Diuretic or sodium-restricted diet for obstructive sleep apnea-a randomized trial.

Study Objectives: Interventions that decrease leg fluid retention reduce obstructive sleep apnea (OSA) severity in nonrandomized experiments. We aimed to investigate in a randomized trial the effect of interventions that reduce fluid volume on OSA severity. Methods: Men diagnosed with severe OSA were randomized to receive daily spironolactone 100 mg + furosemide 20 mg or nutritional counseling to sodium-restricted diet plus placebo pill or placebo pill. All participants underwent home sleep apnea testing at baseline and after 1 week follow-up. The change in apnea-hypopnea index (AHI) was the primary outcome. Results: The study included 54 participants and all were assessed at follow-up. The average baseline value of the AHI was similar among groups and from baseline to follow-up the AHI reduced 14.4 per cent (δ value -7.3 events per hour; 95% confidence interval, -13.8 to -0.9) in the diuretic group, 22.3 per cent (-10.7; 95% CI, -15.6 to -5.7) in the diet group, and 0.8 per cent (0.4; 95% CI, -2.5 to 3.2) in the placebo group (p = .001 for time × group interaction). None of the patients had their AHI returned to normal. The reduction in the total body water was 2.2 ± 2.2 L in the diuretic group (p < .001) and 1.0 ± 1.6 l in the low salt diet group (p = .002). Sleepiness and neck circumference were significantly reduced only in the diet group (p = .007 and p < .001 for the time × group interactions, respectively). Conclusions: Interventions to reduce bodily fluid content in men with severe OSA promoted a limited decrease of apnea frequency. This finding suggests that rostral fluid displacement affects only partially the OSA severity and/or that other factors prevail in determining pharyngeal collapsibility. Clinical Trial: Sodium-Restricted Diet and Diuretic in the Treatment of Severe Sleep Apnea (DESALT), https://clinicaltrials.gov/ct2/show/NCT01945801 ClinicalTrials.gov number: NCT01945801.

Diagnostic performance of cheeks appearance in sleep apnea.

OBJECTIVE: Obstructive sleep apnea (OSA) is a common, potentially life-threatening, but underdiagnosed condition. The study aimed to test the role of facial myofunctional alterations in OSA screening. METHOD: Sixty-one individuals with sleep complaints were evaluated by the Orofacial Myofunctional Evaluation with Scores (OMES) protocol before undergoing polysomnography. The performance of each of the protocol scores in OSA screening was tested. RESULTS: The nonparametric correlation of the apnea-hypopnea index (AHI) was significant for 18 of the 41 variables of the OMES protocol. Cheeks appearance had the best performance, increasing five times the odds for AHI ≥ 15. Its sensitivity was 66%; specificity, 72%; the area under the ROC curve, 0.69; positive and negative likelihood ratios, respectively, 2.38 and 0.47. DISCUSSION: Cheeks appearance may be an instantly visible surrogate of tongue and pharyngeal fat deposition and of muscle function in OSA screening. Adding the item "cheeks appearance" to OSA screening tools and questionnaires may be useful for the identification of OSA risk.

Disrupted day-night pattern of cardiovascular death in obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) patients who suffer sudden cardiac death die predominantly during the night. We aimed to investigate whether all cardiovascular-related deaths display the same night-time peak as sudden cardiac death. METHODS: Data from a large cohort of adults who underwent full-night polysomnography between 1985 and 2015 in a university-affiliated sleep clinic were analyzed. Time and cause of death of these patients and of persons from the general population were identified in death certificates from the State Health Secretariat. The day-night pattern of cardiovascular death was compared among groups of non-OSA, OSA (apnea-hypopnea index, AHI ≥5), CPAP users, and persons from the general population. RESULTS: Among 619 certificates, 160 cardiovascular-related deaths were identified. The time of death of the 142 persons with OSA was uniformly distributed over 24 h, with neither an identifiable peak nor a circadian pattern (Rayleigh test; P = 0.8); the same flat distribution was seen in those with purported CPAP use (n = 49). Non-OSA individuals presented a morning peak and a night nadir of deaths, clearer when analyzed in eight-hour intervals. The same pattern was observed in 92 836 certificates from the State general population, with cardiovascular deaths showing the expected morning peak, night nadir, and a significant circadian pattern (Rayleigh test; P < 0.001). CONCLUSIONS: In OSA patients, the distribution of cardiovascular-related deaths throughout the 24-h period is virtually flat, in contrast with the described nighttime peak of sudden cardiac death. OSA-related phenomena during nighttime might be blunting the mechanisms, arrhythmic or not, behind the morning peak of cardiovascular-related deaths.

