SLEEP

Carley, David W.; Trbovic, Sinisa M.; Radulovacki, Miodrag

doi: 10.1093/sleep/19.5.363pmid: 8843525

SummaryThe effects of lowering blood pressure (BP) by hydralazine (HY) (2 mg/kg) on spontaneous (SA) and post-sigh (PSA) sleep apneas have been studied in spontaneously hypertensive (SHR) rats by monitoring their respiration and sleep by the EEG for 6 hours. Normotensive Wistar-Kyoto (WKY) rats, from which the SHR rat strain was derived, were used as an appropriate control. The SHR rats had more SA (p < 0.02) and PSA (p < 0.0001) apneas/hour than WKY rats during nonrapid eye movement sleep and their mean BP was higher by 40 mm Hg (p < 0.0001) than WKY rats. Administration of HY to SHR rats equalized their BP with the arterial pressure of WKY rats and reduced the SA and the PSA apneas/hour to equivalence with WKY normotensive rats. These results demonstrate that even in the context of lifelong hypertension, acute normalization of BP significantly reduces sleep apneas in rats. They further suggest that improved management of BP may be of clinical benefit to patients with apnea who have long-standing hypertension.

Ferini-Strambi, Luigi; Oldani, Alessandro; Zucconi, Marco; Smirne, Salvatore

doi: 10.1093/sleep/19.5.367pmid: 8843526

SummaryIn REM sleep behavior disorder (RBD) it has been reported that tachycardia may not accompany the impressive movements associated with dream mentation. Up to now there are no data concerning the cardiac autonomic activity during wakefulness, as well as during sleep out of nocturnal dream-enacting behaviors, in RBD. We evaluated 14 RBD patients. Our study shows that only 36% of patients had normal results in all traditional autonomic tests during wakefulness. Moreover, RBD patients had a reduced tonic and phasic heart rate variability during sleep. Autonomic evaluation during sleep may show impairment earlier than the traditional tests during wakefulness. No difference was found between idiopathic RBD patients and symptomatic ones.

Shiomi, Toshiaki; Guilleminault, Christian; Sasanabe, Ryujiro; Hirota, Izumi; Maekawa, Masato; Kobayashi, Tadashi

doi: 10.1093/sleep/19.5.370pmid: 8843527

SummaryAfter documenting the presence of obstructive sleep apnea syndrome (OSAS) through polysomnography monitoring, we performed simultaneous ambulatory recordings of electrocardiogram, oronasal airflow, and pulse oximetry on 12 OSAS patients with normal autonomic nervous function for a period of 24 hours. The power spectrum of heart rate variability was investigated before and during treatments using dental appliances. Frequency domain analysis showed that the very low frequency component of heart rate (0.008–0.04 Hz) was increased in OSAS patients and that a very low frequency peak appeared during episodes of obstructive sleep apnea. The increase in very low frequency identification was synchronized with episodes of absence of air exchange or hypoxemia (decreased arterial oxygen saturation) that occurred repeatedly at a cycle length of 25–120 seconds in our subjects. Frequency domain analysis of heart rate variability before and during prosthetic mandibular advancement treatment showed that only the very low frequency was significantly decreased during prosthetic mandibular advancement treatment, whereas the other frequencies, i.e. high, low, and ultralow frequency component values, showed no significant changes. Time domain analysis of heart rate variability before and during prosthetic mandibular advancement treatment showed no significant changes in any of these parameters. Frequency domain analysis of heart rate variability during nocturnal sleep, especially investigation of very low frequency and very low frequency peak, can be a noninvasive low-cost approach to diagnose and even better monitor subjects undergoing treatment at home, particularly considering that R-R intervals can be extracted from pulse oximetry and that analysis software programs are already commercially available.

