Content uploaded by Renata L Riha
Author content
All content in this area was uploaded by Renata L Riha on Sep 15, 2015
Content may be subject to copyright.
SERIES ‘‘THE GENETIC AND CARDIOVASCULAR ASPECTS OF
OBSTRUCTIVE SLEEP APNOEA/HYPOPNOEA SYNDROME’’
Edited by R.L. Riha and W.T. McNicholas
Number 3 in this Series
Epidemiology of sleep apnoea/hypopnoea
syndrome and sleep-disordered breathing
P. Jennum* and R.L. Riha
#
ABSTRACT: Epidemiological studies have revealed a high prevalence of sleep-disordered
breathing in the community (up to 20%). A subset of these patients has concurrent symptoms of
excessive daytime sleepiness attributable to their nocturnal breathing disorder and is classified
as having obstructive sleep apnoea/hypopnoea syndrome (4–5% of the middle-aged population).
There is strong evidence for an association of sleep apnoea with cardiovascular and
cerebrovascular morbidity, as well as adverse public health consequences. Treatment and
diagnosis have remained largely unchanged over the past 25 yrs. In moderate-to-severe
obstructive sleep apnoea/hypopnoea syndrome, treatment with continuous positive airway
pressure has been shown to be effective. Questions remain as to how to screen patients with
sleep-disordered breathing. Should time-consuming diagnostic procedures with high sensitivity
and specificity be employed, or should simpler methods be applied for screening populations at
risk, e.g. in the primary care sector?
KEYWORDS: Epidemiology, sleep apnoea, sleep-disordered breathing
The epidemiology of obstructive sleep apnoea
(OSA)/hypopnoea syndrome (OSAHS) has
been described in a significant number of
studies. OSAHS affects ,2–4% of the middle-aged
population and is defined on the basis of symptoms
of daytime sleepiness and objective measures of
disordered breathing during sleep. Obstruction of
the upper airway during sleep, resulting in
repetitive breathing pauses accompanied by oxy-
gen desaturation and arousal from sleep, is
characteristic of OSAHS. This results in diurnal
sleepiness leading to cognitive impairment. Sleep-
disordered breathing (SDB; snoring and associated
apnoeas) is common and affects up to 20% of the
population.
OSAHS is common in adults and children. OSAHS
is an independent risk factor for hypertension and
is associated with cardiovascular and cerebrovas-
cular morbidity. OSAHS has consequences for
public health (driving, accidents at work) and the
economy. The benefits and effects of continuous
positive airway pressure (CPAP) treatment have
been described in prospective studies. Despite
increasing awareness of the condition and
improved diagnostic procedures, most patients in
the community remain undiagnosed and
untreated. This is especially true of patients who
may be at high risk for additional complications,
e.g. those with metabolic syndrome, diabetes, or
cardiac, cerebrovascular or other neurological
diseases. Few or no public health programmes
have included systematic screening for OSAHS.
Traditionally, OSAHS is diagnosed using in-hospi-
tal, supervised overnight polysomnography (PSG)
followed by manual titration of CPAP. This is
costly, both time-wise and economically, and since
the capacity of this procedure is limited, waiting
lists tend to lengthen. This calls for discussion of an
organisational model not only for the identification
and management, but also for the prevention, of
OSAHS and its consequences. The present article
focuses on the epidemiological aspects of OSAHS
and SDB, risk associations, socioeconomic conse-
quences and organisational aspects of diagnosing
and managing sleep apnoea.
AFFILIATIONS
*Danish Centre for Sleep Medicine
Glostrup, Denmark.
#
Dept of Sleep Medicine
Royal Infirmary of Edinburgh,
Edinburgh, UK.
CORRESPONDENCE
P. Jennum
Danish Centre for Sleep Medicine,
Dept of Clinical Neurophysiology,
Faculty of Health Sciences
University of Copenhagen
Glostrup Hospital
DK 2600 Glostrup
Denmark
Fax: 45 43233933
E-mail: poje@glo.regionh.dk
Received:
November 27 2008
Accepted after revision:
January 13 2009
STATEMENT OF INTEREST
None declared.
