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Distribution of body mass index (BMI) in patients.

Distribution of body mass index (BMI) in patients.

Table 1. 
Characteristics of the Analyzed Subjects*
Characteristics of the Analyzed Subjects*
Table 2. 
Diagnosis and Treatment of the 400 Analyzed Patients*
Diagnosis and Treatment of the 400 Analyzed Patients*
Table 3. 
Cause of Death Among Patients With Rhonchopathy*
Cause of Death Among Patients With Rhonchopathy*
1.
Koskenvuo  MKaprio  JTelakivi  TPartinen  MHeikkilä  KSarna  S Snoring as a risk factor for ischemic heart disease and stroke in men. Br Med J (Clin Res Ed). 1987;294643Article
2.
Hung  JWhitford  EGParson  RWHillman  DR Association of sleep apnea with myocardial infarction in men. Lancet. 1990;336261- 264Article
3.
Hoffstein  VRubinstein  IMateika  SSlutsky  AS Determinants of blood pressure in snorers. Lancet. 1988;2992- 994Article
4.
Partinen  MJamieson  AGuilleminault  C  et al.  Long-term outcome for obstructive sleep apnea syndrome patients. Chest. 1988;941200- 1204Article
5.
Partinen  MGuilleminault  C Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest. 1990;9727- 32Article
6.
He  JKryger  MHZorick  FJConway  WRoth  T Mortality and apnea index in obstructive sleep apnea. Chest. 1988;949- 14Article
7.
Lindberg  EJanson  CSvärdsudd  KGislason  THetta  JBoman  G Increased mortality among sleepy snorers: a prospective population based study. Thorax. 1998;53631- 637Article
8.
Gonzales-Rothi  RForesman  GEBlock  AJ Do patients with sleep apnea die in their sleep? Chest. 1988;94531- 538Article
9.
Fujita  SConway  WZorick  F  et al.  Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg. 1981;89923- 934
10.
Haraldsson  POBredbacka  S Laser-uvulopalatoplasty (LUPP) under local anesthesia: effective, safe and comfortable. ORL J Otorhinolaryngol Relat Spec. 1996;5899- 104Article
11.
Kamami  YV Laser CO2 for snoring: preliminary results. Acta Otorhinolaryngol Belg. 1990;44451- 456
12.
Larsson  HCarlsson-Nordlander  BSvanborg  E Four-year follow-up after UPPP in 50 unselected patients with obstructive sleep apnea syndrome. Laryngoscope. 1994;1041362- 1368Article
13.
Haraldsson  P-OCarenfelt  CKnutsson  EPersson  HERinder  J Validity of symptom analysis and daytime polysomnography in diagnosis of sleep apnea. Sleep. 1992;15261- 263
14.
Guilleminault  CStoohs  RDuncan  S A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104781- 787Article
15.
Fujita  S Pharyngeal surgery of obstructive sleep apnea and snoring. Fairbanks  DFujita  SIkematsu  TSimmons  Beds.Snoring and Obstructive Sleep Apnea. New York, NY Raven Press1987;101- 128
16.
Powell  NRiley  RGuilleminault  C Maxillofacial surgery for obstructive sleep apnea. Guilleminault  CPartinen  MedsObstructive Sleep Apnea Syndrome Clinical Research and Treatment. New York, NY Raven Press1990;153- 182
17.
Parmar  MMachin  D Log-rank test. Survival Analysis A Practical Approach. Chichester, England John Wiley & Sons Inc1995;66- 75
18.
Hakulinen  TAbeywickrama  K A computor program package for relative survival analysis. Comput Programs Biomed. 1985;19197- 207Article
19.
Ederer  FAxtell  LMCutler  SJ The relative survival rate: a statistical methodology. NCI Monogr. 1961;6101- 121
20.
Not Available, Report of a Joint FAO/WHO UNU Expert Consultation.  Geneva, Switzerland World Health Organization1985;Technical Report Series No. 724.
21.
Keenan  SBurt  HRyan  FFleetham  MB Long-term survival of patients with obstructive sleep apnea treated by uvulopalatopharyngoplasty or nasal CPAP. Chest. 1994;105155- 159Article
22.
Svanborg  ELysdahl  MHaraldsson  P-O Validation of the Apnolog system: digitized portable recordings for diagnosis of obstructive sleep apnea [abstract]. Sleep Res. 1995;24A490
23.
Lavie  PHerer  PPeled  R  et al.  Mortality in sleep apnea patients: a multivariate analysis of risk factors. Sleep. 1995;18149- 157
24.
Socialstyrelsen, Folkhälsorapport 1994.  Stockholm, Sweden Socialstyrelsen1994;51- 56
25.
Kuskowska-Wolk  ARössner  S Det vägar allt tyngre att vara svensk. Läkartidningen. 1992;892282- 2284
26.
Young  TPalta  MDempsey  JSkatrud  JWeber  SBadr  S The occurrence of disordered breathing among middle-aged adults. N Engl J Med. 1993;3281230- 1235Article
27.
Lavie  P Incidence of sleep apnea in a presumably healthy working population: a significant relationship with excessive daytime sleepiness. Sleep. 1983;6312- 318
28.
Sjöström  LV Mortality of severe obese subjects. Am J Clin Nutr. 1992;55(2 suppl)516S- 523S
29.
Rössner  SLagerstrand  LPersson  HESachs  C The sleep apnea syndrome in obesity: risk of sudden death. J Intern Med. 1991;230135- 142Article
Original Article
September 2000

