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Whole blood carbonic anhydrase activity (CAa) is increased in patients with obstructive sleep apnea (OSA). Our study investigated the influence of positive airway pressure (PAP) or CA inhibitor acetazolamide (ACT) therapy on CAa, OSA and blood pressure. Thirty-three OSA patients (21 hypertensive, body mass index (BMI) 37 ± 7 kg/m 2 and apnea-hypopnea index (AHI) of 47 ± 31 events/hr) were followed-up after PAP treatment (compliance, 4.7 ± 1.5 hr/day; duration, median 6 [IQR 6,6] months) (Cohort A). A second OSA Cohort (B) contained nine hypertensive patients (BMI, 29 ± 4 kg/m 2 ; AHI, 39 ± 20 events/hr) with 2-week treatment of ACT, PAP or ACT + PAP in an open crossover study. CAa was assessed at baseline and at the end of each treatment period. In Cohort A, baseline CAa was higher in hypertensive, compared with normotensive, patients (1,033 ± 204 versus 861 ± 201 units, p = .028). PAP treatment reduced systolic/diastolic blood pressure but not CAa (-9 ± 11/-5 ± 7 mmHg and -20 ± 289 units, p < .001, <.001 and .70). In Cohort B, blood pressure was reduced in both ACT-treated groups (-10 ± 10/-5 ± 7 mmHg, p = .043 and .019; and -5 ± 5/-13 ± 13 mmHg, p < .001 and .009). AHI was reduced in both groups: ACT only, -17 ± 9 events/hr p = .001; and ACT + PAP, -39 ± 19 events/hr, p < .001. PAP did not change CAa (p = .98) but activity tended to decrease after ACT with or without PAP (p = .081 and .056). CAa is elevated in hypertensive OSA patients. Long-term PAP reduced blood pressure without affecting CAa. ACT reduced blood pressure and CAa. Increased CAa may constitute a physiological characteristic in OSA, contributing to comorbid hypertension., (© 2019 European Sleep Research Society.)

Sleep bruxism bears several similarities to restless legs syndrome, and a link to changes in central dopamine activity has been considered in both conditions. The dopamine agonist pramipexole is currently indicated for the symptomatic treatment of restless legs. The effect of pramipexole on sleep bruxism was investigated in subjects with 'probable bruxism' recruited at the Orofacial Pain Clinic. Thirteen patients underwent polysomnographic recordings, including bilateral masseter electromyographic activity. Following habituation to the recording equipment, a baseline registration was used to confirm bruxism [total episodes per hour, mean 11.3 (6.3)]. Following randomisation, subjects received no treatment or pramipexole titrated from 0.09 to 0.54 mg, o.d., for 3 weeks according to a crossover procedure. A polysomnographic-electromyographic registration was performed at the end of each period. Pramipexole was associated with more frequent awakenings and a reduction in rapid eye movement sleep (both P ≤ 0.02). Sleep apnea decreased marginally after pramipexole (apnea-hypopnea index 17.1 compared with control 21.5, P ≤ 0.05). The number of bruxism episodes, phasic, tonic and mixed per hour, remained unchanged after pramipexole [total episodes per hour 12.7 (8.5) and 9.8 (5.2) during pramipexole and control conditions, respectively]. It is concluded, from this pilot study, that sleep bruxism is not affected by the dopaminergic agent, pramipexole., (© 2016 European Sleep Research Society.)

