Showing papers by "Peretz Lavie published in 2008"

Shift work in nursing: is it really a risk factor for nurses' health and patients' safety?

Abstract: There is evidence in the scientific literature of the adverse physiological and psychological effects of shift work, including disruption to biological rhythm, sleep disorders, health problems, diminished performance at work, job dissatisfaction, and social isolation. In this study, the results of health problems and sleep disorders between female and male nurses, between daytime and shift nurses, and between sleep-adjusted and non-sleep-adjusted shift nurses were compared. Also the relationship between adjustment to shift work and organizational outcomes (errors and incidents and absenteeism from work) was analyzed. Gender, age, and weight were more significant factors than shift work in determining the well-being of nurses. Shift work by itself was not found to be a risk factor for nurses' health and organizational outcomes in this study. Moreover, nurses who were identified as being "non-adaptive" to shift work were found to work as effectively and safely as their adaptive colleagues in terms of absenteeism from work and involvement in professional errors and accidents. This research adds two additional findings to the field of shift work studies. The first finding is that female shift workers complain significantly more about sleep disorders than male shift workers. Second, although high rates of nurses whose sleep was not adapted to shift work were found, this did not have a more adverse impact on their health, absenteeism rates, or performance (reported errors and incidents), compared to their "adaptive" and "daytime" colleagues.

Delayed neutrophil apoptosis in patients with sleep apnea.

Abstract: Rationale: Obstructive sleep apnea (OSA), characterized by intermittent hypoxia/reoxygenation (IHR), is associated with atherosclerosis. Polymorphonuclear leukocytes (PMNs) are implicated in atherogenesis by producing oxidizing radicals and proteolytic enzymes during PMN–endothelium interactions. PMN apoptosis is a fundamental, injury-limiting mechanism, which prevents their destructive potential.Objectives: To determine whether PMN apoptosis and expression of adhesion molecules are affected by OSA and IHR in vitro.Methods: Apoptosis and expression of adhesion molecules were assessed in whole blood PMNs by flow cytometry, verified by various culture conditions, and morphology. These were complemented by exposing whole blood and purified PMNs to IHR and to sustained hypoxia in vitro.Measurements and Main Results: This study demonstrates for the first time that, in patients with moderate to severe OSA, PMN apoptosis is delayed. Apoptosis was attenuated in patients with an apnea–hypopnea index (AHI) of more ...

Cardiovascular morbidity and mortality in obstructive sleep apnea.

Abstract: Obstructive sleep apnea syndrome (OSA) is a highly prevalent breathing disorder in sleep affecting at least 2-4% of the adult population. A large number of studies have demonstrated that OSA is an independent risk factor of cardiovascular morbidity and mortality. Sleep apnea was shown to be associated with hypertension, ischemic heart disease, stroke, pulmonary hypertension, cardiac arrhythmia, and cardiovascular mortality. The association of OSA with subclinical signs of cardiovascular morbidity such as endothelial dysfunction and vasculature remodeling on the one hand, and with oxidative stress, activation of inflammatory pathways and increased leukocytes/endothelial cells adhesion on the other, implicate that atherogenesis plays a major role in cardiovascular sequela of OSA. Results demonstrating that effective treatment of the syndrome can abort and even reverse the atherogenic process suggest that OSA should be diagnosed and treated as early as possible in order to prevent cardiovascular sequlea.

Upper airway in obstructive sleep apnea--controversies continue.