Long-term Survival After Uvulopalatopharyngoplasty in Nonobese Heavy SnorersA 5- to 9-Year Follow-up of 400 Consecutive Patients

Author Affiliations

From the Respiratory Unit, Division of Anaesthesia and Intensive Care, Danderyd Hospital, Danderyd (Dr Lysdahl), and the Department of Otorhinolaryngology Head & Neck Surgery, Karolinska Hospital, Stockholm (Dr Haraldsson), Sweden.

Arch Otolaryngol Head Neck Surg. 2000;126(9):1136-1140. doi:10.1001/archotol.126.9.1136
Abstract

Background  Heavy snoring and the obstructive sleep apnea syndrome are associated with increased morbidity and mortality in patients with cardiovascular disease. The effect of uvulopalatopharyngoplasty on mortality has been questioned.

Objective  To investigate long-term survival after palatal surgery.

Design  An observational retrospective case-control study with a 5- to 9-year follow-up.

Setting  A university medical center.

Patients  Four hundred consecutive heavy snorers (median age, 47 years), 256 of whom had obstructive sleep apnea syndrome. The mean ± SD body mass index (calculated as weight in kilograms divided by the square of height in meters) of all included patients was 27.1 ± 4.2. Comparison was made with 744 control patients (median age, 43 years) who underwent nasal surgery during the same period and a matched general control population.

Intervention  Uvulopalatopharyngoplasty or laser uvulopalatoplasty between 1986 and 1990.

Main Outcome Measures  Mortality and causes of death up to 9 years after surgery.

Results  High blood pressure at the time of surgery and subsequent death due to cardiovascular disease were 3 times more frequent in the patients with obstructive sleep apnea syndrome than in both control groups (P<.01), but the overall long-term mortality was not increased either in snorers or in persons with sleep apnea. The cumulative survival rate was more than 96% for the 400 patients, the 744 controls, and the matched general population.

Conclusions  No increased mortality was seen following palatal surgery in this long-term follow-up of 400 consecutive, on average, nonobese snorers, 256 of whom had obstructive sleep apnea syndrome. This might indicate a positive survival effect of surgery.

SNORERS' DISEASE—Rhonchopathy—with or without sleep apnea is a sign of intermittent upper airway obstruction during sleep. Epidemiological studies13 have indicated that snoring and sleep apnea are associated with hypertension and cardiovascular morbidity.13 Furthermore, obstructive sleep apnea syndrome (OSAS) has been reported to be a potentially lethal condition,4,5 especially in men younger than 50 years.6 Partinen et al4,5 found an increased death rate in conservatively treated obese patients with OSAS, when compared with those even more obese who were treated with tracheotomy only. He et al,6 without considering body mass index (BMI; calculated as weight in kilograms divided by the square of height in meters) as a confounding factor, reported that an apnea index (AI) above 20 significantly increased the mortality risk as early as 2 years following diagnosis. In a recent large Swedish prospective population study, Lindberg et al7 found a significant increased mortality among men younger than 60 years who were snorers and had excessive daytime sleepiness (EDS), even after adjustment for BMI, compared with those reporting snoring only. Gonzales-Rothi et al,8 although in a limited sample, found no difference in death rates between heavy snorers and patients with OSAS after 8 years of observation.