Engleman, Heather M.; Gough, Kathleen; Martin, Sascha E.; Kingshott, Ruth N.; Padfield, Paul L.; Douglas, Neil J.

doi: 10.1093/sleep/19.5.378pmid: 8843528

SummaryAmbulatory blood pressure (BP) monitoring was performed in 13 patients with the sleep apnea/ hypopnea syndrome (SAHS) during a randomized, placebo-controlled crossover trial of the effects of continuous positive airway pressure (CPAP) therapy. BP was monitored at half-hourly intervals for a 24-hour period both on CPAP and on an oral placebo, each given for a minimum of 3 weeks. Objective effective CPAP use averaged 4.3 hours per night. Weight and anti-hypertensive medications remained stable over the study period. Systolic, diastolic and mean arterial BP for 24-hour, daytime and nighttime periods were not significantly different on placebo compared to CPAP. Those patients with no significant overnight fall in BP on placebo (“non-dippers”) showed a significant improvement in daytime mean arterial BP on CPAP (98 ± 4 mm Hg) compared to placebo (102 ± 4 mm Hg; p = 0.01). These findings, in a well-controlled trial, suggest that BP is not reduced by CPAP in a heterogeneous group of SAHS patients, but it may be selectively improved in those patients most at risk for cardiovascular morbidity and mortality.

Suzuki, Mayumi; Guilleminault, Christian; Otsuka, Kuniaki; Shiomi, Toshiaki

doi: 10.1093/sleep/19.5.382pmid: 8843529

SummaryObstructive sleep apnea syndrome (OSAS) has been associated with a higher than normal cardiovascular morbidity and mortality. Some OSAS patients lack the sleep-related, nocturnal decrease, or 201cdip,201c in blood pressure which is seen in normal individuals. These subjects, called 201cnon-dippers,201c may be at greater risk for cardiovascular problems.We studied 40 OSAS patients (including 3 women) and 6 control subjects, all identified by polysomnography, for nocturnal blood pressure 201cdipping.201c We performed a second nocturnal polysomnogram to determine their apnea and hypopnea indices, (A + H)I, and oxygen saturation levels at the beginning of the study and then initiated 48 hours of ambulatory blood pressure monitoring, with data points collected every 30 minutes.Controls, which included one hypertensive subject, were all dippers. Nineteen OSAS subjects (48% of OSAS individuals) were systolic non-dippers and only 9 of them (22.5%) were diastolic non-dippers. We considered the following clinical variables as potential predictors of non-dipping: age, body mass index, respiratory disturbance index, years of reported loud snoring by bed partners, lowest oxygen saturation during nocturnal sleep, and percentage of sleep time spent with oxygen saturation below 90%. Multiple regression analyses indicated respiratory disturbance index as the only significant variable for systolic (p = 0.04) and diastolic (p = 0.03) blood pressure non-dipping. When we forced the following two nonsignificant variables into the model, they showed a very meager impact: number of years with reported loud snoring (p = 0.4 and p = 0.5, respectively for systolic and diastolic blood pressure non-dipping) and age (p = 0.5 and p = 0.6). The calculated model explained only a low percentage of the variance with an r2 of 0.25 and 0.26 for systolic and diastolic blood pressure non-dipping, respectively.Analysis of hypertension/normotension and dipping/non-dipping failed to show a significant relationship in the studied population. Fifty percent of the normotensive OSAS subjects were non-dippers and 43% of the hypertensive OSAS subjects were also non-dippers. We found a relationship between increasing respiratory disturbance index and increasing average 24-hour systolic blood pressure only when OSAS subjects were non-dippers and hypertensive.

Weiss, J. Woodrow; Remsburg, Stacia; Garpestad, Erik; Ringler, Jack; Sparrow, David; Parker, J. Anthony

doi: 10.1093/sleep/19.5.388pmid: 8843530

SummaryPatients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10–15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.

