelial dysfunction. Several cross-sectional studies have shown consistently that OSA is independently associated with surrogate markers of premature atherosclerosis, most of them in the carotid bed. Moreover, OSA treatment with continuous positive airway pressure may attenuate carotid atherosclerosis, as has been shown in a randomized clinical trial. This review provides an update on the role of OSA in atherogenesis and highlights future perspectives in this important research area.

Obstructive sleep apnea (OSA) and hypertension are independently associated with increased stiffness of large arteries that may contribute to left ventricular (LV) remodeling. We sought to investigate the impact of OSA, hypertension, and their association with arterial stiffness and heart structure.We studied 60 middle-aged subjects classified into four groups according to the absence or presence of severe OSA with and without hypertension. All participants were free of other comorbidities. The groups were matched for age, sex, and body mass index.Full polysomnography, pulse-wave velocity (PWV), and transthoracic echocardiography were performed in all participants. Compared with normotensive subjects without OSA, PWV, left atrial diameter, interventricular septal thickness, LV posterior wall thickness, LV mass index, and percentage of LV hypertrophy had similar increases in normotensive OSA and patients with hypertension and no OSA (p0.05 for all comparisons), with a significant further increase in PWV, LV mass index, and percentage of LV hypertrophy in subjects with OSA and hypertension. Multivariate regression analysis showed that PWV was associated with systolic BP (p0.001) and apnea-hypopnea index (p = 0.002). The only independent variable associated with LV mass index was PWV (p0.0001).Severe OSA and hypertension are associated with arterial stiffness and heart structure abnormalities of similar magnitude, with additive effects when both conditions coexist. Increased large arterial stiffness contributes to ventricular afterload and may help to explain heart remodeling in both OSA and hypertension.

Background OSA has a familial aggregation pattern indicating that it can be partially caused by a genetic component. However, the heritability of OSA has been estimated based on the study of families of obese probands of urban populations with established OSA diagnosis. The objective of this genetic-epidemiologic study is to study families ascertained from a general rural population to determine an unbiased estimate of OSA heritability. Methods We studied a sample of families living in Baependi, a small rural southeastern Brazilian city. Participants were assessed for anthropometric measurements, physical examination, Epworth Sleepiness Scale, blood samples for glucose and cholesterol determination, and overnight home portable monitoring. Results We studied 587 participants (399 women) from 91 families, with a median (interquartile range [IQR]) of 4 (2-8) participants per family. The median age of the population was 44 years (IQR, 29-55 years) and median BMI was 25.0 kg/m2 (IQR, 22.1-28.6 kg/m2). OSA, defined by apnea-hypopnea index (AHI) > 5/h, was diagnosed in 18.6% of the sample. Two polygenic models, model I (no covariate effects) and model II (with covariate effects), were fitted to the data in all analyses. Heritability estimates for AHI were 0.23 and 0.25 for model I and II, respectively. Covariates (age, sex, and BMI) showed no significant effects on the heritability estimate for AHI. Conclusions The heritability of AHI in a rural population with low levels of obesity is intermediate (25%).