The effect of caffeine supplementation on exercise performance evaluated by a novel animal model

Introduction: Caffeinated drinks are used for improve performance. Animal models represent investigational strategy that circumvents most of the drawbacks of research in humans, including motivational factors and the placebo effect. No animal model that could test whether different forms of administering caffeine affect exercise propensity was found in the literature. Methods: An animal model of grouped voluntary exercise was tested. Two-month-old male C57/bl mice were housed in a cage fitted with one running wheel and a monitoring system. Six animals per cage were introduced individually. To assess the sensitivity of the model, the effect of different caffeinated drinks was observed in mice exercising ad libitum. During 2 days, the mice received: 1) pure anhydrous caffeine 0.125 mg/mL (PC), 2) cola drink (CC), and 3) caffeine-taurine-glucuronolactone drink (CTG), intercalating wash-out periods of 2 days, receiving pure water. Results: The distance run during the periods of water ingestion was significantly lower than during the periods of stimulant drinks ingestion: PC (5.6 ± 1.3 km; p = 0.02), of CC ingestion (7.6 ± 0.6 km; p = 0.001), and of CTG ingestion (8.3 ± 1.6 km; p = 0.009). The performances when ingesting the three caffeinated drinks do not follow a dose-response curve. Conclusions: The model described here was able to measure the effect of caffeine intake on voluntary exercise of mice. The sensitivity of the model to the effect of caffeine needs to be further validated. The action of each component of the drinks on exercise performance needs to be clarified in future research. The present model is adequate for such investigation (AU)

Melatonin prevents hyperglycemia in a model of sleep apnea.

OBJECTIVE: Obstructive sleep apnea is a common disorder associated with aging and obesity. Apneas cause repeated arousals, intermittent hypoxia, and oxidative stress. Changes in glucolipidic profile occur in apnea patients, independently of obesity. Animal models of sleep apnea induce hyperglycemia. This study aims to evaluate the effect of the antioxidants melatonin and N-acetylcysteine on glucose, triglyceride, and cholesterol levels in animals exposed to intermittent hypoxia. MATERIALS AND METHODS: Two groups of Balb/c mice were exposed to intermittent hypoxia (n = 36) or sham intermittent hypoxia (n = 36) for 35 days. The intermittent hypoxia group underwent a total of 480 cycles of 30 seconds reducing the inspired oxygen fraction from 21% to 7 ± 1% followed by 30 seconds of normoxia, during 8 hours daily. Melatonin or N-acetylcysteine were injected intraperitonially daily from day 21 on. RESULTS: At day 35, glucose levels were significantly higher in the intermittent hypoxia group than in the control group. The intermittent hypoxia groups receiving N-acetylcysteine and vehicle showed higher glucose levels than the group receiving melatonin. The lipid profile was not affected by intermittent hypoxia or antioxidant administration. CONCLUSIONS: The present results suggest that melatonin prevents the well-recognized increase in glucose levels that usually follows exposure to intermittent hypoxia. Further exploration of the role of melatonin in sleep apnea is warranted.

Uncoupling protein-2 mRNA expression in mice subjected to intermittent hypoxia.