European Respiratory Journal
Print ISSN 0903-1936
Online ISSN 1399-3003
Previous article in this series: No. 1: MacLeod AK, Liewald DCM, McGilchrist MM, Morris AD, Kerr SM, Porteous DJ. Some principles and practices of
genetic biobanking studies. Eur Respir J 2009; 33: 419–425. No. 2: Riha RL, Gislasson T, Diefenbach K. The phenotype and genotype of adult obstructive sleep
apnoea/hypopnoea syndrome. Eur Respir J 2009; 33: 646–655.
EUROPEAN RESPIRATORY JOURNAL VOLUME 33 NUMBER 4 907
Eur Respir J 2009; 33: 907–914
DOI: 10.1183/09031936.00180108
CopyrightßERS Journals Ltd 2009
c
EPIDEMIOLOGY
Sleep apnoea has been recognised throughout human history,
dating as far back as the 4th century BC. Numerous reports
throughout the 19th century and the early part of the 20th
century AD gave way to systematically conducted studies on
patients with OSAHS and related syndromes [1].
OSAHS was first properly documented in neurophysiological
sleep laboratories using techniques developed for the investi-
gation of other conditions such as depression and narcolepsy.
OSAHS was first described as such in 1965 [2] and there has
since been an explosion in the facilities for its diagnosis and
treatment as well as a rapid advancement in the understanding
of its far-reaching consequences.
Reporting of OSAHS was initially confined to case series, but
more recently, large-scale epidemiological studies have
attempted to answer questions on the incidence and preva-
lence of OSAHS. However, few of these have used ideal
methods and it is therefore difficult to draw firm conclusions
from them.
Generally, the best-conducted studies, in terms of method and
rigour of technique employed, have found a prevalence of
OSAHS in the middle-aged male population of up to 4% [3].
The study showing the lowest quoted prevalence may have
underestimated the occurrence of OSAHS in the population by
using oximetry alone, with more than five 4% dips in pulse
oximetry-measured arterial oxygen saturation per hour, as an
initial screening measure [4], while those studies showing the
highest prevalences may have overestimated the prevalence by
including central apnoeas and breath-holds occurring during
wakefulness [5] using inductance plethysmography at home.
Assessment of sleepiness differed between the studies on
account of using self-devised questionnaires specific to each
study. Fewer studies exist examining the prevalence of OSAHS
in females but it is probably half that of males, at 0.5–1% [5].
OSAHS occurs throughout the entire lifespan, from neonates to
the elderly. In adults, the frequency of disordered breathing
during sleep increases with age and is poorly associated with
an increased incidence of daytime sleepiness or other
symptoms of OSAHS [6–10].
ASSESSMENT OF OSAHS
As discussed above, a definitive diagnosis of OSAHS requires
objective recording and measurement of sleep and breathing
during the night in addition to a measure of daytime sleepiness
(objective or subjective) and other symptoms.
SDB
An objective measure of SDB at night is generally required to
confirm the diagnosis of OSAHS. The method most widely
used, and which is considered by some to be the ‘‘gold
standard’’ for diagnosis despite limited evidence, is overnight
PSG. An American Academy of Sleep Medicine (AASM) Task
Force published indications for PSG in 1997 [11] and
measurement techniques and syndrome definitions in 1999
[12]. Most PSG studies monitor the following routinely: nasal
and/or oral airflow; thoracoabdominal movement; snoring;
electroencephalogram (EEG); electro-oculogram; electromyo-
gram; and oxygen saturation. Signal collection and interpreta-
tion is usually computerised, but manual scoring of the trace
should still be performed using guidelines for interpretation of
the EEG published in 1968 by RECHTSCHAFFEN and KALES [13],
and the 1999 AASM criteria [12].
Full-night PSG is generally performed, but split-night studies
are also used [14], in which the first half of the study night is
used for diagnosis and the second half to monitor treatment
response using CPAP.
Cardiorespiratory monitoring alone can also be used. This
involves the measurement of airflow, respiratory effort,
oxygen saturation and cardiac frequency, but not EEG. The
great advantages of these systems are price, portability and the
ability of patients to monitor themselves at home. FERBER et al.