Snoring is extremely common in the general population and may indicate OSA. However, snoring is not objectively measured during polysomnography, and no standard treatment is available for primary snoring or when snoring is associated with mild forms of OSA. This study determined the effects of oropharyngeal exercises on snoring in minimally symptomatic patients with a primary complaint of snoring and diagnosis of primary snoring or mild to moderate OSA.Patients were randomized for 3 months of treatment with nasal dilator strips plus respiratory exercises (control) or daily oropharyngeal exercises (therapy). Patients were evaluated at study entry and end by sleep questionnaires (Epworth Sleepiness Scale, Pittsburgh Sleep Quality Index) and full polysomnography with objective measurements of snoring.We studied 39 patients (age, 46 ± 13 years; BMI, 28.2 ± 3.1 kg/m2; apnea-hypopnea index (AHI), 15.3 ± 9.3 events/h; Epworth Sleepiness Scale, 9.2 ± 4.9; Pittsburgh Sleep Quality Index, 6.4 ± 3.3). Control (n = 20) and therapy (n = 19) groups were similar at study entry. One patient from each group dropped out. Intention-to-treat analysis was used. No significant changes occurred in the control group. In contrast, patients randomized to therapy experienced a significant decrease in the snore index (snores36 dB/h), 99.5 (49.6-221.3) vs 48.2 (25.5-219.2); P = .017 and total snore index (total power of snore/h), 60.4 (21.8-220.6) vs 31.0 (10.1-146.5); P = .033.Oropharyngeal exercises are effective in reducing objectively measured snoring and are a possible treatment of a large population suffering from snoring.ClinicalTrials.gov; No.: NCT01636856; URL: www.clinicaltrials.gov.

Objective This study aimed to investigate nasal mucociliary clearance in acutely ill patients who were clinically stable and had no airway manipulation. Design Prospective clinical study. Setting Medical ICU. Patients and participants Sixteen medical patients admitted to the ICU and 16 healthy subjects were studied. Patients who were receiving airway manipulation, including tracheal suctioning, nasogastric or enteral tubes, noninvasive and invasive mechanical ventilation, were excluded. Interventions Mucociliary clearance was evaluated by saccharine transit time (STT) measurements at ICU admission (admission) and 90 days after hospital discharge (recovery). Healthy subjects were also subjected to two measurements 90 days apart. Measurements and results The STT of patients was 26.4 ± 11.3 min and 17.9 ± 8.6 min at admission and recovery (p = 0.002) [mean ± SD] but did not change along the 90-day interval in healthy subjects (17.2 ± 10.2 min and 16.7 ± 10.3 min), respectively. Smokers (patients and healthy subjects) presented prolonged STT when compared to nonsmokers (p = 0.026). STT at admission correlated positively with heart rate ( r = 0.560; p = 0.024) and hospital stay ( r = 0.634; p = 0.008). Conclusion Mucociliary clearance is impaired in stable acutely ill patients with no airway manipulation and correlates with simple markers of underlying disease severity. Mucociliary dysfunction may help to explain the increased susceptibility of hospital-acquired respiratory infection in critically ill patients.

Refractory angina is a severe form of coronary artery disease (CAD) characterized by persistent angina despite optimal medical therapy. OSA and depression are common in patients with stable CAD and may contribute to a poor prognosis. We hypothesized that OSA and depression are more common and more severe in patients with refractory angina than in patients with stable CAD.We used standardized questionnaires and full polysomnography to compare consecutive patients with well-established refractory angina vs consecutive patients with stable CAD evaluated for coronary artery bypass graft surgery.Patients with refractory angina (n = 70) compared with patients with stable CAD (n = 70) were similar in sex distribution (male, 61.5% vs 75.5%; P = .07) and BMI (29.5 ± 4 kg/m2 vs 28.5 ± 4 kg/m2, P = .06), and were older (61 ± 10 y vs 57 ± 7 y, P = .013), respectively. Patients with refractory angina had significantly more symptoms of daytime sleepiness (Epworth Sleepiness Scale score, 12 ± 6 vs 8 ± 5; P.001), had higher depression symptom scores (Beck Depression Inventory score, 19 ± 8 vs 10 ± 8; P.001) despite greater use of antidepressants, had a higher apnea-hypopnea index (AHI) (AHI, 37 ± 30 events/h vs 23 ± 20 events/h; P = .001), higher proportion of oxygen saturation90% during sleep (8% ± 13 vs 4% ± 9, P = .04), and a higher proportion of severe OSA (AHI ≥ 30 events/h, 48% vs 27%; P = .009) than patients with stable CAD. OSA (P = .017), depression (P.001), higher Epworth Sleepiness Scale score (P = .007), and lower sleep efficiency (P = .016) were independently associated with refractory angina in multivariate analysis.OSA and depression are independently associated with refractory angina and may contribute to poor cardiovascular outcome.