OBJECTIVE: To investigate the effect of intermittent hypoxia-a model of obstructive sleep apnea (OSA)-on pancreatic expression of uncoupling protein-2 (UCP2), as well as on glycemic and lipid profiles, in C57BL mice. METHODS: For 8 h/day over a 35-day period, male C57BL mice were exposed to intermittent hypoxia (hypoxia group) or to a sham procedure (normoxia group). The intermittent hypoxia condition involved exposing mice to an atmosphere of 92% N and 8% CO2 for 30 s, progressively reducing the fraction of inspired oxygen to 8 ± 1%, after which they were exposed to room air for 30 s and the cycle was repeated (480 cycles over the 8-h experimental period). Pancreases were dissected to isolate the islets. Real-time PCR was performed with TaqMan assays. RESULTS: Expression of UCP2 mRNA in pancreatic islets was 20% higher in the normoxia group than in the hypoxia group (p = 0.11). Fasting serum insulin was higher in the hypoxia group than in the normoxia group (p = 0.01). The homeostasis model assessment of insulin resistance indicated that, in comparison with the control mice, the mice exposed to intermittent hypoxia showed 15% lower insulin resistance (p = 0.09) and 21% higher pancreatic ß-cell function (p = 0.01). Immunohistochemical staining of the islets showed no significant differences between the two groups in terms of the area or intensity of α- and ß-cell staining for insulin and glucagon. CONCLUSIONS: To our knowledge, this is the first report of the effect of intermittent hypoxia on UCP2 expression. Our findings suggest that UCP2 regulates insulin production in OSA. Further study of the role that UCP2 plays in the glycemic control of OSA patients is warranted.

Effect of diuretics and sodium-restricted diet on sleep apnea severity: study protocol for a randomized controlled trial.

BACKGROUND: Obstructive sleep apnea occurs as a result of increased collapsibility of the upper airway. Overnight fluid displacement from the legs to the neck causes pharyngeal narrowing and increased apnea severity. Sodium intake is associated with apnea severity. We hypothesized that interventions that decrease bodily fluid content might reduce the severity of sleep apnea. METHODS/DESIGN: This is a randomized clinical trial including men with an apnea-hypopnea index greater than 30 events/hour, previously diagnosed by full-night in-laboratory polysomnography. A total of 54 men will be included and randomly assigned to three groups: Diuretic (n = 18), sodium-restricted diet (n = 18), and control (n = 18). The intervention will last one week. Intention-to-treat and per-protocol analyses will be performed. The diuretic group will receive combined spironolactone 100 mg plus furosemide 20 mg daily, taken in the morning. The diet group will receive a regimen with a maximum intake of 3 g of sodium per day. The control group will receive a placebo pill and will maintain all eating habits while keeping a recall diary of their dietary behavior. The primary outcome measure will be change in apnea-hypopnea index. The secondary outcome measures will be variations of: anthropometric and bioelectrical impedance variables, office blood pressure, respiratory variables from in-home level III polysomnography, excessive daytime sleepiness, glycolipid profile, C-reactive protein, 24 h urinary variables, and adverse events. DISCUSSION: Despite the high efficacy of continuous positive airway pressure to reverse upper airway obstruction in sleep apnea, partial adherence to this form of treatment reduces its efficiency. Thus, additional forms of treating apnea need to be investigated. If the results of this proof-of-concept trial show that decreases in bodily fluid content, either by diuretic or dietary intervention, reduces the severity of sleep apnea, further investigation will be necessary before these results can be translated and adopted as an adjunct apnea therapy. TRIAL REGISTRATION: clinicaltrials.gov NCT01945801.

Uncoupling protein-2 mRNA expression in mice subjected to intermittent hypoxia / Expressão do mRNA da uncoupling protein-2 em camundongos submetidos à hipóxia intermitente