Study Objectives: One of the most important caveats of ambulatory devices is the inability to record and stage sleep. We assessed an algorithm determining 4 different stages: wake, light sleep, deep sleep, and REM sleep using signals derived from the portable monitor Watch-PAT100 (PAT recorder)., Methods: Participants (38 normal subjects and 189 patients with obstructive sleep apnea [OSA]) underwent simultaneous overnight recordings with polysomnography (PSG) and the PAT recorder in a study originally designed to assess the accuracy of the PAT recorder in diagnosing OSA. Light/deep sleep and REM sleep from the PAT recorder recording were automatically scored based on features extracted from time series of peripheral arterial tone amplitudes and inter pulse periods. The PSG scored sleep stages 1 and 2 were classified as light sleep for epoch-by-epoch comparisons., Results: The overall agreement in detecting light/deep and REM sleep were 88.6% ± 5.9% and 88.7% ± 5.5%, respectively. There was a good agreement between PSG and the PAT recorder in quantifying sleep efficiency (78.4% ± 9.9% vs. 78.8% ± 13.4%), REM latency (237 ± 148 vs. 225 ± 159 epochs), and REM percentage (14.4% ± 6.5% vs. 19.3% ± 8.7%). OSA severity did not affect the sensitivity and specificity of the algorithm. The Cohen κ coefficient for detecting all sleep stages: sleep from wake, REM from NREM sleep, and deep from light sleep were 0.48, 0.55, 0.59, and 0.46, respectively., Conclusions: Analysis of autonomic signals from the PAT recorder can detect sleep stages with moderate agreement to more standard techniques in normal subjects and OSA patients. This novel algorithm may provide insights on sleep and sleep architecture when applying the PAT recorder for OSA diagnosis.

Subject Objective: To assess the accuracy of a portable monitoring device based on peripheral arterial tonometry to diagnose obstructive sleep apnea (OSA). To propose a new standard for limited-channel device validation using synchronized polysomnography (PSG) home recordings and a population-based cohort., Design: Single-night, unattended PSG and Watch&#95;PAT 100 (WP&#95;100)., Setting: Home environment., Participants: Ninety-eight subjects (55 men; age, 60 +/- 7 year; body mass index, 28 +/- 4 kg/m2) consecutively recruited from the Skaraborg Hypertension and Diabetes Project., Measurements and Results: The WP&#95;100 records peripheral arterial tone, heart rate, oxygen saturation and actigraphy for automatic analysis of respiratory disturbance index (RDI), apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and sleep-wake state. The accuracy of WP&#95;100 in RDI, AHI, ODI, and sleep-wake detection was assessed by comparison with data from simultaneous PSG recordings. The mean PSG-AHI in this population was 25.5 +/- 22.9 events per hour. The WP&#95;100 RDI, AHI, and ODI correlated closely (0.88, 0.90, and 0.92; p < .0001, respectively) with the corresponding indexes obtained by PSG. The areas under the curve for the receiver-operator characteristic curves for WP&#95;100 AHI and RDI were 0.93 and 0.90 for the PSG-AHI and RDI thresholds 10 and 20 (p < .0001, respectively). The agreement of the sleep-wake assessment based on 30-second bins between the 2 systems was 82 +/- 7%., Conclusions: The WP&#95;100 was reasonably accurate for unattended home diagnosis of OSA in a population sample not preselected for OSA symptoms. The current design, including simultaneous home PSG recordings in population-based cohorts, is proposed as a reasonable validation standard for assessment of simplified recording tools for OSA diagnosis.

Emerging data suggest that determination of physiologic endotypic traits (eg, loop gain) may enable precision medicine in OSA. Does a single-night assessment of polysomnography-derived endotypic traits provide reliable estimates in moderate to severe OSA? Two consecutive in-lab polysomnography tests from a clinical trial (n = 67; male, 69%; mean ± SD age, 61 ± 10 years; apnea-hypopnea index [AHI] 53 ± 22 events/h) were used for the reliability analysis. Endotypic traits, reflecting upper airway collapsibility (ventilation at eupneic drive [V passive ]), upper airway dilator muscle tone (ventilation at the arousal threshold [V active ]), loop gain (stability of ventilatory control, LG1), and arousal threshold (ArTh) were determined. Reliability was expressed as an intraclass correlation coefficient (ICC). Minimal detectable differences (MDDs) were computed to provide an estimate of maximum spontaneous variability. Further assessment across four repeated polysomnography tests was performed in a subcohort (n = 22). Reliability of endotypic traits between the two consecutive nights was moderate to good (ICC: V passive = 0.82, V active = 0.76, LG1 = 0.72, ArTh = 0.83). Variability in AHI, but not in body position or in sleep stages, was associated with fluctuations in V passive and V active (r = –0.49 and r = –0.41, respectively; P <.001 for both). MDDs for single-night assessments were: V passive = 22, V active = 34, LG1 = 0.17, and ArTh = 21. Multiple assessments (mean of two nights, n = 22) further reduced MDDs by approximately 20% to 30%. Endotypic trait analysis using a single standard polysomnography shows acceptable reliability and reproducibility in patients with moderate to severe OSA. The reported MDDs of endotypic traits may facilitate the quantification of relevant changes and may guide future evaluation of interventions in OSA. [ABSTRACT FROM AUTHOR]