Uvulopalatopharyngoplasty (UPPP)9 and palatal laser surgery, like laser uvulopalatoplasty (LUPP)10 or laser-assisted uvulopalatoplasty,11 are the most common surgical treatment modalities for rhonchopathy, for patients with or without OSAS. A decade ago, UPPP fell into disrepute due to poor long-term survival data in the widely referred study by He et al.6 The conclusion was that UPPP did not affect the increased long-term mortality found in untreated patients with an AI of greater than 20. Surgery had, however, been performed on extremely obese patients (mean ± SD BMI, 36.5 ± 7.4) who had severe sleep apnea (mean ± SD AI, 60.0 ± 24.9); both conditions are regarded as contraindications to UPPP.12 Moreover, of the 8 patients who died after UPPP, UPPP was known to have failed in 2, and these 2 were not subsequently treated with continuous positive airway pressure (CPAP) or tracheotomy, and 6 were not restudied. Even patients in other North American mortality studies4,5,8 have shown a degree of obesity far in excess of that seen in the average Scandinavian patient with OSAS.

This study, therefore, ascertains whether increased mortality is still present after palatal surgery in a mainly nonobese patient population and to what extent death is related to cardiovascular disease.

SUBJECTS AND METHODS
SUBJECTS

All adult patients treated for rhonchopathy between February 1986 and March 1990 at the Department of Otorhinolaryngology, Karolinska Hospital, Stockholm, Sweden, were included.

To account for complete consecutive patient material, even patients primarily undergoing CPAP treatment before March 1990 or undergoing CPAP as a secondary treatment during this period were registered.

Control group 1 consisted of patients older than 30 years who underwent nasal surgery between January 1986 and October 1990, because of nasal obstruction. Those who underwent palatal surgery during the control period, because of rhonchopathy, were excluded.

Control group 2 was a sex- and age-matched general population collected from the Cancer Epidemiological Institute in cooperation with Statistics Sweden, both located in Stockholm. It reflected the expected survival of each specific individual.

The survival of patients and controls was followed up to a definite end point of the study, February 6, 1995. Subjects no longer living in Sweden were excluded to avoid inaccurate data.

DIAGNOSIS AND DEFINITIONS

All patients scored their symptoms in a validated self-report questionnaire.13 The questions concerned presence of snoring, daytime sleepiness, involuntary sleep attacks, midsleep awakenings, and breath cessations. Based on this, the patients were classified as having social rhonchopathy if they were nonsleepy snorers. Patients who reported disturbing, habitual snoring (often to always) in combination with EDS were classified as having medical rhonchopathy. These patients were subjected to sleep studies. If this study showed an apnea-hypopnea index or an oxygen desaturation index above 5, the patient was diagnosed as having OSAS. The remaining patients were sleepy snorers clinically diagnosed as having upper airway resistance syndrome.14

PREOPERATIVE EXAMINATION

All patients were subjected to a thorough review of their medical record; a standard preoperative ear, nose, and throat examination; and, in selected patients, cephalometry and fiberoptic rhinolaryngoscopy during voluntary snoring, including the Mueller maneuver. The level of obstruction was classified according to Fujita.15 Treatment for hypertension, if any, was recorded, and so were height and weight for the calculation of the BMI. The types of sleep studies used differed from various screening modalities, including daytime nap polysomnography (without pulse oximetry) after one night of sleep deprivation13 to full-night polysomnography monitoring electroencephalography, electro-oculography, submental electromyography, respiratory effort, nose or mouth airflow, and pulse oximetry. A minimum requirement for sleepy patients, however, was pulse oximetry for qualitative testing.