[15] reviewed seven studies of portable ambulatory monitoring
systems and reported a sensitivity of 78–100% and a specificity
of 67–100% in comparison with in-lab PSG, although ambula-
tory monitoring is of course not a gold standard.
Overnight oximetry is sometimes used as a screening test for
identifying patients who are at risk of significant OSAHS, but
this should never be seen as a substitute for in-lab PSG or
home cardiorespiratory monitoring. There are severe limita-
tions inherent in this technique used in isolation, including the
inability to detect apnoeas or hypopnoeas not associated with
oxygen desaturation and the upper airway resistance synd-
rome. Furthermore, nocturnal oxygen desaturation may be
related to sleep hypoventilation without associated upper
airways obstruction, e.g. in chronic obstructive pulmonary
disease (COPD), severe kyphoscoliosis, muscular dystrophy
and morbid obesity, and in the setting of periodic breathing
associated with severe heart failure.
Daytime sleepiness
Sleepiness is difficult to define (see [16] for a review).
Sleepiness can be regarded as ‘‘normal’’ sleepiness (a result
of the normal circadian rhythm) and ‘‘pathological’’ sleepiness
(a result of altered sleep scheduling). Pathological sleepiness
can be further subdivided into ‘‘habitual’’ (e.g. as the result of
recurring precipitants of sleepiness such as OSA) or ‘‘occa-
sional’’ (e.g. as the result of jet lag or medication).
As proposed by CLUYDTS et al. [16], sleepiness can be
recognised using a number of different measures. 1) Inferring
sleepiness from behaviour, e.g. observation of yawning
frequency, actigraphy, facial expression or performance tests
such as the driving simulator, psychomotor vigilance tests and
reaction time tests. 2) Self-evaluation of sleepiness using rating
scales, e.g. the Stanford Sleepiness Scale to measure sleepiness
at a given instant, and the Epworth Sleepiness Score (ESS) to
measure sleepiness averaged over a month. 3) Direct electro-
physiological measures, e.g. multiple sleep latency test and
multiple wakefulness test [17], pupillometry and cerebral
evoked potentials.
In respect to the diagnosis and monitoring of OSAHS, probably
the most widely used and best-validated scale assessing
daytime sleepiness is the ESS, first devised in 1991 [18]. Its
advantages include ease of administration and low cost.
It assesses global level of sleepiness and is independent of
short-term variations in sleepiness with the time of day and
also of inter-day variations [19]. The ESS aims to measure the
general level of daytime sleepiness as a stable individual
EPIDEMIOLOGY OF SLEEP APNOEA P. JENNUM AND R.L. RIHA
908 VOLUME 33 NUMBER 4 EUROPEAN RESPIRATORY JOURNAL
characteristic and has satisfactory test–retest reliability [20].
The ESS is also able to discriminate between normal and
pathological sleepiness [20]. The accuracy of the ESS depends
on the awareness of subjects falling asleep, which may not
always be the case [21]. Rating of the subject’s sleepiness by
another person may be more precise [22]. The ESS does not
correlate strongly with more objective measures of daytime
sleepiness such as the multiple sleep latency test (MSLT) or
maintenance of wakefulness test (MWT) [23], but this is in
keeping with the fact that sleepiness is not a unitary concept.
ESS reproducibly reflects changes in sleepiness with therapy in
OSAHS [24]. Because of its reliability and its ability to
differentiate between abnormal and normal levels of sleepi-
ness, as well as for its ease of administration, the ESS is one of
the most widely used measures of sleepiness.
In summary, self-reporting of snoring, nocturnal gasping or
apnoeas and measures of sleepiness (e.g. ESS) correspond
relatively poorly with objective measures, such as sound
recording, apnoea/hypopnoea index (AHI) and MSLTs/
MWTs [25]. Any relationship between these factors depends
on the standardisation and the value of the reference test/gold
standard and is subject to high variability in the validity of
questionnaire and test evaluation. Complaints of sleepiness
and/or other indications of hypersomnia are related to many
other conditions, not just SDB, which weakens the relationship
further.
