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Fatureto-Borges F.,Heart Institute InCor | Lorenzi-Filho G.,Sleep Laboratory | Drager L.F.,Heart Institute InCor | Drager L.F.,University of Sao Paulo
Integrated Blood Pressure Control | Year: 2016

Obstructive sleep apnea (OSA) is an extremely common comorbid condition in patients with hypertension, with a prevalence of ∼50%. There is growing evidence suggesting that OSA is a secondary cause of hypertension, associated with both poor blood pressure (BP) control and target organ damage in patients with hypertension. The application of continuous positive airway pressure (CPAP) during sleep is the gold standard treatment of moderate-to-severe OSA and very effective in abolishing obstructive respiratory events. However, several meta-analyses showed that the overall impact of CPAP on BP is modest (∼2 mmHg). There are several potential reasons for this disappointing finding, including the heterogeneity of patients studied (normotensive patients, controlled, and uncontrolled patients with hypertension), nonideal CPAP compliance, clinical presentation (there is some evidence that the positive impact of CPAP on lowering BP is more evident in sleepy patients), and the multifactorial nature of hypertension. In this review, we performed a critical analysis of the literature evaluating the impact of CPAP on BP in several subgroups of patients. We finally discussed perspectives in this important research area, including the urgent need to identify predictors of BP response to CPAP and the importance of precision medicine in this scenario. © 2016 Fatureto-Borges et al.


Panossian L.A.,Sleep Laboratory | Avidan A.Y.,University of California at Los Angeles
Neurologic Clinics | Year: 2016

Sleep disorders are common in neurology practice, but are often undiagnosed and untreated. Specific patient cohorts, such as older adults, patients residing in nursing homes, and patients with underlying chronic neurologic and psychiatric disorders, are at particular risk. If these sleep problems are not properly evaluated and managed the patient may experience exacerbation of the underlying neurologic disorder. This article highlights some of the key sleep disorders relevant to practicing neurologists, emphasizing hypersomnolence, insomnia, and sleep-related movement disorders in the setting of neurologic disorders to enhance the tools available for evaluation, and discusses management strategies. © 2016 Elsevier Inc.


Geovanini G.R.,Sleep Laboratory | Gowdak L.H.W.,Refractory Angina Research Group | Pereira A.C.,Refractory Angina Research Group | De Jesus Danzi-Soares N.,Sleep Laboratory | And 7 more authors.
Chest | Year: 2014

OBJECTIVE: 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. METHODS: 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. R ESULTS: Patients with refractory angina (n 5 70) compared with patients with stable CAD (n 5 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/m 2 , 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 5 .001), higher proportion of oxygen saturation , 90% 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. C ONCLUSIONS: OSA and depression are independently associated with refractory angina and may contribute to poor cardiovascular outcome. © 2014 AMERICAN COLLEGE OF CHEST PHYSICIANS.


Tamisier R.,Sleep Laboratory | Tamisier R.,Joseph Fourier University | Pepin J.L.,Sleep Laboratory | Pepin J.L.,Joseph Fourier University | And 6 more authors.
European Respiratory Journal | Year: 2011

Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms. We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean±SD MSNA increased across the exposure (17.2±5.1 versus 21.7±7.3 bursts?min-1; p<0.01) and baroreflex control of sympathetic outflow declined from -965.3±375.1 to -598.4±162.6 AIU·min-1·mmHg-1 (p<0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS. Copyright©ERS 2011.


Domenico Pinna G.,Fondazione S. Maugeri IRCCS | Robbi E.,Sleep Laboratory | Pizza F.,University of Bologna | Pizza F.,CNR Institute of Neurological Sciences | And 3 more authors.
Journal of Sleep Research | Year: 2014

Fluctuations in sleep-wake state are thought to contribute to the respiratory instability of Cheyne-Stokes respiration in patients with heart failure by promoting the rhythmic occurrence of central apnea and ventilatory overshoot. There are no data, however, on the relationship between vigilance state and respiratory events. In this study we used a novel method to detect the occurrence of state transitions (time resolution: 0.25 s, minimum duration of state changes: 2 s) and to assess their time relationship with apnoeic events. We also evaluated whether end-apnoeic arousals are associated with a ventilatory overshoot. A polysomnographic, daytime laboratory recording (25 min) was performed during Cheyne-Stokes respiration in 16 patients with heart failure. Automatic state classification included wakefulness and non-rapid eye movement sleep stages 1-2. As a rule, wakefulness occurred during hyperpnoeic phases, and non-rapid eye movement sleep occurred during apnoeic events. Ninety-two percent of the observed central apneas (N = 272) were associated with a concurrent wakefulness → non-rapid eye movement sleep → wakefulness transition. The delay between wakefulness → non-rapid eye movement sleep transitions and apnea onset was -0.3 [-3.1, 3.0] s [median (lower quartile, upper quartile); P = 0.99 testing the null hypothesis: median delay = 0], and the delay between non-rapid eye movement sleep → wakefulness transitions and apnea termination was 0.2 [-0.5, 1.2] s (P = 0.7). A positive/negative delay indicates that the state transition occurred before/after the onset or termination of apnea. Non-rapid eye movement sleep → wakefulness transitions synchronous with apnea termination were associated with a threefold increase in tidal volume and a twofold increase in ventilation (all P < 0.001), indicating ventilatory overshoot. These findings highlight that wakefulness → non-rapid eye movement sleep→wakefulness transitions parallel apnoeic events during Cheyne-Stokes respiration in patients with heart failure. The relationships between state changes and respiratory events are consistent with the notion that state fluctuations promote ventilatory instability. © 2014 European Sleep Research Society.