Abstract: The exact pathophysiology leading to pharyngeal collapse in obstructive sleep apnea (OSA) remains incompletely understood. Recent research have focused on the neurochemical and physiological changes occurring at sleep onset that lead to the loss of muscle activity and diminished reflex pharyngeal control, and a loss of the neuromuscular compensation present during wakefulness, resulting in pharyngeal collapse. Regardless of this physiological arm, it is well documented that patients with OSA suffer from compromised upper airway anatomy. Most studies, using a variety of imaging techniques (CT, MRI, acoustic reflection, cephalometrics), have demonstrated a small pharyngeal airway in apnea patients, with the smallest airway luminal size generally occurring at the level of the velopharynx (behind the soft palate) in both patients and controls (Schwab et al., 1993). The finding of Walsh et al. (2008) from the current issue of the JSR supports these findings as well. Utilizing the novel technology of anatomical optical coherence tomography, they showed that the smallest cross-sectional area in 30 patients with OSA and 10 controls is located at the velopharyngeal level. However, they could not corroborate two previous anatomical findings reported in OSA: the role of airway shape and airway length. Several previous studies have reported an oval shape of the pharyngeal airway in individuals with OSA when compared with controls (i.e. a relatively high anteroposterior ⁄ lateral luminal airway dimension). Furthermore, Leiter (1996) have also suggested a reduced ability of muscles to dilate the pharynx when it is oval in shape. The study by Walsh et al. could not demonstrate differences in the AP ⁄ lateral diameter ratio between patients and controls. The importance of airway shape was also found to be less significant in a recent study examining the potential mechanisms contributing to increase in the prevalence of OSA with increasing age. Malhotra et al. (2006) reported that the ratio of the anteroposterior to lateral dimension became progressively lower with increasing age. Thus, the importance of the oval airway shape as an anatomical predisposing factor in the pathophysiology of OSA remains controversial and unclear. The length of the pharyngeal airway has received only minimal attention so far. It was previously reported that upper airway length (UAL) was greater in normal men compared with women, suggesting that it may play a role in the male predisposition to pharyngeal collapse (Malhotra et al., 2002). Furthermore, using computational modeling, a major impact of UAL on pharyngeal mechanics has been demonstrated (Malhotra et al., 2002). In another recent study of 69 healthy boys and girls who had undergone CT scans of the neck, it has been found that the UAL in prepubertal children is equal between genders. However, following puberty, males were found to have longer upper airways than females (independent of systemic growth), thus potentially explaining why pharyngeal collapse has a strong male predominance in adults but not in children (Ronen et al., 2007). In addition, a longer pharyngeal airway has been shown in postmenopausal as compared with premenopausal women (Malhotra et al., 2006). Thus, the existing data suggest that UAL may at least partially explain the male predisposition to airway collapse that occurs at puberty, and the female predisposition that occurs at menopause. Moreover, data from our own laboratory shows that UAL is greater in patients with OSA than in controls, with a positive significant correlation between the UAL and the severity of OSA (paper under consideration for publication). At least three potential reasons can explain the discrepancy between these previous findings and the findings of the current study by Walsh et al.: methodological differences, statistical limitations, and the patient population studied. While previous studies of UAL were based on MRI or CT scans, the current study utilized a relatively novel technology. The anatomical optical coherence tomography is an endoscopic technique, based on infrared light from an optical probe sliding within a preinserted esophageal catheter. While a CT scan is completed within seconds, this technique takes between 9–12 min (for each pullback scan), and may be affected by swallows, head or tongue movements, and by the topical anesthesia applied prior to catheter insertion. In addition, UAL in the Walsh study was determined as the summation of the velopharyngeal, oropharyngeal, and hypopharyngeal segments, thus extending all the way to below the epiglottis, differently from the previous definition for UAL length (between the rigid bony structures of the airway: hard palate to epiglottis). Also, lack of differences in UAL between OSA and controls is based on only 10 subjects in each group, all of whom are men, while the previous studies reporting the importance for UAL had a substantial gender-related effect and were based on substantially larger groups of subjects (Malhotra et al., 2002, 2006; Ronen et al., 2007). Thus, further studies are required to better understand the role of UAL in obstructive sleep apnea syndrome. Controversies in OSA are further exemplified in the discrepancy between the anatomical findings and therapeutic J. Sleep Res. (2008) 17, 123–124 Editorial

On sleepy humans and sleepy rats.