Study objectives: The mechanisms involved in the impairment of mucociliary function after lung transplantation are not completely understood. The purpose of the present study was to isolate the effects of unilateral bronchial transection and reanastomosis in a rat model. Design: In situ bronchial mucociliary transport (MCT) was determined proximal and distal to the bronchial anastomosis, as well as in the right bronchus, in 48 rats classified into six groups: intact rats, and rats at 1 day, 2 days, 7 days, 15 days, and 30 days after bronchial transection and reanastomosis of the left main stem bronchus. In vitro mucus transportability and mucus contact angle were studied in another group of eight rats after 1 week of surgery. Results: Distal to the anastomosis site, left bronchus in situ MCT (mean 6 SD) was 0.26 6 0.19 mm/min for the intact group, and 0.11 6 0.13 mm/min, 0.07 6 0.04 mm/min, 0.03 6 0.04 mm/min, 0.07 6 0.12 mm/min, and 0.05 6 0.06 mm/min for 1 day, 2 days, 7 days, 15 days, and 30 days after surgery, respectively (all significantly reduced, p < 0.05). No intergroup differences were found proximal to the anastomosis (p 5 0.30). When comparing the left and right bronchi, differences were detected in both distal (p < 0.0001) and proximal sides (p 5 0.0001). No significant differences in mucus transportability in vitro were found (p 5 0.15). Mucus contact angle of the left bronchus (52.8 6 20.5°) was significantly greater than that of the mucus from the right bronchus (34.4 6 12.9°; p < 0.05). Conclusions: We conclude that bronchial transection and reanastomosis lead to a marked impairment of MCT in distal airways, which can in part be explained by alterations in the surface properties of mucus. (CHEST 2001; 119:1510 ‐1515)

OSA is extremely common among patients with resistant hypertension (HTN). However, the impact of the treatment of OSA with CPAP on BP in patients with resistant HTN is not well established.In the current study, 40 patients with confirmed resistant HTN and moderate to severe OSA confirmed by full polysomnography were randomized to medical therapy or to medical treatment plus CPAP for 6 months. Patients were evaluated at study baseline and after 6 months by 24-h ambulatory BP monitoring (ABPM).Thirty-five patients (77% men; age, 56 ± 1 years; BMI, median 32 kg/m² [25%-75%, 28-39 kg/m²]; apnea-hypopnea index, 29 events/h [24-48 events/h]; Epworth Sleepiness Scale, 10 ± 1; systolic/diastolic office BP, 162 ± 4/97 ± 2 mm Hg; taking four [four to five] antihypertensive drugs) completed the study. CPAP was used for 6:01 ± 0:20 h/night (3:42-7:44 h/night). Compared with the control group, awake systolic/diastolic ABPM decreased significantly in the CPAP group (Δ: +3.1 ± 3.3 /+2.1 ± 2.7 mm Hg vs -6.5 ± 3.3/-4.5 ± 1.9 mm Hg, respectively, P.05). Interestingly, the BP changes were observed only while patients were awake, but not during nocturnal ABPM (Δ: +2.8 ± 4.5/+1.8 ± 3.5 mm Hg vs +1.6 ± 3.5/+0.8 ± 2.9 mm Hg, P = NS).The treatment of OSA with CPAP significantly reduces daytime BP in patients with resistant HTN. Therefore, our study reinforces the importance of recognizing and treating OSA in patients with resistant HTN.ClinicalTrials.gov; No.: NCT00812695; URL: www.clinicaltrials.gov.