PATIENT SELECTION FOR SURGERY AND CPAP

The decision whether to perform surgery or not was based on the following criteria. Patients with a level of obstruction classified as Fujita 1 (soft palatal and tonsillar hypertrophy) were treated by UPPP, whereas patients classified as Fujita 2a (lax palates only) were treated by LUPP.10 The LUPP technique, introduced at the Karolinska Hospital by Carenfelt and Haraldsson in 198610, is, unlike the later-invented laser-assisted uvulopalatoplasty,11 a one-stage laser procedure. It involves resection of the obstructing lax palate and is performed as an outpatient procedure using local anesthesia. Patients with symptomatic deviation of the nasal septum were subjected to septoplasty to improve nasal patency.

Heavily obese patients (BMI >34), patients with tongue base obstruction (Fujita 2b or 3), and patients with severe sleep apnea syndrome (oxygen desaturation index or apnea-hypopnea index >40 and arterial oxygen saturation nadir <80%) were offered CPAP treatment.

If patients refused CPAP, UPPP was performed anyway to reduce upper airway resistance; in 4 patients, it was complemented with tongue suspension using inferior sagittal osteotomies of the mandible.16 Patients were then referred to weight loss programs.

Patients who did not respond immediately to surgery or who had a relapse of snoring and daytime sleepiness before the end point of the study were offered a CPAP trial, irrespective of BMI and sleep recording results.

MORTALITY

The Swedish Personal Register is based on a specific personal code number given to each citizen at birth. It contained addresses and information concerning patients and controls in group 1 at the study end point; it contained data on those who were still alive and on those who had died. The Swedish Death Register supplied copies of death certificates, stating the cause of death.

STATISTICS

A life table was used. The starting point was the day of surgery, and the unambiguous end point was the day of death. The patients were observed for different lengths, and the end point for survivors was unknown at study termination. The mortality risk rates for patients and controls were compared using the log-rank test, based on the life tables' accounted for censored observations.17 We calculated the 9-year survival chance for all subjects and the cumulative probability of surviving the whole observation time using confidence intervals. For comparison of causes of death between patients and control group 1, the Fisher exact test was used. For comparison of hypertension treatment between patients with OSAS and patients without apnea, the χ2 test was used. P<.05 was considered significant.

Relative survival was analyzed using a computer program designed for cancer survival studies.18 The relative survival rate is defined as the ratio of the observed survival in the studied group to the expected survival in a comparable general population (control group 2), taking into account population, age, sex, and time.19 Statistics Sweden provided data on expected survival probabilities for the general Swedish population.

RESULTS
SUBJECTS AND THEIR CHARACTERISTICS

The demographic data of patients and control group 1 are given in Table 1 and in Figure 1.

Four hundred twenty-six consecutive patients were treated. Seventeen were treated with CPAP primarily or secondarily and were all excluded, as were the 9 patients who had emigrated.

Sixty of the 400 analyzed patients were diagnosed as being nonsleepy snorers (ie, having social rhonchopathy) (Table 2). Twenty-three (38%) were women. The remaining 340 patients were diagnosed as having medical rhonchopathy, of whom 256 were classified as having OSAS. Sixty-nine (27%) of the patients with OSAS had a BMI greater than 30 and were considered obese (Figure 1).20 The mean age of the 400 patients at the time of their first operation was 47.5 years (range, 18-75 years). Thirteen were younger than 30 years. Sixty-three (16%) were women (mean age, 47.2 years; range, 24-74 years). Twenty patients, primarily subjected to LUPP, underwent another operation with UPPP or LUPP up to March 1990, but they were included in the study from the first surgical procedure. Ten percent of the patients underwent additional septoplasty.

Control group 1 comprised 744 patients (mean age, 45.1 years; range, 30-71 years) with nasal obstruction, who had been subjected to nasal surgery such as septorhinoplasty, turbinectomy, or polypectomy but who had never been treated with palatal surgery.

MORBIDITY AND MORTALITY

Treatment for hypertensive blood pressure was found almost 3 times more frequently in the patients with OSAS compared with the nonapneic patients (28.1% vs 9.7%; P<.001).

Thirteen (3.3%) of the 400 analyzed patients died during a cumulative period of 9 years, as did 29 (3.9%) of the 744 controls. The mean ± SD age at the time of death was 58.5 ± 8.1 years for the patients and 59.8 ± 11.6 years for the controls. The mean ± SD BMI of the patients at the time of death was 27.6 ± 4.0. The cause of death among patients is given in Table 3. Six (46%) of the 13 deceased patients died of cerebral and cardiovascular disease, including one with organic heart disease. All 6 had OSAS. Three of the 17 patients (mean BMI, 30.1) receiving CPAP died during the control period, 2 of cardiovascular disease.