Dick R.,Jena University of Applied Sciences | Penzel T.,Charité - Medical University of Berlin | Fietze I.,Charité - Medical University of Berlin | Partinen M.,University of Helsinki | And 2 more authors.
Physiological Measurement | Year: 2010

In recent AASM practice, parameter actimetry is cited to measure total sleep time in obstructive sleep apnoea patients, when polysomnography is not available. An actigraph was therefore compared to polysomnographic data in 28 subjects with known sleep disordered breathing. Total sleep time (TST), sleep period time (SPT), sleep efficiency (SE), sustained sleep efficiency (SSE), sleep onset latency (SL) and sleep/wake pattern were compared to gold standard polysomnography. The results of an epoch-by-epoch comparison of sleep/wake from actigraphy to sleep stages from polysomnography gave a sensitivity of 90.2%, a specificity of 95.2% and an overall accuracy of 85.9%. Correlations were moderately strong for SE (0.71, p < 0.001) and SSE (0.65, p < 0.001) and high for TST (0.89, p < 0.001), SPT (0.91, p < 0.001) and SL (0.89, p < 0.001). It was concluded that actigraphy is not identical with PSG recording but gives good results in sleep/wake patterns and predicting TST, SPT, SSE, SE and SL also in sleep apnoea patients not suffering from other sleep disorders. The difficult detection of correct sleep onset causes SSE and SL to be less predictable. Therefore a 15-epoch criterion was introduced and resulted in high correlation of 0.89 for sleep latency, but has to be tested on a bigger population. © 2010 Institute of Physics and Engineering in Medicine.


Pinna G.D.,Fondazione S. Maugeri IRCCS | Robbi E.,Sleep Laboratory | La Rovere M.T.,Fondazione S. Maugeri IRCCS | Taurino A.E.,Sleep Laboratory | And 3 more authors.
European Journal of Heart Failure | Year: 2015

Aims Obstructive (OSA) and central sleep apnoea (CSA) are a common comorbidity in patients with heart failure. The purpose of this study was to assess and compare the impact of body position on the severity of sleep apnoea in these two groups of patients. Methods and results Standard polysomnography was performed in consecutive, clinically stable, optimally treated patients with moderate-to-severe heart failure and systolic dysfunction. Patients with an apnoea-hypopnoea index (AHI) ≥15/h (n = 120) were included in the study. The severity of sleep-disordered breathing was quantified by the AHI, the mean value of oxygen desaturations (O2desat) and the apnoea ratio. Data from the right and left positions were combined into a single lateral position. Positional sleep apnoea was defined as a >50% reduction in the AHI between the supine and the lateral position. Twenty-nine and 91 subjects had dominant OSA and CSA, respectively. The AHI markedly decreased from the supine to the lateral position in both groups [OSA: (median [q1,q3]) 50.3 [36.9, 67.6]/h vs. 10.4 [7.0, 18.5]/h, P < 0.0001; CSA: 47.4 [37.6, 56.0]/h vs. 19.3 [11.9, 33.3]/h]. The reduction was greater in OSA patients (p = 0.027). Similarly, O2desat and the apnoea ratio decreased in the lateral position (P < 0.0001). Positional sleep apnoea was observed in 76% of OSA and 53% of CSA patients (P = 0.028). Conclusion This study demonstrates that the lateral sleeping position has a major beneficial effect on the severity of sleep-disordered breathing in heart failure patients, and that this improvement is greater in subjects with OSA than in those with CSA. © 2015 The Authors European Journal of Heart Failure.


