UNITED KINGDOM – The widespread coverage of sleep disorders found its way to the United Kingdom recently when the BBC News reported that a whopping 30% of the UK population suffers from insomnia and other sleep disorders. And in an unusual twist, the Nov 27 article reports that increasing numbers are doing “rather strange things during the night.”

“Clinics say they are getting up to 50 new referrals a week,” writes BBC Magazine reporter Denise Winterman. “It’s a fivefold increase in just a decade for some. This big rise has been put down to raised awareness of sleep disorders and more people reporting them. The clinics are also dealing with some strange new sleep behavior, while other rather odd sleep disorders are becoming more common.”

One such strange behavior is sending text messages while asleep. The head of a Neurology Sleep Service facility in London says, “It is very common for people to do things in their sleep that they do repeatedly during the day,” with other extremes including driving a car while sleeping, and even having sex while asleep—so-called “sexsomnia.”

“The problem is people rarely do such acts under controlled conditions at a sleep clinic,” adds sleep specialist Dr Chris Idzikowski, director of the Edinburgh Sleep Clinic. “But this area of research is going to really move forward in the next few years because we now have the necessary equipment to record people in their own homes.”

Source: BBC Magazine

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Sleep   apnea   may   capture   more   headlines   these   days, but sleep veteran Russell Rosenberg, PhD, points out that every good sleep center can capture the full slumber spectrum with a serious focus on insomnia.

It’s not easy to find a clinical psychologist and board certified sleep specialist with more than 25 years experience in the sleep world. Russell Rosenberg, PhD, director and CEO, NeuroTrials Research, and Atlanta School of Sleep Medicine, fits that rare description and brings his considerable experi- ence to international courses on a range of sleep medicine topics—including the occasionally neglected realm of insomnia.

The   National   Sleep   Foundation   estimates   that   about a third of Americans have symptoms of insomnia. It’s a massive number, but it should not be confused with the disorder of insomnia. “Everybody has an occasional night of sleeplessness, or occasionally can’t get back to sleep,” says Rosenberg, who also serves as chairman of the National Sleep Foundation. “But that number does not represent the number of Americans who meet the criteria for a diagnosis of insom- nia. About 6% of adults have diagnosable primary insomnia based on strict criteria from the Diagnostic and Statistical Manual of Psychiatric Disorders (DSM IV-TR).”

Insomnia has been a primary focus of Rosenberg’s clinical work, along with research and teaching. Rosenberg has seen many insomnia patients who simply did not realize the sheer amount of available treatments.

Worse   yet,   far   too   many   walking   around   with   the disorder have yet to be evaluated, much less treated. Many sleep disorder centers do not have enough staff who feel comfortable treating insomnia. The situation is caused by an emphasis on sleep apnea, but Rosenberg maintains that sleep centers can successfully treat both disorders. After all, “There are far more people who have insomnia than who have sleep apnea,” says Rosenberg.

Primary Care Practioners First Line of Defense

Primary care physicians (PCPs) are still the first line of treatment for most sleep disorders, including insomnia. Rosenberg does not necessarily have a problem with this phenomenon, but he points out that PCPs are more likely to be medically focused, and less likely to use behavioral approaches.

“Not every sleep center has someone who can provide cognitive behavioral therapy (CBT) for insomnia,” he says. “I want more primary care providers to recognize poor sleep in their patients as a serious health problem—whether it be sleep apnea or insomnia—and whether the treatment is medication, a medical device, or behavior therapy.”

Most of the time, says Rosenberg, PCPs will tend to prescribe a hypnotic or sleeping agent of some sort for insomnia. While these medications can be used long term, they can have side effects.  Psychologically-based  behavior  treatments  are  also valid, but their use usually depends on the PCP establishing solid sleep center referral networks.

New Drug Fits “As Needed” Niche

The first and only FDA-approved drug for treating patients who have middle-of-the-night awakenings—and can’t get back to sleep—was approved late last year. It’s called Inter- mezzo, and Rosenberg is confident that the new offering can serve as a valid option for years to come.

Since   most   insomniacs   do   not   have   horrible   sleep 7 nights a week, 365 days of the year, the new drug fits the “as needed” niche. “Previously, patients were given hypnotics in anticipation that they might not sleep well,” explains Rosen- berg. “When you wake up in the middle of the night, you can take Intermezzo only if you have 4 or more hours to remain in bed. It takes 4 hours to get it out of your system so it’s safe to drive.”

Administered   under   the   tongue,   the   minty   flavored tablet has a 3.5-milligram dose for men and 1.75 milligrams for women. “Drugs like intermezzo are not for everyone,” cautions Rosenberg. “I don’t think every insomnia patient should be on a sleeping pill. This is something that should be carefully considered by a patient’s physician, whether it’s a PCP or a specialist who has a lot of experience with these drugs. Remember that CBT has been shown to be quite effective—as effective as treatments with medications.”

Too often, the problem is that CBT is not as widely available, largely because clinical psychologists and mental health professionals do not put in the time to study it. “Sleep specialists may do a more thorough evaluation to detect breathing disorders and movement disorders,” adds Rosen- berg. “They are more likely to use a combination approach of medication and CBT then PCPs. There are lots of sleep centers across the country that do have a specialist in CBT, but not all do at this point.”

Where are the Insomniacs?

Why do sleep labs see so many apnea patients, but relatively few insomniacs? Rosenberg boils it down to the simple fact that insomniacs rarely, if ever, require a polysomnography. The American Academy of Sleep Medicine does not recom- mend the use of polysomnography as a routine evaluation for insomnia, and most insomniacs do not need a full sleep study.

Certainly there are those that are also suspected to have sleep apnea, but Rosenberg says these patients are not the “bread  and  butter”  of  sleep  disorder  centers.  “If  there  is a sleep disorder center that wants to present itself as a full service center,” he says, “it should have the capability, or at least a specialist for treating insomnia.”

Rosenberg  hopes  the  full  spectrum  approach  will  catch on nationwide, and he’ll do his part to further that mission while he educates physicians in the clinical and basic science of sleep medicine—and the therapeutic interventions for sleep disorders. “I’m also interested in is identifying an efficient way to integrate behavioral approaches with medication treatments for insomnia,” muses Rosenberg. “In the last 15 years, there has been a tremendous amount of research on insomnia, but very few breakthroughs. The reason is that these things take time. We are in a bit of a lull in terms of advances—other than this new drug Intermezzo—which is probably the most exciting advance in at least the last 5 years.”