Among group 1 controls, the cause of death could be obtained in 27 of 29 cases. The death certificate could not be located for one case, while the other had not been discovered until putrefaction had set in. Five (18.5%) of the 27 died of vascular disease.

The 95% confidence interval for the probability of the patients dying within the 9-year observation period was 3.3% ± 1.7%; for control group 1, 3.9% ± 1.4%.

There was no difference in relative mortality for all patients (13 of 400) (P =.77), those diagnosed as having OSAS (10 of 256) (P =.99), sleepy snorers (2 of 84) (P =.85), or nonsleepy snorers (1 of 60) (P =.66), compared with control group 1 (29 of 744), irrespective of surgical method used (all P values obtained using the log-rank test). The cumulative 9-year survival for patients and control group 1 was more than 96%, even though the relative risk of dying of vascular disease was increased 3-fold in patients with OSAS (6 of 10 patients) compared with control group 1 (5 of 27 controls) (P<.01).

COMMENT

Few earlier studies exist dealing with long-term mortality after palatal surgery for patients with OSAS, and the samples have so far been limited. Keenan et al21 included 149 patients with a mean ± SD BMI of 30 ± 5 who were treated with UPPP in an up to 6-year follow-up, while He et al6 included 60 UPPP-treated patients with a mean ± SD BMI of 36.5 ± 7.4 in an 8-year follow-up. To our knowledge, no such study concerning nonobese patients has been performed.

Although the rate of hypertension and cardiovascular disease–related death was increased among patients, the present investigation did not indicate any increased mortality of the 400 surgically treated patients when compared with a sex- and age-matched general Swedish population. Also, control group 1, operated on for nasal obstruction, had a similar mortality rate. These controls lived in an environment similar to the patients and were, therefore, valid for comparison for causes of death.

Patients who underwent UPPP and LUPP had a similar BMI and showed no difference in mortality. Laser uvulopalatoplasty was used on patients obstructed by lax palates only, a common finding in the nonobese, which explains why most patients were treated by this procedure.

Only a few patients were treated for heavy snoring alone. More than 85% combined heavy snoring with EDS. The OSAS diagnosis was based on clinical findings,13 but then confirmed by sleep studies measuring either the apnea-hypopnea index or the oxygen desaturation index.

Over time, the sleep respiratory diagnostic recordings in our department varied and data are, therefore, not immediately comparable.13,22 The overall results of this study showed, however, that most of our patients with OSAS had moderate obstructive sleep apnea (index values around 30-40). Desaturation below 85% of arterial oxygen saturation was uncommon.

Lindberg et al7 have, in a recently published 10-year prospective study on 3100 male subjects in Uppsala, Sweden, investigated self-reported symptoms related to OSAS and long-term mortality. They showed that nonsnoring subjects complaining of EDS and simple snorers did not have any increased mortality. Sleepy snorers, on the contrary, displayed a significant increase in overall mortality, decreasing after age 50 years and disappearing after age 60 years, even when adjusting for BMI, reported hypertension, cardiac disease, and diabetes. This study was performed in a city only 70 km from Stockholm and the subjects were nonobese and are, therefore, comparable to patients in the present study. Partinen and Guilleminault5 and Lavie et al23 found increased cardiovascular disease–related mortality among untreated patients with OSAS but could not find any correlation to the AI. Excessive daytime sleepiness, on the other hand, is not only an important clinical symptom but also appears to have an impact on mortality among snorers.7

In the Stockholm region, cardiovascular disease is the most common cause of death among the middle aged, followed by malignant neoplasms and trauma or suicide.24 Because of the unique citizen code number system in Sweden, it was possible to investigate all subjects in a national database with no loss to follow-up. Moreover, the cause of death could be stated for all the 42 deceased patients and controls (except for 2 cases as previously described). Cardiovascular disease was found to have caused death in 6 (60%) of the 10 deceased patients with OSAS (Table 3). In contrast, only 5 (19%) of the 27 controls died of vascular disease (P<.01). Partinen and Guilleminault5 and Lavie et al23 demonstrated similar vascular death rates in patients with OSAS. Most (5 of 6) of the patients dying from vascular disease had hypertension, a risk factor related to BMI and sleep apnea but not clearly to simple snoring.3 This may explain the predominance of vascular disease–related death among patients with OSAS.