Epidemiological studies have used a variety of methods to
measure OSA, including self-reported markers such as snor-
ing, apnoeas, daytime sleepiness, in-laboratory PSG, unat-
tended in-home PSG, and unattended polygraphic or other
recordings of a few physiological parameters. Studies using
objective measures of apnoea and hypopnoea have employed
variable respiratory event definitions. Moreover, there has
been no standardisation of the method used to quantify
airflow, with methods such as thermistry, inductance plethys-
mography and nasal cannula/pressure transducer systems
providing different sensitivities to changes in airflow. Like
other conditions based on a severity continuum, the definition
of the units of the continuum and the ultimate thresholds used
to designate the presence of OSA will affect the magnitude of
prevalence and estimates of associations with risk factors and
outcomes. The use of more-restrictive definitions of apnoea
and hypopnoea, higher AHI cut-off points, or an additional
requirement for symptoms of sleepiness, will obviously lower
prevalence estimates and affect values expressing associations,
such as odds ratios. Like other conditions, OSAHS presents a
severity spectrum which affects the estimates of prevalences.
Studies have consistently found that symptomatic OSAHS
occurs in o2–4% of the adult population. Studies evaluating
the occurrence of SDB, independently of symptoms, show a
much higher prevalence of 6–24% among adults (tables 1–3).
SEX AND AGE
OSAHS is more common in males than in females, with a ratio
of 2:1. Menopause is a risk factor for sleep apnoea [26]. OSAHS
prevalence increases in mid-life, but the existence of OSAHS in
childhood, adolescence and older age means that there is no
simple positive correlation of OSAHS with age [27]. A multi-
modal distribution of prevalence by age is often indicative of
distinct disease subtypes with different aetiologies and health
consequences. SDB occurs commonly in populations aged
.65 yrs (tables 1–3), but there is controversy regarding its
significance in older people and its relationship to OSAHS that
occurs in middle age [28, 29].
RISK ASSOCIATIONS
Smoking
Smoking is one of the strongest risk factors for cardiovascular
disease. The association with OSAHS is relatively weak, but
smoking may interact with and add to the cardiovascular risk
associated with OSA [30].
Genetics/family history
Reports published in the 1990s suggested a relationship
between self-reported snoring and familial occurrence of
snoring and sleep apnoea, with a relative risk association of
3–5 [31–33]. The risk has been demonstrated to increase if both
parents are affected. A number of studies have documented
this association. A recent review of this evidence has evaluated
this relationship [34]. In addressing this topic, future studies
should address the hereditary components of OSAHS by
subdividing the disease according to different subgroups, e.g.
sleep apnoea with age of onset of disease, hypertension,
metabolic syndrome, propensity to cerebrovascular disease
and other risk associations.
TABLE 1 Age- and sex-specific prevalence rates of the
apnoea/hypopnoea index (AHI) based on
polysomnographic (PSG) results for a sample of
1,050 males and 1,098 females from the Vitoria-
Gasteiz region of Spain
Age yrs AHI
o5o10 o15 o20 o30
Males
30–39 9.0 (2–16) 7.6 (0–15) 2.7 (1–5) 2.1 (0–4) 2.1 (0–4)
40–49 25.6 (14–37) 18.2 (9–27) 15.5 (7–24) 10.1 (5–15) 7.0 (3–11)
50–59 27.9 (17–38) 24.1 (15–34) 19.4 (11–27) 14.7 (8–21) 11.4(6–17)
60–70 52.1 (33–71) 32.2 (17–48) 24.2 (12–37) 15.0 (8–22) 8.6 (4–14)
Females
30–39 3.4 (0–7) 1.7 (0–4) 0.9 (0–2)
40–49 14.5 (3–25) 9.7 (0–19)
50–59 35.0 (20–50) 16.2 (5–27) 8.6 (1–17) 8.3 (0–16) 4.3 (0–10)
60–70 46.9 (31–63) 25.6 (13–38) 15.9 (6–26) 13.0 (3–22) 5.9 (0–13)
Data are presented as % (95% confidence interval). Data were collected as
follows. The MESAM IV portable recording system (Medizintechnik fu
¨rArtzund
Patient, Munich, Germany) was used overnight. PSG was recorded using Alice 3
(Respironics, Pittsburgh, PA, USA). Manual scoring using conventional criteria
was employed. An abnormal breathing event was defined as complete cessation
of airflow for o10 s (apnoea) or a discernible 50% reduction in respiratory airflow
accompanied by a decrease of o4% in arterial oxygen saturation measured by
pulse oximetry and/or electroencephalogram arousal (hypopnoea). Arousals
were defined according to American Sleep Disorders Association criteria [15].