Russell Rosenberg, PhD, D.ABSM, is the founder and director of the Atlanta School of Sleep Medicine and Technology. In addition to teaching, Rosenberg is actively involved in clinical research at Neuro- Trials Research Inc. He currently serves on the board of directors of the National Sleep Foundation.

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A novel brain mechanism mediating the inhibition of the critical breathing muscles during rapid  eye movement (REM) sleep has been identified for the first time in a new study titled “Identification of the Mechanism Mediating Genioglossus Muscle Inhibition in REM Sleep” published online ahead of print in the American Thoracic Society’s American Journal of  Respiratory and Critical Care Medicine., offering the possibility of a new treatment target for  sleep-related breathing problems.

“REM sleep is accompanied by profound  inhibition of muscle activity,” said researcher Richard Horner, PhD, professor of medicine and  physiology at the University of Toronto. This “paralysis” affects  breathing muscles and “is  a cause of snoring and other breathing problems in sleep, especially  obstructive sleep apnea.”

Sleep apnea is a common and serious problem that  increases the risk for heart attacks, high blood pressure, stroke, diabetes and  daytime sleepiness.

According to Dr. Horner, “the brain  mechanism mediating inhibition of the critical breathing muscles in REM sleep was  unknown, but a novel and powerful inhibitory mechanism is identified for the  first time in our study.”

In the study, performed by PhD student Kevin Grace, rats were studied across sleep-wake states. The  researchers targeted manipulation of the brain region that controls tongue  muscles during sleep.

To read the full article online, please visit: http://www.thoracic.org/media/press-releases/resources/Grace.pdf.

The tongue is an important breathing muscle because its activity keeps the airspace open behind the tongue  to allow for the effective passage of air into the lungs. Inhibition of tongue  muscle activity in sleep in some people leads to backward movement of the  tongue and blockage of the airspace. This blockage in sleep leads to episodes  of self-suffocation (sleep apnea) that are rescued by waking up from sleep.  Such episodes can occur hundreds of times a night.

Importantly, the muscle activating  effects of these interventions were largest during REM sleep and minimal or  absent in other sleep-wake states. The brain chemical mediating this powerful  inhibition of breathing muscle activity in REM sleep is acetylcholine, acting  via muscarinic receptors that are functionally linked to a particular class of  potassium channel.

“Since REM sleep recruits mechanisms that can abolish or suppress tongue  muscle activity during periods of REM sleep and cause obstructive sleep apnea,  identification of a mechanism mediating this inhibition is a significant  discovery,” said Dr. Horner.

“This newly identified process has fundamental  implications for understanding the common and serious problems of snoring and  other breathing problems such as obstructive sleep apnea, which are worse in  REM sleep,” said Dr. Horner. “Moreover, identifying the fundamental mechanism  responsible for the shutting down of a muscle in sleep that is critical for  effective breathing also identifies a rational drug target designed to prevent  this inactivity and so prevent obstructive sleep apnea and other sleep-related  breathing problems.”

Source: Provided by the American Thoracic Society

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Ernesto Kufoy,1† Jose-Alberto Palma,1,2†  Jon Lopez,3 Manuel Alegre,1,3 Elena Urrestarazu,1,3Julio Artieda1,3 and Jorge Iriarte1*

Abstract

Introduction: Obstructive Sleep Apnea (OSA) is a major risk factor for cardiovascular disease. The goal of this study was to demonstrate whether the use of CPAP produces significant changes in the heart rate or in the heart rate variability of patients with OSA in the first night of treatment and whether gender and obesity play a role in these differences.

Methods: Single-center transversal study including patients with severe OSA corrected with CPAP. Only patients with total correction after CPAP were included. Patients underwent two sleep studies on consecutive nights: the first night a basal study, and the second with CPAP. We also analyzed the heart rate changes and their relationship with CPAP treatment, sleep stages, sex and body mass index. Twenty-minute segments of the ECG were selected from the sleep periods of REM, no-REM and awake. Heart rate (HR) and heart rate variability (HRV) were studied by comparing the R-R interval in the different conditions. We also compared samples from the basal study and CPAP nights.

Results: 39 patients (15 females, 24 males) were studied. The mean age was 50.67 years old, the mean AHI was 48.54, and mean body mass index was 33.41 kg/m2  (31.83 males, 35.95 females). Our results showed that HRV (SDNN) decreased after the use of CPAP during the first night of treatment, especially in non-REM sleep. Gender and obesity did not have any influence on our results.

Conclusions: These findings support that cardiac variability improves as an acute effect, independently of gender or weight, in the first night of CPAP use in severe OSA patients, supporting the idea of continuous use and emphasizing that noncompliance of CPAP treatment should be avoided even if it is just once.

Introduction

Obstructive Sleep Apnea (OSA) is considered a cardiovascular risk factor, which increases the likely of suffering stroke, con- gestive heart failure, arterial hypertension, pulmonary hyper- tension, coronary artery disease, cardiac arrhythmias, and acute myocardial infarction.1–6  Although OSA has been associated with each of these diseases, the exact etiopathogenic mechanisms

†These authors contributed equally to this work.

1Clinical  Neurophysiology  Service,  University  Clinic  of  Navarra, Pamplona, Spain.

2Department of Neurology, University Clinic of Navarra, Pamplona, Spain.

3Neurophysiology   Laboratory,   Neurosciences   Area,   Centro   de Investigación  Médica  Aplicada  (CIMA),  University  of  Navarra, Pamplona, Spain.

Reprinted PLoS ONE 7(3) ©2012 Kufoy et al.

are unclear for most of these disorders. Among many of the systems affected by OSA, changes in the autonomic nervous system (ANS) are frequently studied.7,8

In healthy people, sleep stages have a great impact on sympathetic nervous system (SNS) activity, while the circadian system predominantly affects the parasympathetic nervous system (PNS) activity.9,10 Even people with altered sleep patterns (e.g. night shift workers) have an increased SNS activation.11

In OSA patients, both sympathetic and parasympathetic nervous system control of the heart rate become unstable, with enhanced parasympathetic tone during the apneas and hypo- pneas punctuated with enhanced sympathetic nervous system activation subsequent to the apneic events.12,13  Although other cardiovascular diseases, such as hypertension (which is a com- mon co-morbidity of OSA), are related to irregularities to both the PNS and SNS, dysregulation in these systems is noted during the daytime and nighttime in OSA patients even without evidence of cardiovascular diseases.14,15