Continuous positive airway pressure treatment was uncommon in Sweden in the mid-1980s. Therefore, it was initially offered to and accepted by a limited number of patients. This situation, however, appears to have been of limited importance for the mortality in this study as there was, nevertheless, no increased mortality among the patients with OSAS even though the decision to give complementary treatment with CPAP was not based on sleep study results but on the clinical outcome alone. In contradiction to other studies, an increased death rate was seen among those treated with CPAP (3 of 17 patients). All had severe OSAS and cardiovascular disease at the time of initial treatment. The few subjects do not, however, allow any conclusion.

The patients included in the present study had a mean BMI of 27.1, which is not substantially different from the average BMI of the general Swedish male population (mean ± SD, 24.4 ± 3.2).25 Only 15 (3.8%) of the 400 patients had a BMI exceeding 36 (Figure 1), the figure given as a mean for those 60 patients treated by UPPP in the study by He et al.6 North American studies46,8,21 indicate that most patients with OSAS are obese, whereas the present study, probably representative for most Scandinavian patients with OSAS, shows a much slimmer patient population. A conclusion to be drawn from the present and the referred studies is that investigations performed on populations of patients with OSAS with a mean excessive BMI may not be representative for a more weightwise normal population and are, therefore, not valid worldwide. That the reported prevalence of OSAS is about 4-fold in a working population of the United States compared with one of Israel26,27 further stresses this point.

Obesity contributes to upper airway obstruction, hypertension, and cardiovascular disease. Obesity itself has been reported to be a major mortality risk factor,28 influencing mortality far more than the AI.23 The combination of extreme obesity and OSAS, however, is a significant risk factor for sudden cardiovascular death, even in the absence of other conventional risk factors.29

The predominance of heavily obese patients with severe sleep apnea in the studies by Partinen et al4,5 and in that by He et al6 may also explain the high mortality rate found in conservatively treated patients. Not less than 17% of those 127 patients with OSAS who were conservatively treated by recommended weight loss died within 7 years.5 In contrast, only 2.8% of the 71 patients with OSAS who underwent tracheotomy died during the same period, figures similar to our controls and nonobese patients with OSAS treated with palatal surgery.

The beneficial effect of tracheotomy and CPAP treatment in these obese subjects with OSAS46 indicates that the abolishing of upper airway obstruction may eradicate the apparent synergistic effect on morbidity of obesity and sleep apnea.

In conclusion, the present study did not disclose any increased mortality at long-term follow-up after palatal surgery. With respect to the findings by Lindberg et al,7 this indicates that palatal surgery might have a positive effect on long-term mortality in nonobese sleepy snorers with or without OSAS.

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Article Information

Accepted for publication April 11, 2000.

We thank Ulf Brodin, Margareta Krook-Brandt, and Bo Nilsson for their valuable statistical support, and Eva Svanborg, MD, PhD, for revising the manuscript.

Reprints: Michael Lysdahl, MD, Respiratory Unit, Division of Anaesthesia and Intensive Care, Danderyd Hospital, S182,88 Danderyd, Sweden (e-mail: michael.lysdahl@ane.ds.sll.se).