Background and objective: OSA and PLMS are known to induce acute BP swings during sleep. Our current study aimed to address the independent effect of PLMS on BP in an unselected OSA patient cohort. Methods: This cross‐sectional analysis included 1487 patients (1110 males, no previous hypertension diagnosis or treatment, mean age: 52.5 years, mean BMI: 30.5 kg/m2) with significant OSA (defined as AHI ≥ 10) recruited from the European Sleep Apnoea Cohort. Patients underwent overnight PSG. Patients were stratified into two groups: patients with significant PLMS (PLMSI > 25 events/hour of sleep) and patients without significant PLMS (PLMSI < 25 events/hour of sleep). SBP, DBP and PP were the variables of interest. For each of these, a multivariate regression linear model was fitted to evaluate the relationship between PLMS and outcome adjusting for sociodemographic and clinical covariates (gender, age, BMI, AHI, ESS, diabetes, smoking and sleep efficiency). Results: The univariate analysis of SBP showed an increment of BP equal to 4.70 mm Hg (P < 0.001) in patients with significant PLMS compared to patients without significant PLMS. This increment remained significant after implementing a multivariate regression model (2.64 mm Hg, P = 0.044). No significant increment of BP was observed for DBP and PP. Conclusion: PLMS is associated with a rise in SBP regardless of AHI, independent of clinical and sociodemographic confounders. A PLMS phenotype may carry an increased risk for cardiovascular disease in OSA patients. The link between PLMS and cardiovascular alterations is still debated. Our current study aimed to address the effects of PLMS on BP in a large unselected OSA patient cohort, showing that the PLMS phenotype is associated with significantly elevated clinical SBP independent of confounders. See relatedEditorial [ABSTRACT FROM AUTHOR]

Background: Obstructive sleep apnea is characterized by intermittent hypoxia and hypercapnia. CO2 production, transport and elimination are influenced by the carbonic anhydrase enzyme. We hypothesized that elevated standard bicarbonate, a proxy for increased carbonic anhydrase activity, is associated with apnea severity and higher blood pressure in patients with obstructive sleep apnea.Methods: A retrospective analysis of a sleep apnea cohort (n = 830) studied by ambulatory polygraphy. Office systolic/diastolic blood pressure, lung function, and arterial blood gases were assessed during daytime.Results: Arterial standard bicarbonate was increased with apnea severity (mild/moderate/severe 24.1 ± 1.8, 24.4 ± 1.7 and 24.9 ± 2.9 mmol/l, respectively, Kruskal-Wallis test p < 0.001). Standard bicarbonate was independently associated with apnea hypopnea index after adjustment for sex, age, body mass index, smoking, alcohol, hypertension, pO2 and pCO2 (standard bicarbonate quartile 1 vs. quartile 4, β = 10.6, p < 0.001). Log-transformed standard bicarbonate was associated with a diagnosis of hypertension or diastolic blood pressure but not systolic blood pressure adjusting for cofounders (p = 0.007, 0.048 and 0.45, respectively).Conclusions: There was an independent association between sleep apnea severity and arterial standard bicarbonate. The link between high standard bicarbonate and daytime hypertension suggests that carbonic anhydrase activity may constitute a novel mechanism for blood pressure regulation in sleep apnea. [ABSTRACT FROM AUTHOR]