One of the simplest non-invasive methods to monitor changes in cardiovascular control is by measuring heart rate variability (HRV), which can be defined as a physiological phenomenon where the time interval between heart beats varies. It is measured by the variation in the beat-to-beat interval. HRV reflects the relationship between the PNS and SNS, which is a good predictor of future cardiovascular problems.19  HRV can be analyzed by using a time-domain analysis which measures beat to beat intervals (R-R, also known as NN intervals).19Since OSA causes irregularities in the SNS function, OSA has been associated with an increased risk of cardiovascular events and mortality.16  Besides, OSA severity is also linked to distur- bances of PNS activity.17 PNS activity is higher in non-REM sleep (NREM), particularly in stage 2 sleep, as compared with REM sleep. This increase in PNS activity during stage 2 can be seen in healthy subjects, but is even more noticeable in OSA, suggesting that increased parasympathetic activity is a consequence of mechanisms to compensate oxygen saturation (SatO ) fluctuations during NREM.18,3

The most commonly used time-domain HRV measure is SDNN (the standard deviation of all NN intervals). Changes and var- iability in heart rate are strongly influenced by sleep stages, and for some authors these changes do not differ significantly when comparing OSA and non-OSA patients.20–22 R-R intervals have been shown to be at their highest in the early morning between the sleep and wake periods.23  R-R intervals have also been shown to steadily increase from wake to non-REM sleep then decrease during REM sleep in healthy subjects.24 Changes in the variances in R-R intervals have been associated with the severity of OSA,25,26  although other recent studies have argued that spectral analysis of HRV may serve as a better method to determine of OSA severity.27

Methods

This was a single-center transversal retrospective study involving  patients  with  severe  OSA  (AHI  >  30).  Subjects were selected from the sleep database of the Sleep Unit of the University Clinic of Navarra. Patients were either referred to the Sleep Unit from other departments within the University Clinic of Navarra (Neurology, Pulmonology, ENT, etc.) or from other hospitals of Spain. Most patients were referred because of primary complaints of snoring, daytime somnolence, restless sleep or other symptoms suggesting sleep apnea. Before PSG studies, all patients filled a questionnaire to determine clinical

Medicine  (AASM)  scoring  criteria.46    Following  the  baseline study, subjects underwent a second PSG study to treat the OSA using the suitable CPAP pressure. The CPAP pressure was calculated according to neck circumference (NC), body mass index (BMI) and IAH, following the widely used equation previously described by Hoffstein et al: P = (0.16 × BMI)+(0.13 × NC)+(0.04+AHI)–5.1247  Only patients with total correction of apneas with CPAP were included. CPAP treatment was considered successful if AHI in the night with CPAP was less than 10 and the lowest oxygen value was higher than 89%.

Sleep Data Conversion and HRV Analysis

In order to assess changes in HRV from the patient’s baseline study to their second study with CPAP treatment, 20-minute concatenated segments were selected from the sleep periods of REM, non-REM (NREM) and awake (WAKE), avoiding awak- enings and artifacts. Although concatenated segments were taken, an attempt was made to select consecutive or relatively close sleep stages in the selection process for REM and NREM segments, based on previous studies that show that HRV varies significantly throughout the night.19  Most of the selected REM segments were not from the first quarter of sleep, but exceptions were made for certain CPAP studies which only consisted of one REM cycle. NREM segments were taken from stage 3 and stage 2 sleep and were excluded if they occurred in the first quarter of the night. Periods with ectopic cardiac beats and arousals were excluded from analysis.

Sleep data in the form of digital files were collected using the Stellate Reviewer software program. The sleep segments were saved as text files from their digital recording in Stellate

Statistical Analysis

All statistical tests were performed using SPSS version 15.0.1 (SPSS Inc., Chicago, IL, USA). To investigate the effect of CPAP treatment by group, one-way ANOVA was performed. For categorical (qualitative) data, the c2 test was used to check the differences between the two groups. When the expected frequencies were less than 5, Fisher’s exact test was performed. For comparisons of two or more means, the analysis of variance (ANOVA) was performed. When a significant result was obtained in the ANOVA test, a post-hoc analysis (Scheffé’s test) was carried out to perform multiple comparisons. In all cases, statistical significance was defined as p < 0.05. A multivariate test was performed to test the effect of gender and obesity on weight was similar, they tended to have lower BMI, but the difference was not significant. Twenty subjects were obese (BMI > 30) and 6 had morbid obesity (BMI > 35).

Relationship between HR Parameters in OSA with CPAP Treatment

The primary aim of this study was to determine how HRV in OSA patients is affected after acute CPAP treatment, in a single night of treatment. First we compared heart rate mean (HRM) and HRV, considering all the patients and stages together. With these data, no significant differences were seen in the HRM when comparing the basal study to the CPAP study (p > 0.05). On the other hand, significant differences were seen when comparing HRV before and after CPAP treatment (p < 0.05). As expected, significant differences did occur when comparing the variation

Table 6. Analysis of the Data in Non-REM, REM and WAKE

between Male and Female Groups.

HRM: Heart Rate Mean. HRV: Heart Rate Variability. Var. SatO2: Variance of Oxygen Saturation. *Statistical significance.

obesity seen in the patient group. The lack of significant changes in HRV in REM after CPAP treatment could be explained by the REM interference theory in PNS activity. The clinical implica- tion of these results may suggest that patients who suffer from OSA with apneas occurring predominantly during REM sleep, may not enjoy the same cardiovascular benefits compared to OSA patients whose apneic episodes are scattered between REM and NREM. However, further studies are required to determine whether the unique properties of REM sleep influence autonomic function in patients with OSA.

The heart rate mean did not decrease significantly from NREM to REM during CPAP studies. This result is similar to previous studies in healthy individuals.24  The decrease HRV from NREM to REM was seen in basal studies, which suggests that OSA may influence the variance of the heart rate, but does not vary the natural change of overall beats per minute from NREM to REM. The lack of change in HRM during the CPAP study suggests that CPAP treatment lowers the variance of heart rate during NREM, as well as eliminates the change in the heart rate between NREM and REM.

Previous studies showed obese patients to have lower variations in total HRV.49  Our results also showed significant differences in HRV in obese patients during REM when com- pared to the non-obese group in both CPAP and basal studies. From these results, it seems plausible that CPAP treatment may improve HRV in obese patients, sufficiently so as to resemble the improved HRV seen in non-obese patients with CPAP treatment. In our study, another aim was to study the effects of obesity on CPAP treatment in severe OSA (AHI > 30) patients, as CPAP treatment has shown to lower night time blood pres- sure and increase SNS activity in OSA patients.50  The results from our study showed that obesity does not influence HRV or HRM during CPAP treatment when compared to non-obese patients. Based on these results, obesity does seem to influence heart rate mean in WAKE and REM, but not enough to be statistically significant. Therefore, from a clinical perspective, additional or differential forms of treatment do not seem neces- sary when combating ANS dysfunction in obese patients.