Edinger, Jack D.; Fins, Ana I.; Goeke, John M.; McMillan, Donna K.; Gersh, Tracey L.; Krystal, Andrew D.; McCall, W. Vaughn

doi: 10.1093/sleep/19.5.398pmid: N/A

SummaryOver the past 15 years, there has been considerable debate concerning the extent to which insomnia patients can be classified into diagnostic subtypes. Despite this debate, relatively little research has been conducted to empirically determine whether naturally occurring insomnia subtypes might be identified within populations of sleep clinic patients. In the current study we used a hierarchical cluster analysis to empirically identify subtypes among a mixed group of normal sleepers and the insomnia outpatients who presented to our sleep center over the past decade. Using factor-analytically derived composite variables that summarized data obtained from sleep history questionnaires and polysomnographic monitoring, this clustering procedure resulted in the identification of 14 subgroups that varied between four and 34 patients/subjects in size. Subsequently, subgroup mean scores for the composite variables used in the clustering procedure were used to construct profiles for each of the 14 clusters. A multivariate profile analysis, employed to elucidate subgroup differences, showed that these cluster profiles differed in terms of their configural shapes, average elevations, and degrees of interscale differences. Furthermore, both DSM-III-R (American Psychiatric Association) and International Classification of Sleep Disorders (ICSD) insomnia diagnoses, assigned independent of cluster findings, suggested that these subtypes differed significantly in regard to their diagnostic compositions. Nevertheless, a far-from-perfect concordance was observed between such clinically assigned diagnoses and cluster group membership. In fact, many of the empirically identified groups were composed of various DSM-III-R and/or ICSD diagnostic subtypes. These results provided only partial support for current DSM and ICSD insomnia categories. However, our results support the existence of multiple, clinically discrete insomnia subtypes and provide information that may be useful in future revisions of current insomnia nosologies.

Costa E Silva, Jorge Alberto; Chase, Michael; Sartorius, Norman; Roth, Thomas

doi: 10.1093/sleep/19.5.412pmid: 8843532

Roehrs, Timothy; Salin-Pascual, Raphael; Merlotti, Lori; Rosenthal, Leon; Roth, Thomas

doi: 10.1093/sleep/19.5.417pmid: 8843533

SummaryPhase advanced sleep (by 4 hours) was studied in 28 healthy, normal men and women, aged 21–50 years, without nocturnal sleep or daytime sleepiness complaints. Eleven subjects (6 men and 5 women) with moderately short (≤10 minutes) average daily sleep latencies on the multiple sleep latency test (MSLT) were compared to 17 (11 men and 6 women) with relatively long (≥12 minutes) latencies. Nocturnal sleep on both a baseline and a shift night differed between the groups. The moderately “sleepy” group had shorter sleep latencies and less wakefulness during sleep than the moderately “alert” group. The phase advanced sleep schedule reduced sleep efficiency in both groups, but the moderately sleepy group showed a lessened effect of the shift. Additionally, sleep efficiency was reduced in the moderately sleepy group only during the first 2 hours of the sleep period, while sleep efficiency was uniformly disturbed in the moderately alert group throughout the night during the phase advance.

Zhdanova, Irina V.; Wurtman, Richard J.; Morabito, Claudia; Piotrovska, Veronika R.; Lynch, Harry J.

doi: 10.1093/sleep/19.5.423pmid: 8843534

SummaryLow oral doses of melatonin raise serum melatonin concentrations to those normally occurring noc-turnally and facilitate polysomnographically assessed sleep onset when given at different time points throughout the day, without altering mood or performance on the morning following treatment. In the present study, 12 young healthy volunteers, free of sleep disturbances, received 0.3 or 1.0 mg of melatonin or placebo at 2100 hours, 2–4 hours prior to their habitual bedtime. Polysomnographic recording of overnight sleep began at 2200 hours and continued until 0700 hours the following morning, when subjects were awakened. Sleep onset latency and latency to stage 2 sleep were significantly decreased as a result of melatonin treatment. Neither dose of melatonin significantly altered sleep architecture. Administration of the lower dose of melatonin (0.3 mg) at 2100 hours elevated serum melatonin to levels within the normal nocturnal range (113 ± 13.5 pg/ml) at the time the sleep test was initiated. Neither melatonin dose caused “hangover effects”, as assessed by self-reports or by mood and performance tests administered on the morning following treatment. These observations provide additional evidence that nocturnal melatonin secretion has a sleep-promoting function. They also indicate that an increase in serum melatonin concentrations, within the normal physiologic range, does not significantly alter sleep architecture in subjects with normal sleep who receive the treatment several hours prior to their habitual bedtime.