The cross-sectional relationship of obstructive sleep apnea with moderate to severe chronic kidney disease, defined as an estimated glomerular filtration rate <60 mL min−1∙1.73 m−2, was investigated in a large cohort of patients with suspected obstructive sleep apnea studied by nocturnal polysomnography or cardiorespiratory polygraphy. Data were obtained from the European Sleep Apnea Database, where information from unselected adult patients with suspected obstructive sleep apnea afferent to 26 European sleep centres had been prospectively collected. Both the Modification of Diet in Renal Disease and the Chronic Kidney Disease-Epidemiology Collaboration equations were used for the assessment of estimated glomerular filtration rate. The analysed sample included 7700 subjects, 71% male, aged 51.9 ± 12.5 years. Severe obstructive sleep apnea (apnea-hypopnea index ≥30) was found in 34% of subjects. The lowest nocturnal oxygen saturation was 81 ± 10.2%. Chronic kidney disease prevalence in the whole sample was 8.7% or 6.1%, according to the Modification of Diet in Renal Disease or the Chronic Kidney Disease-Epidemiology Collaboration equations, respectively. Subjects with lower estimated glomerular filtration rate were older, more obese, more often female, had worse obstructive sleep apnea and more co-morbidities ( P < 0.001, each). With both equations, independent predictors of estimated glomerular filtration rate <60 were: chronic heart failure; female gender; systemic hypertension; older age; higher body mass index; and worse lowest nocturnal oxygen saturation. It was concluded that in obstructive sleep apnea, chronic kidney disease is largely predicted by co-morbidities and anthropometric characteristics. In addition, severe nocturnal hypoxaemia, even for only a small part of the night, may play an important role as a risk factor for kidney dysfunction. [ABSTRACT FROM AUTHOR]

Background: Clinical presentation phenotypes of obstructive sleep apnoea (OSA) and their association with comorbidity as well as impact on adherence to continuous positive airway pressure (CPAP) treatment have not been established. Methods: A prospective follow-up cohort of adult patients with OSA (apnoea-hypopnoea index (AHI) of ≥5/h) from 17 European countries and Israel (n = 6,555) was divided into four clinical presentation phenotypes based on daytime symptoms labelled as excessive daytime sleepiness (“EDS”) and nocturnal sleep problems other than OSA (labelled as “insomnia”): 1) EDS (daytime+/nighttime-), 2) EDS/insomnia (daytime+/nighttime+), 3) non-EDS/non-insomnia (daytime-/nighttime-), 4) and insomnia (daytime-/nighttime+) phenotype. Results: The EDS phenotype comprised 20.7%, the non-EDS/non-insomnia type 25.8%, the EDS/insomnia type 23.7%, and the insomnia phenotype 29.8% of the entire cohort. Thus, clinical presentation phenotypes with insomnia symptoms were dominant with 53.5%, but only 5.6% had physician diagnosed insomnia. Cardiovascular comorbidity was less prevalent in the EDS and most common in the insomnia phenotype (48.9% vs. 56.8%, p<0.001) despite more severe OSA in the EDS group (AHI 35.0±25.5/h vs. 27.9±22.5/h, p<0.001, respectively). Psychiatric comorbidity was associated with insomnia like OSA phenotypes independent of age, gender and body mass index (HR 1.5 (1.188–1.905), p<0.001). The EDS phenotype tended to associate with higher CPAP usage (22.7 min/d, p = 0.069) when controlled for age, gender, BMI and sleep apnoea severity. Conclusions: Phenotypes with insomnia symptoms comprised more than half of OSA patients and were more frequently linked with comorbidity than those with EDS, despite less severe OSA. CPAP usage was slightly higher in phenotypes with EDS. [ABSTRACT FROM AUTHOR]