The final aim of our study was to determine the role of gender in HRV during short-term CPAP treatment of severe OSA (AHI > 30) patients, as women with breathing disorders have been shown to have increased SNS activity during NREM, and men with breathing disorders have been shown to have lower PNS activity during wake,51  and women with high AHI had low SNS activation during REM.52  Our results did show a difference in HRV between men and women in

wakefulness. In addition, HRM was different in all the sleep stages. Our results showed a significant difference in HRV and heart rate mean between our male and female groups during wake. However, the changes were similar in the basal and in the CPAP nights, which suggests that gender does not influence the improvements seen in ANS activity from CPAP treatment. Nevertheless, the absence of statistical significance when assessing the effects of gender and obesity on HRV may be a consequence of the small sample size of our study, which is one of its limitations.

The main limitation of our study is a consequence of its transversal nature. In these regard, there is a possibility that changes in HRV during acute CPAP treatment may reflect a normalization of the respiratory pattern or may be due to changes in venous return secondary to the dramatic changes of intrathoracic pressure that occur during the apneic event rather than changes in cardiovascular control mechanisms. Thus, caution must be used when analyzing our results, as the effect of OSA in autonomic activity may perhaps more likely to be detected by comparing HRV on the first night of treatment with a sleep study on CPAP after weeks of treatment, and not with a single-night study, such as the present one. We neither studied whether the changes in HRV were associated with the severity of OSA, as we only selected patients with an AHI > 30. Moreover, we do not provide data regarding the percentage of stage 2 and stage 3 sleep in the NREM segments, in spite of the fact that several studies show that ANS balance differs between these 2 stages. Finally, we did not study frequency- domain measures (i.e. HF, LF, and VLF); hence, further studies may be needed to understand our findings in depth.

Nonetheless, all these limitations do not hamper the fact that cardiac variability improves as an acute effect, indepen- dently of gender or weight, in the first night of CPAP use in severe OSA patients. Thus, we think that the CPAP treatment should not be delayed. Severe OSA patients should be advised that even a single night without CPAP has changes in the cardiac rate, which are corrected with CPAP. Hence, to use or not to use the CPAP for a single night does matter.

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36. Limphanudom P, Chierakul N, Pinyopattarakul N, Nana A, Naruman C, et al. (2007) Recovery of heart rate variability in patients with moderate to severe obstructive sleep apnea after 6-month continuous positive airway pressure treatment. J Med Assoc Thai 90: 1530-1535.

37.   Mayer J, Becker H, Brandenburg U, Penzel T, Peter JH, et al. (2001) Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. Cardiology 79: 84–92.

38.   Chrysostomakis  SI,  Simantirakis  EN,  Schiza  SE,  Karalis  IK, Klapsinos NC, et al. (2006) Continuous positive airway pressure therapy lowers vagal tone in patients with obstructive sleep apnea-hypopnea syndrome. Hellenic J Cardiol 47: 13–20.

39.  Kasai T, Narui K, Dohi T, Yanagisawa N, Ishiwata S, et al. (2008) Prognosis of patients with heart failure and obstructive sleep apnea treated with continuous positive airway pressure. Chest 133: 690–696.

40.  Dursunoglu D, Dursunoglu N (2007) Effect of CPAP on QT interval dispersion in obstructive sleep apnea patients without hypertension. Sleep Med 8: 478–483.

41.   Patruno V, Aiolfi S, Costantino G, Murgia R, Selmi C, et al. (2007) Fixed  and  autoadjusting  continuous  positive  airway  pressure treatments are not similar in reducing cardiovascular risk factors in patients with obstructive sleep apnea. Chest 131: 1393–1399.

42.  Antczak J, Horn B, Richter A, Jernajczyk W, Bodenschatz R, et al. (2008) The influence of obesity on sleep quality in male sleep apnea patients before and during therapy. J Physiol Pharmacol 59: 123–1234.

43.   Lin CM, Davidson TM, Ancoli-Israel S (2008) Gender differences in obstructive sleep apnea and treatment implications. Sleep Med Rev 12: 481–496.

44.  Sztajzel J, Jung M, Bayes de Luna A (2008) Reproducibility and gen-der-related differences of heart rate variability during all-day activity in young men and women. Ann Noninvasive Electrocardiol 13: 270–277.

45.  Ye L, Pien GW, Weaver TE (2009) Gender differences in the clinical manifestation of obstructive sleep apnea. Sleep Med 10: 1075–1084.

46.   AASM (2005) The International Classification of Sleep Disorders 2nd ed.: Diagnostic and Coding Manual American Academy of Sleep Medicine, Westchester.

47.  Hoffstein V, Mateika S (1994) Predicting nasal continuous positive airway pressure. Am J Respir Crit Care Med 150: 486–488. 48.   Dursunoglu  N,  Dursunoglu  D,  Cuhadaroglu  C,  Kilicaslan  Z (2005)  Acute  effects  of  automated  continuous  positive  airway pressure on blood pressure in patients with sleep apnea and hypertension. Respiration 72: 150–155.

49.   Reynolds EB, Seda G, Ware JC, Vinik AI, Risk MR, et al. (2007) Autonomic  function  in  sleep  apnea  patients:  increased  heart rate variability except during REM sleep in obese patients. Sleep Breath 11: 53–60.

50.   Ferland A, Poirier P, Series F (2009) Sibutramine versus CPAP in the treatment of obese patients with obstructive sleep apnea. Eur Respir J 34: 694–701.

51.   Wang W, Tretriluxana S, Redline S, Surovec S, Gottlieb DJ, et al. (2008) Association of cardiac autonomic function measures with severity  of  sleep-disordered  breathing  in  a  community-based sample. J Sleep Res 17: 251–262.

52.  Kesek M, Franklin KA, Sahlin C, Lindberg E (2009) Heart rate variability during sleep and sleep apnea in a population based study of 387 women. Clin Physiol Funct Imaging 29: 309–315.

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Abstract

Introduction: Obstructive Sleep Apnea (OSA) is a major risk factor for cardiovascular disease. The goal of this study was to demonstrate whether the use of CPAP produces significant changes in the heart rate or in the heart rate variability of patients with OSA in the first night of treatment and whether gender and obesity play a role in these differences.