Reproduced from [6], with permission from the publisher.
P. JENNUM AND R.L. RIHA EPIDEMIOLOGY OF SLEEP APNOEA
c
EUROPEAN RESPIRATORY JOURNAL VOLUME 33 NUMBER 4 909
Obesity and metabolic syndrome
There is strong epidemiological and clinical evidence for a
relationship between sleep apnoea, central obesity and meta-
bolic syndrome. Despite the lack of controlled studies, several
studies have presented data showing that weight reduction
through dieting or bariatric surgery is followed by a reduction
in AHI and incidence of diabetes, improved glucose control
and reductions in hyper-triglyceridaemia [35–37]. This impor-
tant area will be discussed further in the last paper in the
current series.
Polycystic ovary syndrome
There is some evidence that sleep apnoea is associated with
polycystic ovary syndrome [38, 39]; however, no epidemiolo-
gical, cross-sectional or prospective studies have addressed
this important issue.
CONSEQUENCES OF OSA
Morbidity and mortality associated with OSAHS
Untreated OSAHS can contribute to the development or
progression of other disorders. OSAHS has now been shown
to be a cause for systemic hypertension [40] and there is some
evidence suggesting that it can also cause pulmonary
hypertension [41, 42]. OSAHS is also associated with ischaemic
heart disease.
SDB has been found to be a significant clinical feature in a
proportion of patients with cerebrovascular disease: stroke and
transient ischaemic attacks [40]. However, published results are
contradictory, with some showing no increase in OSAHS in those
with transient ischaemic attacks [43], while others show a high
prevalence of OSAHS in those with stroke (see [44] for review).
Treating OSAHS in stroke is also controversial. Some studies
show a significant reduction in SDB and improvement in quality
of life, while others do not [45, 46]. Patients with OSAHS and
moderate-to-severe coexistent lung disease, such as COPD, are
more likely to develop type II respiratory failure that will
improve with treatment of the obstructive apnoeas [47, 48].
Likewise, nocturnal asthma may be worsened by sleep apnoea
and treatment may lead to improvement [49].
OSAHS leads to neuropsychological impairment that includes
deficits in attention, concentration, vigilance, manual dexterity,
visuomotor skills, memory, verbal fluency and executive
function [50]. Perhaps the most important complication of
OSAHS, and the one that has the greatest impact from the
public health perspective, is driving accidents. More than one-
third of patients with OSAHS report having had an accident or
near-accident on account of falling asleep while driving [51].
There is also objective evidence of 1.3–12-fold increases in
accident rates among those with sleep apnoea, and accident
rates in OSAHS patients have been found to be 1.3 to seven
times higher than those in the general population [52–54].
Vigilance testing and driving simulators in studies assessing
driving performance in patients with OSAHS reveal that
performance is markedly reduced and the impairment is not
limited to periods when patients actually fall asleep but also
occurs when they are awake, owing to reduced vigilance.
There is also evidence that OSAHS patients have a 50%
increased risk of workplace accidents [55, 56].
OSAHS thus leads to several complications, including:
impairment in education, quality of life and work capacity;
traffic accidents; cardiac and cerebrovascular morbidity and
mortality; and increased economic burden.