Polygraphy ( PG) and polysomnography ( PSG) are used in clinical settings in Europe for diagnosing obstructive sleep apnea ( OSA), but their equivalence in unselected clinical cohorts is unknown. We hypothesized that the method would affect both diagnostic outcomes and disease severity stratification. Data from 11 049 patients in the multi-centre European Sleep Apnea Cohort ( ESADA) with suspected OSA (male and female, aged 18-80 years) were used in two groups of patients to compare PG ( n = 5745) and PSG ( n = 5304). Respiratory events were scored using the 2007 American Association of Sleep Medicine ( AASM) criteria. In subjects who underwent PSG, mean apnea-hypopnea index ( AHI) using sleep time ( AHIPSG 31.0 ± 26.1 h−1) and total analysed time ( TAT) ( AHITAT 24.7 ± 22.0 h−1) were higher than in subjects who underwent PG ( AHIPG 22.0 ± 23.5 h−1) ( P < 0.0001). The oxygen desaturation index ( ODI) was lower in subjects investigated with PG ( ODIPG 18.4 ± 21.7 h−1) compared to subjects investigated with PSG ( ODIPSG 23.0 ± 25.3 h−1) but not different when the PSG was indexed by TAT ( ODITAT 18.6 ± 21.4 h−1, P < 0.65). The proportion of patients with an AHI ≥ 15 was 64% in the subjects who underwent PSG and 47% in the subjects who underwent PG ( P < 0.001). Overall, patients investigated using PG are likely to have a 30% lower AHI on average, compared to patients investigated by PSG. This study suggests that PG interpreted using standard guidelines results in underdiagnosis and misclassification of OSA. We advocate the development of PG-specific guidelines for the management of OSA patients. [ABSTRACT FROM AUTHOR]

Summary Obstructive sleep apnea diagnosis is based on the manual scoring of respiratory events. The agreement in the manual scoring of the respiratory events lacks an in‐depth investigation as most of the previous studies reported only the apnea–hypopnea index or overall agreement, and not temporal, second‐by‐second or event subtype agreement. We hypothesized the temporal and subtype agreement to be low because the event duration or subtypes are not generally considered in current clinical practice. The data comprised 50 polysomnography recordings scored by 10 experts. The respiratory event agreement between the scorers was calculated using kappa statistics in a second‐by‐second manner. Obstructive sleep apnea severity categories (no obstructive sleep apnea/mild/moderate/severe) were compared between scorers. The Fleiss' kappa value for binary (event/no event) respiratory event scorings was 0.32. When calculated separately within N1, N2, N3 and R, the Fleiss' kappa values were 0.12, 0.23, 0.22 and 0.23, respectively. Binary analysis conducted separately for the event subtypes showed the highest Fleiss' kappa for hypopneas to be 0.26. In 34% of the participants, the obstructive sleep apnea severity category was the same regardless of the scorer, whereas in the rest of the participants the category changed depending on the scorer. Our findings indicate that the agreement of manual scoring of respiratory events depends on the event type and sleep stage. The manual scoring has discrepancies, and these differences affect the obstructive sleep apnea diagnosis. This is an alarming finding, as ultimately these differences in the scorings affect treatment decisions. [ABSTRACT FROM AUTHOR]