Abstract: In view of the present day practice of sleep medicine, it is rather surprising that until the mid-1970s, scientific literature dealing with sleep disorders in the general population hardly touched on the complaint of excessive sleepiness. This, however, does not mean that sleepy patients were completely absent from the medical literature. In Dickens s Pickwick Papers, Joe, the boy servant who impressed Mr Pickwick by his constant tendency to fall asleep, inspired several physicians to coin the phrase Pickwickian to denote sleepy patients. In the 21st century, sleepiness has become a major clinical and research subject. Suffice to mention that Murray John s paper describing the Epworth Sleepiness Scale (ESS), the popular subjective self-completed questionnaire to assess sleepiness, is the second most cited paper among all sleep-related publications (Johns, 1991). The 2008 December issue of Journal of Sleep Research includes a collection of papers addressing the subject of sleepiness from several interesting angles such as how to measure sleepiness objectively in an animal model? what are the determinants of sleepiness in sleep apnoea patients? is it possible to differentiate between the overlapping complaints of fatigue and sleepiness in patients with chronic fatigue syndrome? what are the consequences of sleep debt on daytime sleepiness? and what are the effective countermeasures of sleepiness? There is a great number of methodologies to measure sleepiness objectively in humans. The most widely used are the multiple sleep latency test (MSLT) in which sleepiness is operationally defined as the propensity to fall asleep during 4– 5 planned naps during the day, and the psychomotor vigilance test (PVT) that measures sleepiness by performance impairment (Carskadon et al., 1986; Jewett et al., 1999). So far, validated techniques to measure sleepiness in animals are sparse. The first two papers in the this issue of JSR by McKenna et al. Assessing sleepiness in the rat: a multiple sleep latencies test compared to polysomonographic measures of sleepiness , and by Christie et al. 24 hours of sleep deprivation in the rat increases sleepiness and decreases vigilance: introduction of the rat-psychomotor vigilance test , both from the same research group from Harvard Medical School, provide animal versions of the MSLT and PVT analogous to the human tests. The rat MSLT requires only 3 h of testing and, similar to the human version, produces a minimal amount of additional sleep loss associated with the procedure itself. McKenna et al. showed that 6 h of sleep deprivation significantly shortened the rat MSLT latencies regardless of circadian and illumination influences, and that it was as sensitive a measure as conventional polysomnographic indirect measures of sleepiness. Christie et al. developed a rat PVT that closely resembles the human version. In an operant conditioning paradigm, rats are required to monitor a central stimulus location (light) for a brief and unpredictable signal (flash of light) to which they respond with simple intrinsic behaviour (a nose-poke) rewarded with water. Rats experiencing 24-h sleep deprivation just prior to performing the rat PVT demonstrated behavioural impairment analogous to that of sleep-deprived humans – i.e. response latencies slowed and lapses increased. Both the rat MSLT and PVT will allow investigation of the neurobiological mechanisms underlying sleepiness in the rat model. Although clinical experience shows that sleepiness is the cardinal symptom of sleep-disordered breathing, Koutsourelakis et al. convincingly demonstrate that the origin of sleepiness in patients with sleep apnoea syndrome is multifactorial, and that sleep apnoea severity is only one of three independent factors that contribute to sleepiness. In their paper Determinants of subjective sleepiness in suspected obstructive sleep apnoea , they report that the severity of sleep apnoea, depression and diabetes, contributed the lion share of the variance in the ESS score, used to measure subjective sleepiness. Interestingly, polysomnographically determined sleep measures were not independently related to sleepiness. Thus, the results of Koutsourelakis et al. should warn sleep clinicians from assuming that the apnoeas and sleep fragmentation are the sole causes of excessive daytime sleepiness in sleep apnoea syndrome. Neu et al., in their paper Are patients with chronic fatigue syndrome just tired or also sleepy ? addressed the interesting question of the possible overlapping between complaints of fatigue and sleepiness . Using the MSLT to measure daytime sleepiness in two groups of patients with chronic fatigue syndrome and sleep apnoea syndrome, and in healthy controls, they report that chronic fatigue patients, free of any other medical or psychiatric co-morbidities, showed normal sleep latencies in spite of their subjective complaints of fatigue and sleepiness that were significantly higher than in healthy controls, and no different from patients with sleep apnoea. Noteworthy, although patients with chronic fatigue could not be considered objectively sleepy, their sleep latencies were significantly shorter than in the control group. The question how to counteract mid-afternoon and evening sleepiness is the subject of Horne, Anderson and Platten s paper: Sleep extension versus nap or coffee, within the context of ‘‘sleep debt.’’ They compared the effects of three counterJ. Sleep Res. (2008) 17, 363–364 Editorial