Hypertension
A relationship between sleep apnoea, snoring and hypertension
was proposed in the first half of the 1980s. This relationship was
TABLE 2 Age- and sex-specific prevalence rates of the
apnoea/hypopnoea index (AHI) based on
polysomnographic (PSG) results for a sample of
352 males and 250 females from Wisconsin, USA
Age yrs AHI
o5o10 o15
Males
30–39 17.0 (9.6–25) 12.0 (5.4–19) 6.2 (1.9–10)
40–49 25.0 (18–32) 18.0 (11–24) 11.0 (6.7–16)
50–60 31.0 (21–40) 14.0 (7.5–20) 9.1 (5.1–13)
Females
30–39 6.5 (1.4–11) 4.9 (0.6–9.8) 4.4 (1.1–7.3)
40–49 8.7 (4.2–13) 4.9 (1.7–8.1) 3.7 (1.0–6.5)
50–60 16.0 (5.2–26) 5.9 (0.0–12.0) 4.0 (0.0–10)
Data are presented as % (95% confidence interval). Data were collected as
follows. Overnight in-lab PSG recording was carried out in sound-attenuated,
light- and temperature-controlled rooms using standard set-up and a 16-
channel polygraph (Model 78d; Grass Instrument, Quincy, MA, USA). Manual
scoring using conventional criteria was employed. An abnormal breathing event
was defined as complete cessation of airflow for o10 s (apnoea) or a
discernible 50% reduction in respiratory airflow accompanied by a decrease of
o4% in arterial oxygen saturation measured by pulse oximetry. Reproduced
from [3], with permission from the publisher.
TABLE 3 Prevalence rates of the apnoea and hypopnoea
index (AHI) by age based on polysomnographic
(PSG) results for a sample of 741 males from
two counties in Southern Pennsylvania, USA
Age yrs Subjects AHI
o5o10 o20
20–44 236 7.9 (5.0–12.1) 3.2 (1.6–6.4) 1.7 (0.6–4.4)
45–64 430 19.7 (16.2–23.7) 11.8 (9.1–15.3) 23.9 (15.7–34.9)
65–100 75 30.5 (21.1–41.7) 23.9 (15.7–34.9) 13.3 (7.3–23)
Data are presented as n or % (95% confidence interval). Data were collected as
follows. Overnight in-lab PSG recording was carried out in sound-attenuated,
light- and temperature-controlled rooms using standard set-up and a 16-
channel polygraph (Model 78d; Grass Instrument, Quincy, MA, USA). Manual
scoring using conventional criteria was employed. An abnormal breathing event
was defined as complete cessation of airflow for o10 s (apnoea) or a
discernible 50% reduction in respiratory airflow accompanied by a decrease of
o4% in arterial oxygen saturation measured by pulse oximetry. Reproduced
from [7], with permission from the publisher.
EPIDEMIOLOGY OF SLEEP APNOEA P. JENNUM AND R.L. RIHA
910 VOLUME 33 NUMBER 4 EUROPEAN RESPIRATORY JOURNAL
initially supported by epidemiological studies using self-
reported snoring as a surrogate marker for sleep apnoea [55,
57]. Later follow-up studies suggested that sleep apnoea was
correlated with increased cardiovascular risk [58]. Although
snoring is associated with hypertension, several studies ques-
tioned the link, taking other risk factors into consideration [59].
This is due to the problem with self-reported snoring: it shows
only a partial relationship to sleep apnoea, with moderate
sensitivity and specificity. Since then, several studies have
shown a relationship between sleep apnoea, apnoea severity
and the occurrence of hypertension, independently of risk
factors, such as age and obesity [40].
Cardiac disease
Over the past 25 yrs, several studies have documented snoring
and OSAHS as risk factors for cardiac disease (artherosclerotic,
acute myocardial infarction, arrhythmias). Morbidity and
mortality risk is increased in the context of SDB, even when
taking other risk factors into consideration [40].
Sleep apnoea and stroke
Based on cross-sectional epidemiological studies primarily
using self-reported snoring, a relationship between snoring
and stroke was proposed in the mid-1980s. Prospective studies
have supported this relationship. The drawback of these
studies, however, was the inaccuracy of the report of snoring
due to the sensitivity, specificity and the individuality of this
symptom, which weakens a potential relationship between
sleep apnoea and stroke. Case–control studies suggest a
potential relationship based upon historical report of sleep
apnoea and PSG findings in stroke patients compared with
control groups [60, 61]. There are, however, several issues in
these patients, especially patients with stroke and sleep-related
breathing problems. These include selection problems and
stroke-induced SDB (e.g. pseudo-bulbar OSA, central apnoea
and hypoventilation) which may add to the occurrences of
sleep-related breathing disorders [62].