Methods: Single-center transversal study including patients with severe OSA corrected with CPAP. Only patients with total correction after CPAP were included. Patients underwent two sleep studies on consecutive nights: the first night a basal study, and the second with CPAP. We also analyzed the heart rate changes and their relationship with CPAP treatment, sleep stages, sex and body mass index. Twenty-minute segments of the ECG were selected from the sleep periods of REM, no-REM and awake. Heart rate (HR) and heart rate variability (HRV) were studied by comparing the R-R interval in the different conditions. We also compared samples from the basal study and CPAP nights.

Results: 39 patients (15 females, 24 males) were studied. The mean age was 50.67 years old, the mean AHI was 48.54, and mean body mass index was 33.41 kg/m2  (31.83 males, 35.95 females). Our results showed that HRV (SDNN) decreased after the use of CPAP during the first night of treatment, especially in non-REM sleep. Gender and obesity did not have any influence on our results.

Conclusions: These findings support that cardiac variability improves as an acute effect, independently of gender or weight, in the first night of CPAP use in severe OSA patients, supporting the idea of continuous use and emphasizing that noncompliance of CPAP treatment should be avoided even if it is just once.

Introduction

Obstructive Sleep Apnea (OSA) is considered a cardiovascular risk factor, which increases the likely of suffering stroke, con- gestive heart failure, arterial hypertension, pulmonary hyper- tension, coronary artery disease, cardiac arrhythmias, and acute myocardial infarction.1–6  Although OSA has been associated with each of these diseases, the exact etiopathogenic mechanisms

†These authors contributed equally to this work.

1Clinical  Neurophysiology  Service,  University  Clinic  of  Navarra, Pamplona, Spain.

2Department of Neurology, University Clinic of Navarra, Pamplona, Spain.

3Neurophysiology   Laboratory,   Neurosciences   Area,   Centro   de Investigación  Médica  Aplicada  (CIMA),  University  of  Navarra, Pamplona, Spain.

Reprinted PLoS ONE 7(3) ©2012 Kufoy et al.

are unclear for most of these disorders. Among many of the systems affected by OSA, changes in the autonomic nervous system (ANS) are frequently studied.7,8

In healthy people, sleep stages have a great impact on sympathetic nervous system (SNS) activity, while the circadian system predominantly affects the parasympathetic nervous system (PNS) activity.9,10 Even people with altered sleep patterns (e.g. night shift workers) have an increased SNS activation.11

In OSA patients, both sympathetic and parasympathetic nervous system control of the heart rate become unstable, with enhanced parasympathetic tone during the apneas and hypo- pneas punctuated with enhanced sympathetic nervous system activation subsequent to the apneic events.12,13  Although other cardiovascular diseases, such as hypertension (which is a com- mon co-morbidity of OSA), are related to irregularities to both the PNS and SNS, dysregulation in these systems is noted during the daytime and nighttime in OSA patients even without evidence of cardiovascular diseases.14,15

One of the simplest non-invasive methods to monitor changes in cardiovascular control is by measuring heart rate variability (HRV), which can be defined as a physiological phenomenon where the time interval between heart beats varies. It is measured by the variation in the beat-to-beat interval. HRV reflects the relationship between the PNS and SNS, which is a good predictor of future cardiovascular problems.19  HRV can be analyzed by using a time-domain analysis which measures beat to beat intervals (R-R, also known as NN intervals).19Since OSA causes irregularities in the SNS function, OSA has been associated with an increased risk of cardiovascular events and mortality.16  Besides, OSA severity is also linked to distur- bances of PNS activity.17 PNS activity is higher in non-REM sleep (NREM), particularly in stage 2 sleep, as compared with REM sleep. This increase in PNS activity during stage 2 can be seen in healthy subjects, but is even more noticeable in OSA, suggesting that increased parasympathetic activity is a consequence of mechanisms to compensate oxygen saturation (SatO ) fluctuations during NREM.18,3

The most commonly used time-domain HRV measure is SDNN (the standard deviation of all NN intervals). Changes and var- iability in heart rate are strongly influenced by sleep stages, and for some authors these changes do not differ significantly when comparing OSA and non-OSA patients.20–22 R-R intervals have been shown to be at their highest in the early morning between the sleep and wake periods.23  R-R intervals have also been shown to steadily increase from wake to non-REM sleep then decrease during REM sleep in healthy subjects.24 Changes in the variances in R-R intervals have been associated with the severity of OSA,25,26  although other recent studies have argued that spectral analysis of HRV may serve as a better method to determine of OSA severity.27

Methods

This was a single-center transversal retrospective study involving  patients  with  severe  OSA  (AHI  >  30).  Subjects were selected from the sleep database of the Sleep Unit of the University Clinic of Navarra. Patients were either referred to the Sleep Unit from other departments within the University Clinic of Navarra (Neurology, Pulmonology, ENT, etc.) or from other hospitals of Spain. Most patients were referred because of primary complaints of snoring, daytime somnolence, restless sleep or other symptoms suggesting sleep apnea. Before PSG studies, all patients filled a questionnaire to determine clinical

Medicine  (AASM)  scoring  criteria.46    Following  the  baseline study, subjects underwent a second PSG study to treat the OSA using the suitable CPAP pressure. The CPAP pressure was calculated according to neck circumference (NC), body mass index (BMI) and IAH, following the widely used equation previously described by Hoffstein et al: P = (0.16 × BMI)+(0.13 × NC)+(0.04+AHI)–5.1247  Only patients with total correction of apneas with CPAP were included. CPAP treatment was considered successful if AHI in the night with CPAP was less than 10 and the lowest oxygen value was higher than 89%.

Sleep Data Conversion and HRV Analysis

In order to assess changes in HRV from the patient’s baseline study to their second study with CPAP treatment, 20-minute concatenated segments were selected from the sleep periods of REM, non-REM (NREM) and awake (WAKE), avoiding awak- enings and artifacts. Although concatenated segments were taken, an attempt was made to select consecutive or relatively close sleep stages in the selection process for REM and NREM segments, based on previous studies that show that HRV varies significantly throughout the night.19  Most of the selected REM segments were not from the first quarter of sleep, but exceptions were made for certain CPAP studies which only consisted of one REM cycle. NREM segments were taken from stage 3 and stage 2 sleep and were excluded if they occurred in the first quarter of the night. Periods with ectopic cardiac beats and arousals were excluded from analysis.