Objective: To investigate the effect of intermittent hypoxia-a model of obstructive sleep apnea (OSA)-on pancreatic expression of uncoupling protein-2 (UCP2), as well as on glycemic and lipid profiles, in C57BL mice. Methods: For 8 h/day over a 35-day period, male C57BL mice were exposed to intermittent hypoxia (hypoxia group) or to a sham procedure (normoxia group). The intermittent hypoxia condition involved exposing mice to an atmosphere of 92% N and 8% CO2 for 30 s, progressively reducing the fraction of inspired oxygen to 8 ± 1%, after which they were exposed to room air for 30 s and the cycle was repeated (480 cycles over the 8-h experimental period). Pancreases were dissected to isolate the islets. Real-time PCR was performed with TaqMan assays. Results: Expression of UCP2 mRNA in pancreatic islets was 20% higher in the normoxia group than in the hypoxia group (p = 0.11). Fasting serum insulin was higher in the hypoxia group than in the normoxia group (p = 0.01). The homeostasis model assessment of insulin resistance indicated that, in comparison with the control mice, the mice exposed to intermittent hypoxia showed 15% lower insulin resistance (p = 0.09) and 21% higher pancreatic β-cell function (p = 0.01). Immunohistochemical staining of the islets showed no significant differences between the two groups in terms of the area or intensity of α- and β-cell staining for insulin and glucagon. Conclusions: To our knowledge, this is the first report of the effect of intermittent hypoxia on UCP2 expression. Our findings suggest that UCP2 regulates insulin production in OSA. Further study of the role that UCP2 plays in the glycemic control of OSA patients is warranted. .

Objetivo: Investigar o efeito da hipóxia intermitente com um modelo de apneia obstrutiva do sono (AOS) sobre a expressão de uncoupling protein-2 (UCP2), assim como sobre perfis glicêmicos e lipídicos, em camundongos C57BL. Métodos: Camundongos C57BL machos foram expostos a hipóxia intermitente ou hipóxia simulada (grupo controle) 8 h/dia durante 35 dias. A condição de hipóxia intermitente envolveu a exposição dos camundongos a uma atmosfera de 92% de N e 8% de CO2 por 30 s, com redução progressiva de fração de O2 inspirado até 8 ± 1%, seguida por exposição a ar ambiente por 30 s e repetições do ciclo (480 ciclos no período experimental de 8 h). Os pâncreas foram dissecados para isolar as ilhotas. Foi realizada PCR em tempo real utilizando o método TaqMan. Resultados: A expressão do mRNA da UCP2 nas ilhotas pancreáticas foi 20% maior no grupo controle que no grupo hipóxia (p = 0,11). A insulina sérica de jejum foi maior no grupo hipóxia do que no grupo controle (p = 0,01). O modelo de avaliação da homeostase de resistência à insulina indicou que, em comparação com os camundongos controle, aqueles expostos à hipóxia intermitente apresentaram 15% menor resistência à insulina (p = 0,09) e 21% maior função das células beta (p = 0,01). A coloração das ilhotas pancreáticas por imuno-histoquímica não mostrou diferenças significativas entre os grupos em termos da área ou da intensidade das células alfa e beta, marcadas por insulina e glucagon. Conclusões: Segundo nosso conhecimento, esta é a primeira descrição do efeito da hipóxia intermitente sobre a expressão da UCP2. Nossos achados sugerem que UCP2 regula a produção de insulina na AOS. Futuras investigações sobre o papel da UCP2 no controle glicêmico em pacientes com AOS são justificadas. .

Melatonin prevents hyperglycemia in a model of sleep apnea

Objective Obstructive sleep apnea is a common disorder associated with aging and obesity. Apneas cause repeated arousals, intermittent hypoxia, and oxidative stress. Changes in glucolipidic profile occur in apnea patients, independently of obesity. Animal models of sleep apnea induce hyperglycemia. This study aims to evaluate the effect of the antioxidants melatonin and N-acetylcysteine on glucose, triglyceride, and cholesterol levels in animals exposed to intermittent hypoxia. Materials and methods Two groups of Balb/c mice were exposed to intermittent hypoxia (n = 36) or sham intermittent hypoxia (n = 36) for 35 days. The intermittent hypoxia group underwent a total of 480 cycles of 30 seconds reducing the inspired oxygen fraction from 21% to 7 ± 1% followed by 30 seconds of normoxia, during 8 hours daily. Melatonin or N-acetylcysteine were injected intraperitonially daily from day 21 on. Results At day 35, glucose levels were significantly higher in the intermittent hypoxia group than in the control group. The intermittent hypoxia groups receiving N-acetylcysteine and vehicle showed higher glucose levels than the group receiving melatonin. The lipid profile was not affected by intermittent hypoxia or antioxidant administration. Conclusions The present results suggest that melatonin prevents the well-recognized increase in glucose levels that usually follows exposure to intermittent hypoxia. Further exploration of the role of melatonin in sleep apnea is warranted. Arch Endocrinol Metab. 2015;59(1):66-70 .

Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea.

BACKGROUND: Sleep apnea causes intermittent hypoxia (IH). We aimed to investigate the proteins related to oxidative stress, inflammation and apoptosis in liver tissue subjected to IH as a simulation of sleep apnea in conjunction with the administration of either melatonin (MEL, 200 µL/kg) or N-acetylcysteine (NAC, 10 mg/kg). METHODS: Seventy-two adult male Balb-C mice were divided: simulation of IH (SIH), SIH + MEL, SIH + NAC, IH, IH + MEL and IH + NAC. The animals were subjected to simulations of sleep apnea for 8 h a day for 35 days. The data were analyzed with ANOVA and Tukey tests with the significance set at p < 0.05. RESULTS: In IH, there was a significant increase in oxidative stress and expression of HIF-1a. In addition, we observed increase in the activation levels of NF-kB. This increase may be responsible for the increased expression of TNF-alpha and iNOS as well as the significant increase of VEGF signaling and expression of caspase-3 and caspase-6, which suggests an increase in apoptosis. In the groups treated with antioxidants, the analysis showed that the enzyme activity and protein levels were similar to those of the non-simulated group. CONCLUSIONS: Thus, we show that IH causes liver inflammation and apoptosis, which may be protected with either MEL or NAC.

Hypomyelination, memory impairment, and blood-brain barrier permeability in a model of sleep apnea.

We investigated the effect of intermittent hypoxia, mimicking sleep apnea, on axonal integrity, blood-brain barrier permeability, and cognitive function of mice. Forty-seven C57BL mice were exposed to intermittent or sham hypoxia, alternating 30s of progressive hypoxia and 30s of reoxigenation, during 8h/day. The axonal integrity in cerebellum was evaluated by transmission electron microscopy. Short- and long-term memories were assessed by novel object recognition test. The levels of endothelin-1 were measured by ELISA. Blood-brain barrier permeability was quantified by Evans Blue dye. After 14 days, animals exposed to intermittent hypoxia showed hypomyelination in cerebellum white matter and higher serum levels of endothelin-1. The short and long-term memories in novel object recognition test was impaired in the group exposed to intermittent hypoxia as compared to controls. Blood-brain barrier permeability was similar between the groups. These results indicated that hypomyelination and impairment of short- and long-term working memories occurred in C57BL mice after 14 days of intermittent hypoxia mimicking sleep apnea.

Ecocardiografia em pacientes com apneia do sono grave com e sem pressão arterial controlada: estudo transversal / Echocardiography in patients with severe sleep apnea with and without controlled blood pressure: cross sectional study

A apneia obstrutiva do sono (AOS) afeta a anatomia e função do coração. Ocorre hipertensão arterial em metade dos casos de AOS, dificultando atribuir a etiologia dessas alterações separadamente à hipertensão arterial ou à apneia do sono. Métodos: Estudo transversal de pacientes com índice de apneia-hipopneia maior que 50 eventos por hora. As variáveis ecocardiográficas comparadas em indivíduos com hipertensão arterial controlada e não controlada foram: 1) fração de ejeção, 2) diâmetro da aorta, 3) diâmetro do átrio esquerdo, 4) diâmetro de ventrículo direito, 5) diâmetros do ventrículo esquerdo diastólico e sistólico, 6) percentagem delta, 7) espessura do septo, 8) espessura da parede posterior. Resultados: Foram incluídos 83 voluntários, 50 com pressão arterial não controlada. Em média, a idade era 47 ± 9,5 anos, o índice de massa corporal 34 ± 5,4 Kg/m2 , o índice de apneia-hipopneia 86 ± 18 eventos/hora. Sessenta pacientes apresentaram anormalidade no ecocardiograma. A hipertrofia de ventrículo esquerdo foi o achado mais comum, sem diferença de frequência em controles (39%) e em hipertensos (48%), seguida por disfunção diastólica em controles (27%) e em hipertensos (32%). Conclusões: Indivíduos com apneia do sono grave e pressão arterial controlada apresentam alterações no ecocardiograma de tipo e frequência semelhantes aos com hipertensão não controlada. Isso sugere que a apneia do sono pode causar dano cardíaco independentemente de hipertensão. Quando não explicáveis por hipertensão arterial, achados como hipertrofia de ventrículo esquerdo podem ser provocados por apneia do sono...