We showed previously that nasal mucociliary clearance was decreased in critically ill elderly subjects, most of whom had diabetes mellitus (DM) and/or hypertension (HTN). To determine if these changes were due to the effects of aging, disease, or critical illness, we studied nasal mucociliary clearance and mucus properties in an ambulatory population consisting of young, elderly, and healthy subjects and those with DM, HTN, or both.Of 440 subjects contacted, 252 entered the study. The subjects were divided into the following groups: (1) healthy (n 5 79, 18-94 years, 50 men) and (2) DM and/or HTN, of which 37 had DM (14-90 years, 12 men), 52 had HTN (23-90 years, 12 men), and 84 had both DM and HTN (25-82 years, 33 men). Subjects were also grouped by age: , 40 years, 40 to 59 years, and 60 years. We assessed demographic and clinical data, quality of life using the 36-Item Short Form Health Survey (SF-36) questionnaire, nasal mucociliary clearance using the saccharine transit test (STT), and in vitro mucus properties by examining the sneeze (high airflow) clearability and contact angle. A logistic regression analysis for prolonged STT . 12 min was used, and we controlled for age, sex, and diseases.Subjects aged . 60 years reported a decreased SF-36 physical component relative to other age groups. Sex, BMI, BP, heart rate, pulse oximetry, blood glucose level, and mucus properties were not associated with prolonged STT. Aging and DM and/or HTN independently increased the risk of prolonged STT.Aging and DM, HTN, or both diseases are independently associated with decreased nasal mucociliary clearance. This may predispose toward respiratory infections.

Obstructive sleep apnea (OSA) is independently associated with death from cardiovascular diseases, including myocardial infarction and stroke. Myocardial infarction and stroke are complications of atherosclerosis; therefore, over the last decade investigators have tried to unravel relationships between OSA and atherosclerosis. OSA may accelerate atherosclerosis by exacerbating key atherogenic risk factors. For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. In addition, clinical data and experimental evidence in animal models suggest that OSA can have direct proatherogenic effects inducing systemic inflammation, oxidative stress, vascular smooth cell activation, increased adhesion molecule expression, monocyte/lymphocyte activation, increased lipid loading in macrophages, lipid peroxidation, and endothelial dysfunction. Several cross-sectional studies have shown consistently that OSA is independently associated with surrogate markers of premature atherosclerosis, most of them in the carotid bed. Moreover, OSA treatment with continuous positive airway pressure may attenuate carotid atherosclerosis, as has been shown in a randomized clinical trial. This review provides an update on the role of OSA in atherogenesis and highlights future perspectives in this important research area.

Hypertrophic cardiomyopathy (HCM) is associated with arrhythmias and cardiovascular death. Left atrial enlargement and atrial fibrillation (AF) are considered markers for death due to heart failure in patients with HCM. Obstructive sleep apnea (OSA) is independently associated with heart remodeling and arrhythmias in other populations. We hypothesized that OSA is common and is associated with heart remodeling and AF in patients with HCM.We evaluated 80 consecutive stable patients with a confirmed diagnosis of HCM by sleep questionnaire, blood tests, echocardiography, and sleep study (overnight respiratory monitoring).OSA (apnea-hypopnea index [AHI]15 events/h) was present in 32 patients (40%). Patients with OSA were significantly older (56 [41-64] vs 38.5 [30-53] years, P.001) and presented higher BMI (28.2 +/- 3.5 vs 25.2 +/- 5.2 kg/m(2), P.01) and increased left atrial diameter (45 [42-52.8] vs 41 [39-47] mm, P = .01) and aorta diameter (34 [30-37] vs 29 [28-32] mm, P.001), compared with patients without OSA. Stepwise multiple linear regression showed that the AHI (P = .05) and BMI (P = .06) were associated with left atrial diameter. The AHI was the only variable associated with aorta diameter (P = .01). AF was present in 31% vs 6% of patients with and without OSA, respectively (P.01). OSA (P = .03) and left atrial diameter (P = .03) were the only factors independently associated with AF.OSA is highly prevalent in patients with HCM and it is associated with left atrial and aortic enlargement. OSA is independently associated with AF, a risk factor for cardiovascular death in this population.