Sleep data in the form of digital files were collected using the Stellate Reviewer software program. The sleep segments were saved as text files from their digital recording in Stellate

Statistical Analysis

All statistical tests were performed using SPSS version 15.0.1 (SPSS Inc., Chicago, IL, USA). To investigate the effect of CPAP treatment by group, one-way ANOVA was performed. For categorical (qualitative) data, the c2 test was used to check the differences between the two groups. When the expected frequencies were less than 5, Fisher’s exact test was performed. For comparisons of two or more means, the analysis of variance (ANOVA) was performed. When a significant result was obtained in the ANOVA test, a post-hoc analysis (Scheffé’s test) was carried out to perform multiple comparisons. In all cases, statistical significance was defined as p < 0.05. A multivariate test was performed to test the effect of gender and obesity on weight was similar, they tended to have lower BMI, but the difference was not significant. Twenty subjects were obese (BMI > 30) and 6 had morbid obesity (BMI > 35).

Relationship between HR Parameters in OSA with CPAP Treatment

The primary aim of this study was to determine how HRV in OSA patients is affected after acute CPAP treatment, in a single night of treatment. First we compared heart rate mean (HRM) and HRV, considering all the patients and stages together. With these data, no significant differences were seen in the HRM when comparing the basal study to the CPAP study (p > 0.05). On the other hand, significant differences were seen when comparing HRV before and after CPAP treatment (p < 0.05). As expected, significant differences did occur when comparing the variation

Table 6. Analysis of the Data in Non-REM, REM and WAKE

between Male and Female Groups.

HRM: Heart Rate Mean. HRV: Heart Rate Variability. Var. SatO2: Variance of Oxygen Saturation. *Statistical significance.

obesity seen in the patient group. The lack of significant changes in HRV in REM after CPAP treatment could be explained by the REM interference theory in PNS activity. The clinical implica- tion of these results may suggest that patients who suffer from OSA with apneas occurring predominantly during REM sleep, may not enjoy the same cardiovascular benefits compared to OSA patients whose apneic episodes are scattered between REM and NREM. However, further studies are required to determine whether the unique properties of REM sleep influence autonomic function in patients with OSA.

The heart rate mean did not decrease significantly from NREM to REM during CPAP studies. This result is similar to previous studies in healthy individuals.24  The decrease HRV from NREM to REM was seen in basal studies, which suggests that OSA may influence the variance of the heart rate, but does not vary the natural change of overall beats per minute from NREM to REM. The lack of change in HRM during the CPAP study suggests that CPAP treatment lowers the variance of heart rate during NREM, as well as eliminates the change in the heart rate between NREM and REM.

Previous studies showed obese patients to have lower variations in total HRV.49  Our results also showed significant differences in HRV in obese patients during REM when com- pared to the non-obese group in both CPAP and basal studies. From these results, it seems plausible that CPAP treatment may improve HRV in obese patients, sufficiently so as to resemble the improved HRV seen in non-obese patients with CPAP treatment. In our study, another aim was to study the effects of obesity on CPAP treatment in severe OSA (AHI > 30) patients, as CPAP treatment has shown to lower night time blood pres- sure and increase SNS activity in OSA patients.50  The results from our study showed that obesity does not influence HRV or HRM during CPAP treatment when compared to non-obese patients. Based on these results, obesity does seem to influence heart rate mean in WAKE and REM, but not enough to be statistically significant. Therefore, from a clinical perspective, additional or differential forms of treatment do not seem neces- sary when combating ANS dysfunction in obese patients.

The final aim of our study was to determine the role of gender in HRV during short-term CPAP treatment of severe OSA (AHI > 30) patients, as women with breathing disorders have been shown to have increased SNS activity during NREM, and men with breathing disorders have been shown to have lower PNS activity during wake,51  and women with high AHI had low SNS activation during REM.52  Our results did show a difference in HRV between men and women in

wakefulness. In addition, HRM was different in all the sleep stages. Our results showed a significant difference in HRV and heart rate mean between our male and female groups during wake. However, the changes were similar in the basal and in the CPAP nights, which suggests that gender does not influence the improvements seen in ANS activity from CPAP treatment. Nevertheless, the absence of statistical significance when assessing the effects of gender and obesity on HRV may be a consequence of the small sample size of our study, which is one of its limitations.

The main limitation of our study is a consequence of its transversal nature. In these regard, there is a possibility that changes in HRV during acute CPAP treatment may reflect a normalization of the respiratory pattern or may be due to changes in venous return secondary to the dramatic changes of intrathoracic pressure that occur during the apneic event rather than changes in cardiovascular control mechanisms. Thus, caution must be used when analyzing our results, as the effect of OSA in autonomic activity may perhaps more likely to be detected by comparing HRV on the first night of treatment with a sleep study on CPAP after weeks of treatment, and not with a single-night study, such as the present one. We neither studied whether the changes in HRV were associated with the severity of OSA, as we only selected patients with an AHI > 30. Moreover, we do not provide data regarding the percentage of stage 2 and stage 3 sleep in the NREM segments, in spite of the fact that several studies show that ANS balance differs between these 2 stages. Finally, we did not study frequency- domain measures (i.e. HF, LF, and VLF); hence, further studies may be needed to understand our findings in depth.

Nonetheless, all these limitations do not hamper the fact that cardiac variability improves as an acute effect, indepen- dently of gender or weight, in the first night of CPAP use in severe OSA patients. Thus, we think that the CPAP treatment should not be delayed. Severe OSA patients should be advised that even a single night without CPAP has changes in the cardiac rate, which are corrected with CPAP. Hence, to use or not to use the CPAP for a single night does matter.

References

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17.   Tabata R, Yin M, Nakayama M, Ikeda M, Hata T, et al. (2008) A preliminary study on the influence of obstructive sleep apnea upon cumulative parasympathetic system activity. Auris Nasus Larynx 35: 242–246.

18.   Silva A, Andersen ML, De Mello MT, Bittencourt LR, Peruzzo D, et al. (2008) Gender and age differences in polysomnography findings and sleep complaints of patients referred to a sleep laboratory. BrazJ Med Biol Res 41: 1067–1075.

19.   Rajendra AU, Paul JK, Kannathal N, Lim CM, Suri JS (2006) Heart rate variability: a review. Med Biol Eng Comput 44: 1031–1051.

20.   Dumont M, Jurysta F, Lanquart JP, Noseda A, van de Borne P, et al. (2007) Scale-free dynamics of the synchronization between sleep  EEG  power  bands  and  the  high  frequency  component of heart rate variability in normal men and patients with sleep apnea-hypopnea syndrome. Clin Neurophysiol 118: 2752–2764.

21.   Penzel T, Kantelhardt JW, Lo CC, Voigt K, Vogelmeier C (2003) Dynamics of heart rate and sleep stages in normals and patients with sleep apnea. Neuropsychopharmacology 28 Suppl 1: S48–53.