Obstructive sleep apnea (OSA) affects the cardiac anatomy and function. Hypertension occurs in half the OSA cases, making it difficult to attribute the cause of these changes separately to arterial hypertension or sleep apnea. Methods: Prospective cross-sectional study of volunteers with apnea-hypopnea index >50 events per hour. The echocardiographic variables were analyzed: 1) ejection fraction, 2) aortic diameter, 3) left atrial diameter, 4) right ventricular diameter, 5) diastolic and systolic diameters of the left ventricle, 6) delta percentage, 7) septum thickness, 8) posterior wall thickness. Results: There were 83 participants, 74 men, 50 with hypertension. The average age was 47 ± 9.5 years, body mass index of 34 ± 5.4 kg/m2 , apnea-hypopnea index of 86±18 events/hour, and minimum oxygen saturation of 55 ± 17%. Left ventricular hypertrophy was the most common echocardiographic abnormality in subjects without hypertension (39%) and with hypertension (48%), followed by diastolic dysfunction in subjects with normal blood pressure (27%) and with high blood pressure (32%). There was no statistically significant difference in echocardiographic characteristics between hypertensive subjects with those with normal pressure. Conclusions: Individuals with normal blood pressure and severe sleep apnea show abnormalities in the echocardiogram with frequency similar to that observed in patients with high blood pressure. This suggests that sleep apnea can cause ventricular overload independently of hypertension. When not explained by high blood pressure, left ventricular hypertrophy can be caused by sleep apnea...

Downregulation of uncoupling protein-1 mRNA expression and hypoadiponectinemia in a mouse model of sleep apnea.

PURPOSE: The knowledge on the effect of intermittent hypoxia on adipose tissue-mediated processes is incipient. The aim of the present study was to assess the effect of a sleep apnea model on a limited set of specific molecular, biochemical, histological, and behavioral parameters of adipose tissue function. METHODS: Mice were exposed to either intermittent hypoxia or sham hypoxia during 8 h a day for 37 days. Uncoupling protein-1 expression in brown adipose tissue was measured by real-time PCR and immunohistochemistry. Digital quantification of adipose cells and immunohistochemistry of uncoupling protein-1 were performed to determine cell dimensions, positive area, and staining intensity. Serum levels of leptin, adiponectin, and cortisol were measured by ELISA. RESULTS: In comparison with the control group, animals in the hypoxia group had significantly lower chow ingestion, weight gain, and smaller white and brown adipocytes on histological examination. Adiponectin levels were also lower in the hypoxia group. Uncoupling protein-1 mRNA was abolished in the mice exposed to hypoxia; accordingly, fewer cells positive for uncoupling protein-1 and lighter staining intensity were observed in brown adipocytes. CONCLUSIONS: An experimental model of sleep apnea produced changes in uncoupling protein-1 expression and adiponectin levels. These results confirm previous findings on the response of brown adipose tissue to intermittent hypoxia and indicate a yet-unknown interference of intermittent hypoxia on energy control, which may participate in the propensity to weight gain observed in patients with sleep apnea. Brown adipose tissue activity in this patient population needs to be further investigated.

Altered aquaporins in the brains of mice submitted to intermittent hypoxia model of sleep apnea.