Background and Objective: Obstructive sleep apnoea (OSA) and hyperlipidaemia are independent risk factors for cardiovascular disease. This study investigates the association between OSA and prevalence of hyperlipidaemia in patients of the European Sleep Apnea Database (ESADA) cohort.Methods: The cross-sectional analysis included 11 892 patients (age 51.9 ± 12.5 years, 70% male, body mass index (BMI) 31.3 ± 6.6 kg/m2 , mean oxygen desaturation index (ODI) 23.7 ± 25.5 events/h) investigated for OSA. The independent odds ratio (OR) for hyperlipidaemia in relation to measures of OSA (ODI, apnoea-hypopnoea index, mean and lowest oxygen saturation) was determined by means of general linear model analysis with adjustment for important confounders such as age, BMI, comorbidities and study site.Results: Hyperlipidaemia prevalence increased from 15.1% in subjects without OSA to 26.1% in those with severe OSA, P < 0.001. Corresponding numbers in patients with diabetes were 8.5% and 41.5%, P < 0.001. Compared with ODI quartile I, patients in ODI quartiles II-IV had an adjusted OR (95% CI) of 1.33 (1.15-1.55), 1.37 (1.17-1.61) and 1.33 (1.12-1.58) (P < 0.001), respectively, for hyperlipidaemia. Obesity was defined as a significant risk factor for hyperlipidaemia. Subgroups of OSA patients with cardio-metabolic comorbidities demonstrated higher prevalence of HL. In addition, differences in hyperlipidaemia prevalence were reported in European geographical regions with the highest prevalence in Central Europe.Conclusion: Obstructive sleep apnoea, in particular intermittent hypoxia, was independently associated with the prevalence of hyperlipidaemia diagnosis. [ABSTRACT FROM AUTHOR]

Summary In‐laboratory polysomnography, the gold‐standard for diagnosing sleep disorders, is resource‐demanding and not conducive to multiple night evaluations. Ambulatory polysomnography, especially when self‐applied, could be a viable alternative. This study aimed to assess the feasibility and reliability of self‐applied polysomnography over three consecutive nights in untrained participants, assessing: technical success rate; comparing sleep diagnostic variables from single and multiple nights; and evaluating participants' subjective experience. Data were collected from 78 participants (55.1% females) invited to test a self‐applicable polysomnography device for three consecutive nights at home. The technical success rate for valid sleep recordings was 82.5% out of 234 planned study nights, with 87.2% of participants obtaining at least two valid nights. Misclassification of obstructive sleep apnea severity was higher in participants with mild OSA (21.4%) compared with those with moderate‐to‐severe obstructive sleep apnea or no obstructive sleep apnea. Sleep efficiency and wake after sleep onset showed improvement from Night 1 to Night 3 (p < 0.001), and the mean polysomnography set‐up time decreased significantly over this period. Participants reported moderate‐to‐high satisfaction with the device (System Usability Scale score 71.2 ± 12.4). The findings suggest that self‐applied polysomnography is a feasible diagnostic method for untrained individuals at risk for sleep disorders, and that multiple night assessments can improve diagnostic precision for mild obstructive sleep apnea cases. [ABSTRACT FROM AUTHOR]