Nena E.,Sleep Laboratory | Nena E.,Laboratory of Hygiene and Environmental Protection | Papanas N.,Democritus University of Thrace | Steiropoulos P.,Sleep Laboratory | And 7 more authors.
Platelets | Year: 2012

Aim of the study: To evaluate Mean Platelet Volume (MPV) and Platelet Distribution Width (PDW) in non-diabetic subjects, according to obstructive sleep apnoea syndrome (OSAS) severity and the associations of these indices with anthropometric characteristics and parameters of breathing function during sleep. Materials and methods: We included 610 non-diabetic subjects with suspected OSAS, evaluated by polysomnography. According to their apnoea-hypopnoea index (AHI), patients were divided into Group A (n148) with AHI<5/h; Group B (n121) with AHI: 514.9/h; Group C (n85) with AHI: 1529.9/h and Group D (n256) with AHI≥30/h. MPV and PDW were measured using an automated blood cell counter. Results: MPV was significantly higher in group D (mean value 12.1±1.3 fl) than in groups A (9.8±1.1 fl), B (9.8±1.6 fl), and C (11.5±1.3 fl) (p<0.001). The same pattern was observed in PDW values (15.9±2.2 fl for group D and 13.2±2.2 fl for group A, 14.1±2.8 fl for group B, and 15±2.2 fl for group C, p<0.001). Significant correlations were seen between MPV and AHI (p<0.001), average pulse oxygen saturation (SpO2) (p<0.001), minimum SpO2 (p<0.001) and percent of the total sleep time with SpO2 lower than 90 (t<90) (p<0.001) during sleep, Arousal Index (p<0.001) and Epworth sleepiness scale (ESS) (p=0.028). Similarly, PDW was correlated with AHI (p<0.001), average SpO2 (p=0.001), minimum SpO2 (p<0.001), t<90 (p=0.002), and Arousal Index (p<0.001). Conclusions: MPV and PDW are higher in non-diabetic patients with severe OSAS and are correlated with different parameters of breathing function during sleep. © 2012 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.


Rogev E.,Sleep Laboratory | Pillar G.,Sleep Laboratory | Pillar G.,Technion - Israel Institute of Technology
Israel Medical Association Journal | Year: 2013

Background: Insomnia is the most common sleep disorder. Treatment options are improved sleep hygiene, relaxation, cognitive behavioral therapy, and medications. Studies examining the effect of hypnotics on insomnia reported that placebo had a substantial beneficial effect. Objectives: To evaluate whether placebo is an effective treatment for insomnia. Methods: We assessed 25 patients with insomnia who were enrolled in a hypnotic study but prior to the study were asked to undergo two full nights in laboratory polysomnography studies: with and without a placebo. Although they were not explicitly told that they were receiving a placebo, the participants knew that the results of these studies would determine whether they met the criteria to participate in the pharmaceutical study. Results: Although the participants acknowledged that they were given a placebo, almost all measures of their sleep improved. With placebo, sleep latency was shortened from 55.8 ± 43.5 to 39.8 ± 58.5 minutes (P < 0.05); total sleep time was extended from 283 ± 72.5 to 362.9 ± 56.3 minutes, and sleep efficiency improved from 59.57 ± 14.78 to 75.5 ± 11.70% (P < 0.05). Interestingly, placebo had no effect on the relative sleep stage distribution (percentage of total sleep time), except for a trend toward increased percentage of REM sleep. Conclusions: Our findings show a clear and significant beneficial effect of placebo on insomnia, despite participants' understanding that they were receiving placebo. These results emphasize the importance of the patients' perception and belief in insomnia treatment, and suggest that in some cases placebo may serve as a treatment.


Billiard M.,Gui Of Chauliac Hospital | Podesta C.,Sleep Laboratory
Sleep Medicine | Year: 2013

Background: Recurrent hypersomnia (RH) following a traumatic brain injury (TBI) is a rare form of RH. According to the International Classification of Sleep Disorders, 2nd edition (ICSD-2), RH must be considered in the differential diagnosis as secondary to an organic insult of the central nervous system and not as the clinical subtype of RH, Kleine-Levin syndrome (KLS). The aim of our study was to investigate if cases of RH following TBI should be considered in the differential diagnosis of RH as indicated by the International Classification of Sleep Disorders, 2nd edition or as genuine, or indicated by ICSD-2, RH must cases of KLS. Methods: Twelve cases of RH developed after TBI were collected and analyzed for circumstance at onset, severity of TBI, delay between TBI and occurrence of first episode of RH, symptoms of RH, duration and cycle length of episodes of hypersomnia, physical signs, and brain morphological imaging at the time of hypersomnia episodes. Results: Factors such as the delay between TBI and the first episode of RH, the presence of other triggering factors and potential genetic factors, the degree of the severity of TBI, the presence or absence of any consistent brain imaging abnormality, provided the following results: (1) two of the cases could be considered as symptomatic of the underlying pathological brain process, (2) eight of the cases could be considered as simply triggered by TBI in patients at risk for KLS, and (3) two cases could be considered neither symptomatic nor triggered by TBI, due to the long delay between TBI and occurrence of symptoms. Conclusion: Cases of RH following TBI do not present under a single mechanism. Clinical assessment and laboratory tests are necessary to correctly classify them. © 2013.

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