References
1.
Koskenvuo  MKaprio  JTelakivi  TPartinen  MHeikkilä  KSarna  S Snoring as a risk factor for ischemic heart disease and stroke in men. Br Med J (Clin Res Ed). 1987;294643Article
2.
Hung  JWhitford  EGParson  RWHillman  DR Association of sleep apnea with myocardial infarction in men. Lancet. 1990;336261- 264Article
3.
Hoffstein  VRubinstein  IMateika  SSlutsky  AS Determinants of blood pressure in snorers. Lancet. 1988;2992- 994Article
4.
Partinen  MJamieson  AGuilleminault  C  et al.  Long-term outcome for obstructive sleep apnea syndrome patients. Chest. 1988;941200- 1204Article
5.
Partinen  MGuilleminault  C Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest. 1990;9727- 32Article
6.
He  JKryger  MHZorick  FJConway  WRoth  T Mortality and apnea index in obstructive sleep apnea. Chest. 1988;949- 14Article
7.
Lindberg  EJanson  CSvärdsudd  KGislason  THetta  JBoman  G Increased mortality among sleepy snorers: a prospective population based study. Thorax. 1998;53631- 637Article
8.
Gonzales-Rothi  RForesman  GEBlock  AJ Do patients with sleep apnea die in their sleep? Chest. 1988;94531- 538Article
9.
Fujita  SConway  WZorick  F  et al.  Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg. 1981;89923- 934
10.
Haraldsson  POBredbacka  S Laser-uvulopalatoplasty (LUPP) under local anesthesia: effective, safe and comfortable. ORL J Otorhinolaryngol Relat Spec. 1996;5899- 104Article
11.
Kamami  YV Laser CO2 for snoring: preliminary results. Acta Otorhinolaryngol Belg. 1990;44451- 456
12.
Larsson  HCarlsson-Nordlander  BSvanborg  E Four-year follow-up after UPPP in 50 unselected patients with obstructive sleep apnea syndrome. Laryngoscope. 1994;1041362- 1368Article
13.
Haraldsson  P-OCarenfelt  CKnutsson  EPersson  HERinder  J Validity of symptom analysis and daytime polysomnography in diagnosis of sleep apnea. Sleep. 1992;15261- 263
14.
Guilleminault  CStoohs  RDuncan  S A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104781- 787Article
15.
Fujita  S Pharyngeal surgery of obstructive sleep apnea and snoring. Fairbanks  DFujita  SIkematsu  TSimmons  Beds.Snoring and Obstructive Sleep Apnea. New York, NY Raven Press1987;101- 128
16.
Powell  NRiley  RGuilleminault  C Maxillofacial surgery for obstructive sleep apnea. Guilleminault  CPartinen  MedsObstructive Sleep Apnea Syndrome Clinical Research and Treatment. New York, NY Raven Press1990;153- 182
17.
Parmar  MMachin  D Log-rank test. Survival Analysis A Practical Approach. Chichester, England John Wiley & Sons Inc1995;66- 75
18.
Hakulinen  TAbeywickrama  K A computor program package for relative survival analysis. Comput Programs Biomed. 1985;19197- 207Article
19.
Ederer  FAxtell  LMCutler  SJ The relative survival rate: a statistical methodology. NCI Monogr. 1961;6101- 121
20.
Not Available, Report of a Joint FAO/WHO UNU Expert Consultation.  Geneva, Switzerland World Health Organization1985;Technical Report Series No. 724.
21.
Keenan  SBurt  HRyan  FFleetham  MB Long-term survival of patients with obstructive sleep apnea treated by uvulopalatopharyngoplasty or nasal CPAP. Chest. 1994;105155- 159Article
22.
Svanborg  ELysdahl  MHaraldsson  P-O Validation of the Apnolog system: digitized portable recordings for diagnosis of obstructive sleep apnea [abstract]. Sleep Res. 1995;24A490
23.
Lavie  PHerer  PPeled  R  et al.  Mortality in sleep apnea patients: a multivariate analysis of risk factors. Sleep. 1995;18149- 157
24.
Socialstyrelsen, Folkhälsorapport 1994.  Stockholm, Sweden Socialstyrelsen1994;51- 56
25.
Kuskowska-Wolk  ARössner  S Det vägar allt tyngre att vara svensk. Läkartidningen. 1992;892282- 2284
26.
Young  TPalta  MDempsey  JSkatrud  JWeber  SBadr  S The occurrence of disordered breathing among middle-aged adults. N Engl J Med. 1993;3281230- 1235Article
27.
Lavie  P Incidence of sleep apnea in a presumably healthy working population: a significant relationship with excessive daytime sleepiness. Sleep. 1983;6312- 318
28.
Sjöström  LV Mortality of severe obese subjects. Am J Clin Nutr. 1992;55(2 suppl)516S- 523S
29.
Rössner  SLagerstrand  LPersson  HESachs  C The sleep apnea syndrome in obesity: risk of sudden death. J Intern Med. 1991;230135- 142Article
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