Background and Objectives: The orally active dual OX1R and OX2R antagonist, almorexant, targets the orexin system for the treatment of primary insomnia. This clinical trial assessed the effect of almorexant on sleep maintenance and other sleep endpoints, and its safety and tolerability in adults.Patients and Methods: Prospective, randomized, double-blind, placebo-controlled, active referenced trial in male and female adults aged 18-64 years with chronic, primary insomnia. Patients were randomized 1:1:1:1 to receive placebo, almorexant 100 mg, almorexant 200 mg, or zolpidem 10 mg (active reference) for 16 days. Primary efficacy assessments were objective (polysomnography-measured) and subjective (patient-recorded) wake time after sleep onset (WASO). Further sleep variables were also evaluated.Results: From 709 randomized patients, 707 (mean age 45.4 years; 61.7% female) received treatment and 663 (93.8%) completed the study. A significant decrease versus placebo in median objective WASO was observed with almorexant 200 mg at the start and end of randomized treatment (-26.8 min and -19.5 min, respectively; both p < 0.0001); subjective WASO also decreased over the two-week treatment period (p = 0.0006). Objective and subjective total sleep time (TST) were increased with almorexant 200 mg (p < 0.0001). Almorexant 200 mg significantly reduced objective and subjective latency to persistent sleep and latency to sleep onset at initiation of therapy, and provided longer duration of sleep stages with no suppression of slow-wave sleep. No impaired next-day performance, rebound insomnia, or withdrawal effects were observed. Adverse events were similar with almorexant and placebo.Conclusion: Almorexant reduced time to sleep onset and maintained sleep without residual effects on next-day performance or safety concerns. This study provides further support for the role of the endogenous orexin system in insomnia disorder. CLINICALTRIALS.Gov Registration: NCT00608985. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Pulse wave attenuation, which occurs in association with obstructive sleep apnea (OSA), is sympathetically mediated. We compared the effect of Doxazosin (DO, a peripheral α-receptor inhibitor) and Enalapril (EN, an ACE inhibitor) on digital vasoconstriction and nocturnal blood pressure (BP) in hypertensive OSA patients. Methods: A double-blind, crossover study comparing equipotent dosages of DO (4mg/day for 2weeks with 8mg/day for an additional 2weeks) and EN (10mg/day and 20mg/day, respectively) was undertaken in 16 male OSA patients (age 55±7years, body mass index 30.1±3.8kg/m2) with hypertension. Assessments including ambulatory 24-h BP, full-night polysomnography with simultaneous peripheral arterial tone (PAT) and beat-to-beat finger BP monitoring (Finapres) were made at the end of each treatment period. Nighttime BP and digital vasoconstrictions associated with apneic events (measured as the ratio of PAT amplitudes during and after apneas) were analyzed. Results: There were no differences between the two treatments in the 24-h BP profile and OSA severity. But the nighttime average beat-to-beat finger BP was significantly higher under DO treatment (systolic BP 129±13 vs. 119±23mm Hg, P =0.02; diastolic BP 81±12 vs. 74±14mm Hg, P =0.04, DO and EN respectively). In a linear mixed effects regression model, the PAT ratio during apnea increased 5.3% under DO compared with EN (P <0.0001). Each percentage decrease of apneic related oxygen desaturation was associated with 0.9% decrease in the PAT ratio (P <0.0001). REM sleep was associated with 2.2% decrease of PAT ratio compared to NREM sleep (P =0.002). Conclusion: Digital vasoconstrictions associated with apneic events are α-receptor mediated. DO compared to EN has a proportionally poor effect on nocturnal BP control in OSA patients, which may be due to the enhanced sympathetic nervous system activity characteristic of this condition. [Copyright &y& Elsevier]

Abstract: Objective and Background: Pulse wave amplitude (PWA) derived from the digital vascular bed has been used in sleep studies. The nocturnal attenuation of PWA has been shown to reflect sympathetic activation during sleep. We assessed the relationship between nocturnal PWA attenuation and office blood pressure (BP). Methods: Eighty-one subjects (46 men; age 60±7 years; body mass index [BMI] 28.2±4.3kg/m2; apnea hypopnea index [AHI], 25.4±22.6 events/h; systolic BP 137±15mmHg; diastolic BP 79±7mmHg) recruited from a population based cohort underwent simultaneous ambulatory polysomnography (PSG) and peripheral arterial tonometry (PAT) recording. Episodic attenuations of PWA derived from the pulse waveform of the PAT signal were identified and characterized. Generalized least squares regression models were used to identify the associations between median PWA attenuation (PWA.att), office BP and sleep-related disordered breathing. Results: We found that the association between PWA.att and office BP was independent of gender, age, BMI, antihypertensive medication, number of attenuation episodes, AHI, oxygen desaturation ⩾4% index (ODI4) and arousal index. Each 10% increase in PWA.att was associated with increases of 5.0mmHg systolic BP (P =0.02) and 3.0mmHg diastolic BP (P =0.005). We also found independent relationships between systolic/diastolic BP and BMI (P =0.0006/0.001), AHI (P =0.03/0.1) and ODI4 (P =0.03/0.03). Conclusions: The degree of PWA attenuation during the night is associated with office BP independent of sleep-disordered breathing. Continuous assessment of PWA during sleep may provide novel insights into cardiovascular physiology and morbidity. [Copyright &y& Elsevier]