22.  Penzel T, Kantelhardt JW, Grote L, Peter JH, Bunde A (2003) Comparison of detrended fluctuation analysis and spectral analysis for heart rate variability in sleep and sleep apnea. IEEE Trans Biomed Eng 50: 1143–1151.

23.   Halasz P, Terzano M, Parrino L, Bodizs R (2004) The nature of arousal in sleep. J Sleep Res 13: 1–23.

24.   Jurysta F, van de Borne P, Migeotte PF, Dumont M, Lanquart JP, et al. (2003) A study of the dynamic interactions between sleep EEG and heart rate variability in healthy young men. Clin Neuro-physiol 114: 2146–2155.

25.   Aytemir K, Deniz A, Yavuz B, Ugur DA, Sahiner L, et al. (2007) Increased  myocardial  vulnerability  and  autonomic  nervous system imbalance in obstructive sleep apnea syndrome. Respir Med 101: 1277–1282.

26.   Baumert M, Smith J, Catcheside P, McEvoy RD, Abbott D, et al. (2008) Variability of QT interval duration in obstructive sleep apnea: an indicator of disease severity. Sleep 31: 959–966.

27.   Park DH, Shin CJ, Hong SC, Yu J, Ryu SH, et al. (2008) Correlation between the severity of obstructive sleep apnea and heart rate variability indices. J Korean Med Sci 23: 226–231.

28.  Penzel T (2003) Is heart rate variability the simple solution to diagnose sleep apnea? Eur Respir J 22: 870–871.

29.  Roche F, Celle S, Pichot V, Barthelemy JC, Sforza E (2007) Analysis of the interbeat interval increment to detect obstructive sleep apnea/hypopnea. Eur Respir J 29: 1206–1211.

30.   Roche F, Xuong AN, Court-Fortune, Costes F, Pichot V, et al. (2003) Relationship among the severity of sleep apnea syndrome, cardiac  arrhythmias,  and  autonomic  imbalance.  Pacing  Clin Electrophysiol 26: 669–677.

31.  Burr RL (2007) Interpretation of normalized spectral heart rate vari- ability indices in sleep research: a critical review. Sleep 30: 913–919.

32.   Frazier SK, Moser DK, Stone KS (2001) Heart rate variability and hemodynamic alterations in canines with normal cardiac function during exposure to pressure support, continuous positive airway pressure, and a combination of pressure support and continuous positive airway pressure. Biol Res Nurs 2: 167–174.

33.   Gates GJ, Mateika SE, Mateika JH (2005) Heart rate variability in non-apneic snorers and controls before and after continuous positive airway pressure. BMC Pulm Med 5: 9.

34.   Dursunoglu D, Dursunoglu N (2006) Cardiovascular diseases in obstructive sleep apnea. Tuberk Toraks 54: 382–396.

35.   Gilman MP, Floras JS, Usui K, Kaneko Y, Leung RS, et al. (2008) Continuous positive airway pressure increases heart rate variability in heart failure patients with obstructive sleep apnea. Clin Sci (Lond) 114: 243–249.

36. Limphanudom P, Chierakul N, Pinyopattarakul N, Nana A, Naruman C, et al. (2007) Recovery of heart rate variability in patients with moderate to severe obstructive sleep apnea after 6-month continuous positive airway pressure treatment. J Med Assoc Thai 90: 1530-1535.

37.   Mayer J, Becker H, Brandenburg U, Penzel T, Peter JH, et al. (2001) Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. Cardiology 79: 84–92.

38.   Chrysostomakis  SI,  Simantirakis  EN,  Schiza  SE,  Karalis  IK, Klapsinos NC, et al. (2006) Continuous positive airway pressure therapy lowers vagal tone in patients with obstructive sleep apnea-hypopnea syndrome. Hellenic J Cardiol 47: 13–20.

39.  Kasai T, Narui K, Dohi T, Yanagisawa N, Ishiwata S, et al. (2008) Prognosis of patients with heart failure and obstructive sleep apnea treated with continuous positive airway pressure. Chest 133: 690–696.

40.  Dursunoglu D, Dursunoglu N (2007) Effect of CPAP on QT interval dispersion in obstructive sleep apnea patients without hypertension. Sleep Med 8: 478–483.

41.   Patruno V, Aiolfi S, Costantino G, Murgia R, Selmi C, et al. (2007) Fixed  and  autoadjusting  continuous  positive  airway  pressure treatments are not similar in reducing cardiovascular risk factors in patients with obstructive sleep apnea. Chest 131: 1393–1399.

42.  Antczak J, Horn B, Richter A, Jernajczyk W, Bodenschatz R, et al. (2008) The influence of obesity on sleep quality in male sleep apnea patients before and during therapy. J Physiol Pharmacol 59: 123–1234.

43.   Lin CM, Davidson TM, Ancoli-Israel S (2008) Gender differences in obstructive sleep apnea and treatment implications. Sleep Med Rev 12: 481–496.

44.  Sztajzel J, Jung M, Bayes de Luna A (2008) Reproducibility and gen-der-related differences of heart rate variability during all-day activity in young men and women. Ann Noninvasive Electrocardiol 13: 270–277.

45.  Ye L, Pien GW, Weaver TE (2009) Gender differences in the clinical manifestation of obstructive sleep apnea. Sleep Med 10: 1075–1084.

46.   AASM (2005) The International Classification of Sleep Disorders 2nd ed.: Diagnostic and Coding Manual American Academy of Sleep Medicine, Westchester.

47.  Hoffstein V, Mateika S (1994) Predicting nasal continuous positive airway pressure. Am J Respir Crit Care Med 150: 486–488. 48.   Dursunoglu  N,  Dursunoglu  D,  Cuhadaroglu  C,  Kilicaslan  Z (2005)  Acute  effects  of  automated  continuous  positive  airway pressure on blood pressure in patients with sleep apnea and hypertension. Respiration 72: 150–155.

49.   Reynolds EB, Seda G, Ware JC, Vinik AI, Risk MR, et al. (2007) Autonomic  function  in  sleep  apnea  patients:  increased  heart rate variability except during REM sleep in obese patients. Sleep Breath 11: 53–60.

50.   Ferland A, Poirier P, Series F (2009) Sibutramine versus CPAP in the treatment of obese patients with obstructive sleep apnea. Eur Respir J 34: 694–701.

51.   Wang W, Tretriluxana S, Redline S, Surovec S, Gottlieb DJ, et al. (2008) Association of cardiac autonomic function measures with severity  of  sleep-disordered  breathing  in  a  community-based sample. J Sleep Res 17: 251–262.