Rostral fluid displacement has been proposed as a pathophysiologic mechanism of both central and obstructive sleep apnea. Aquaporins are membrane proteins that regulate water transport across the cell membrane and are involved in brain edema formation and resolution. The present study investigated the effect of intermittent hypoxia (IH), a model of sleep apnea, on brain aquaporins. Mice were exposed to intermittent hypoxia to a nadir of 7% oxygen fraction. Brain water content, Aquaporin-1 and Aquaporin-3 were measured in the cerebellum and hippocampus. Hematoxylin-eosin and immunohistochemistry stainings were performed to evaluate cell damage. Compared to the sham group, the hypoxia group presented higher brain water content, lower levels of Aquaporin-1 and similar levels of Aquaporin-3. Immunoreactivity to GFAP and S100B was stronger in the hypoxia group in areas of extensive gliosis, compatible with cytotoxic edema. These findings, although preliminary, indicate an effect of IH on aquaporins levels. Further investigation about the relevance of these data on the pathophysiology of OSA is warranted.

High risk for sleep apnea in the Berlin questionnaire and coronary artery disease.

INTRODUCTION: Obstructive sleep apnea (OSA) affects up to 30% of the adult population and is a risk factor for coronary artery disease (CAD). The diagnostic process, involving polysomnography, may be complex. Berlin questionnaire (BQ) is a validated and economical screening tool. PURPOSE: The aim of this study was to assess the performance of the BQ for the diagnosis of OSA in individuals with angina complaints. METHODS: Patients undergoing diagnostic cineangiography, portable type III polysomnography to determine the apnea-hypopnea index (AHI), and who answered the BQ were included. We excluded patients older than 65 years that were smokers, diabetics, and morbidly obese. High risk for OSA was based on positive responses in two of three symptom criteria of the BQ. CAD was defined by the presence of >50% lesion in coronary arteries. RESULTS: In 57 included cases, high risk in the BQ indicates significant odds ratio [95% confidence interval] for the presence of CAD (4.5[1.03-19.25], P = 0.045), adjusted for usual confounders: gender, age, and body mass index. The sensitivity and the specificity of BQ for CAD were 70% and 48%, respectively; the positive and negative predictive values are 56% and 64%. CONCLUSIONS: In conclusion, simple questionnaire-based diagnostic tools can be included in the screening procedures of patients with angina to detect the need for further OSA evaluation. In conclusion, the BQ is an effective instrument for this purpose.

Sleep apnea is a stronger predictor for coronary heart disease than traditional risk factors.

BACKGROUND: Sleep apnea (SA) may be linked to coronary artery disease (CAD). Both conditions have similar risk factors, confounding the analyses. Investigation of the lipid profile is routine in the adult population, even without symptoms or suspected cardiac ailment. SA, however, remains underdiagnosed even in the presence of unambiguous clinical manifestations. PURPOSE: The aim of this study was to verify the association between SA and CAD, adjusting for usual CAD risk factors. METHODS: Patients who underwent diagnostic or therapeutic coronariography and portable type III polysomnography were studied. The severity of SA was determined by the apnea-hypopnea index (AHI). We measured classic CAD risk factors: fasting glucose; total, HDL, and LDL cholesterols; triglycerides; uric acid, and high-sensitivity C-reactive protein. We excluded patients older than 65 years, with body mass index higher than 40 kg/m(2), with diabetes, and with history of smoking in the last year. RESULTS: Of 55 included patients, 28 had AHI > 14, showing an odds ratio of 8.7 for CAD. Patients without (n = 29) and with CAD (n = 26), showed AHI of, respectively, 11 ± 11 and 23 ± 14 per hour (P = 0.001). In a binary logistic regression to predict CAD, controlling for all the above risk factors, the only variables entered in the stepwise model were AHI (either as continuous or categorical variable) and uric acid. CONCLUSION: In a sample without smokers, morbidly obese, or diabetic patients, AHI is the main predictor of CAD. SA should integrate the set of risk factors routinely assessed in clinical investigation for coronary disease risk stratification.