52.  Kesek M, Franklin KA, Sahlin C, Lindberg E (2009) Heart rate variability during sleep and sleep apnea in a population based study of 387 women. Clin Physiol Funct Imaging 29: 309–315.

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SAN JOSE, Calif., Ventus Medical announces that their Theravent Advanced Nightly Snore Therapy has received the prestigious Spark Award.  Theravent won silver in the 2012 Spark competition for Product Design. The Spark Awards reward innovative design that helps humanity or the environment we live in. The mission of the award is to promote better living through better design.

“The Theravent product is already helping a lot of couples get a better night’s sleep,” says Peter Wyles, CEO and President of Ventus Medical.  “Ventus worked with LUNAR on developing the very innovative Theravent product and we were able to create an elegant design that gives people an easy to use solution to effectively treat their snoring.  This is an important accomplishment in a market where 45 million people snore and their bed partners suffer.”

“We are thrilled to see Theravent win this recognition,” said John Edson, LUNAR’s president.  “This simple, ingenious product is the most recent result of a lot of hard work and an amazing collaboration between the teams at Ventus and LUNAR. Even more satisfying than the award is seeing these products help a lot of people.”

Theravent is a unique, disposable nightly snoring device that is FDA-cleared to reduce or eliminate snoring.  It has been proven to reduce snoring in clinical studies and is available without a prescription.  On average, successful Theravent users reduced snoring by 76%, as measured using a decibel meter worn on the forehead. Theravent uses the same patented MicroValve Technology that was previously only available with a prescription.

It is available exclusively on-line at http://www.theravent.com

Source: Ventus Medical

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A new analysis backs up what sleep doctors have known for a long time—sleep disorders should be addressed first if companies want to boost productivity.

Are ubiquitous corporate wellness programs focusing on the wrong health problems? If the goal is to avoid sick days and lost productivity, the answer may be yes.

Wellness programs are a staple of American corporations, but a new analysis from a global human resources (HR) firm concludes that sleep disorders should be at the top of the list of health concerns. Using data from sources new and old, analysts listed the top 15 drivers of lost work time. Sleep disorders topped the list.

The remaining top 14 drivers were: depression; fatigue; back/neck; anxiety; hypertension; other emotional; arthritis; obesity; chronic pain; headache; irritable bowel; high cholesterol; heart disease; and allergies. As it happens, OSA increases the risk of developing heart disease, hypertension, stroke, diabetes, and even obesity according to some studies—that’s another four of the 15 drivers.

The new study obtained by Sleep Diagnosis and Therapy (but not yet ready for official release), reiterates that obstructive sleep apnea (OSA) impacts one in 12 employees, yet 85% remain undiagnosed. Employers incur an estimated $3,200 to $4,000 in incremental annual health care spending for employees with unmanaged OSA.

For corporations, the numbers are powerful evidence that the time may be right to retool wellness programs to focus on sleep problems. Such a switch could yield considerable bang for the buck.

Various HR companies could fill this demand by taking over ineffective wellness programs and working with select manufacturers. Who will these manufacturers be? The good news for corporations looking for better options for employees is that treatment options are more diverse than ever.

Retooling is already happening in some quarters, with sleep entities partnering to offer employers a program focused solely on sleep health. The solution incorporates early identification and intervention to deliver medical cost savings while improving employee productivity and quality of life. The good news for persons needing treatment is that there is a diverse range of treatment options. Beyond the gold standard of CPAP, sleep physicians are increasingly recommending dental sleep appliances and expiratory positive air pressure (EPAP).

Source: Greg Thompson, Staff Writer

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Life can be hard for people who suffer from Obstructive Sleep Apnea (OSA), especially those who want an active lifestyle or whose lives depend on being active and getting a good night of sleep. Peter Rowe is one of those people and he recently took the portable Transcend CPAP, rechargeable battery and solar battery charger with him on a trek towards Mount Everest in the Himalayas.  Rowe shared his experience with the Transcend CPAP in a YouTube video explaining how easy and convenient it was to use Transcend, even at 16,000 feet elevation. (visit http://www.youtube.com/watch?v=0opX3jjXAhw&feature=share)

Peter Rowe is a world-renowned filmmaker, director, actor and adventurer known for his work in exploration and adventure around the world. His recent work includes producing the 39-part television series Angry Planet, which airs worldwide.

Sleep apnea sufferers around the world who use continuous positive airway pressure (CPAP) therapy are finding that portability of their CPAP machine is an important factor in getting a good night’s sleep and enjoying an active lifestyle. But, most CPAPs are not portable nor are they designed for an active lifestyle. Only Transcend^®, the innovation leader in sleep apnea therapy, brings reliable CPAP therapy where power is limited or not available. Its flexibility and portability provide on-the-go CPAP users with therapy no matter whether they are a mountain climber, over-the-road trucker, boating enthusiast, camper or business traveler.

Source: www.mytranscend.com

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Dublin, Ireland – Jazz Pharmaceuticals plc (Nasdaq: JAZZ) today announced financial results for the third quarter ended September 30, 2012.  These results reflect the first full quarter of operations following completion of the EUSA Pharma acquisition in June.  The company also reported the results of its women’s health business, which was sold in October, as discontinued operations.

“During the third quarter, we completed the integration of EUSA Pharma’s U.S. commercial business, and our R&D group is working to coordinate worldwide Erwinaze^® and Asparec^® development activities,” said Bruce Cozadd, chairman and chief executive officer of Jazz Pharmaceuticals.  “I am very pleased that we have been able to complete two important acquisitions and a divestiture of our non-core women’s health business this year, while continuing to deliver solid results fueled by growing sales of key products.”

Third quarter 2012 adjusted income from continuing operations, which excluded contributions from the discontinued women’s health business, was $78.6 million, or $1.29 per diluted share.  Adjusted income for the discontinued women’s health business was $3.0 million, or $0.05 per diluted share, for a total of $1.34 per share on a combined basis.

GAAP income from continuing operations for the third quarter of 2012 was $33.6 million, or $0.56 per diluted share, and GAAP loss from the discontinued women’s health business was $0.4 million, or$0.01 per diluted share.  GAAP net income for the third quarter of 2012 was $33.2 million, or $0.55 per diluted share.

GAAP net income was impacted by various acquisition-related expenses, which included transaction, integration and restructuring expenses, as well as certain non-cash expenses.  A reconciliation of certain GAAP to non-GAAP adjusted information is included with this press release.

Source: Jazz Pharmaceuticals

Click here to read full announcement

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