Traffic accidents
Noncommercial drivers with sleep apnoea are at a statistically
significant increased risk of having a motor vehicle crash.
Magnitude of daytime sleepiness and the severity of SDB were
correlated with crash risk, while full treatment of sleep apnoea
improves driver performance [63]. Untreated OSAHS increases
societal costs due to traffic accidents and their consequences
[64–66].
Socioeconomic consequences
The social and cardiovascular consequences of OSAHS seem
most pronounced among patients of low socioeconomic status.
This was found to be the case in a clinic population [67], but in
a discharge register study from Sweden, socioeconomic status
had a minor effect on the likelihood of hospitalisation and it
was suggested that other factors, e.g. smoking and obesity, may
influence this observed relationship [68]. It should be noted,
however, that there is a tendency towards lower screening and
diagnostic activity among people of lower social status.
OSAHS presents a significant socioeconomic burden due to
comorbidity, healthcare utilisation in the primary and second-
ary healthcare sectors, use of medication, effects on employ-
ment and lost income. Treatment of OSAHS causes reduced
morbidity, mortality and hospitalisation rates and this has
been demonstrated to be cost effective [69–73].
SCREENING AND MANAGEMENT OF SLEEP APNOEA
Undiagnosed OSAHS is likely to be highly prevalent, even in
countries where diagnostic facilities have been available for a
long time. A significant proportion of the potential for
improved diagnosis is in the primary care sector, and in
high-risk groups, e.g. patients with acute and chronic cardio-
vascular or cerebrovascular disease, or diabetics. There is a
need to evaluate the optimal organisational model for patient
identification and management. Few studies have presented
the optimal economic model for the evaluation of OSAHS. In a
Danish Health Technology Assessment, the use of ambulatory
portable diagnostic procedures using partial polygraphy
followed by auto-adjusted CPAP was superior to the use of
in-hospital, supervised PSG (which is time consuming and
costly) and oximetry (which has low sensitivity and diagnostic
accuracy) among patients without major comorbidity in the
primary care sector [74]. Similar results have been obtained by
others, who found oximetry to present low diagnostic
accuracy, but also pointed out the use of split-night PSG
studies as an alternative diagnostic and therapeutic approach
[75]. Thus, there is a need to evaluate the organisation of
diagnosing and managing patients with OSAHS, with and
without major comorbidities. In patients without major
comorbidity suspected of OSAHS, a portable study approach
is possible [76], whereas in patients with significant neurolo-
gical, cardiac or pulmonary disease it is likely that a supervised
study is desirable [77].
CONCLUSION
In conclusion, it is impossible, in view of the vast quantity of
literature that has burgeoned in the field of obstructive sleep
apnoea/hypopnoea syndrome, to present an exhaustive over-
view of all its aspects. However, the following main messages
remain: obstructive sleep apnoea/hypopnoea syndrome and
sleep-disordered breathing are very common, affecting a
significant proportion of the population and, when untreated,
cause significant increased social, cardiac and cerebrovascular
morbidity and mortality; a significant proportion of patients
with obstructive sleep apnoea/hypopnoea syndrome remain
undiagnosed and untreated due to inadequate resources for
case detection and investigation. There is a need to identify
optimal organisational and economic models to identify
patients at risk for additional screening and management,
especially in ‘‘at-risk’’ populations.
ACKNOWLEDGEMENTS
Thanks to S. Rafferty (Royal Infirmary of Edinburgh,
Edinburgh, UK) for her help in the preparation of the present
manuscript.
REFERENCES
1Lavie P. Nothing new under the moon. Historical accounts
of sleep apnea syndrome. Arch Intern Med 1984; 144:
2025–2028.
2Jung R, Kuhlo W. Neurophysiological studies of abnormal
night sleep and the Pickwickian syndrome. Prog Brain Res
1965; 18: 140–159.
P. JENNUM AND R.L. RIHA EPIDEMIOLOGY OF SLEEP APNOEA
c
EUROPEAN RESPIRATORY JOURNAL VOLUME 33 NUMBER 4 911
3Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S.
The occurrence of sleep-disordered breathing among
middle-aged adults. N Engl J Med 1993; 328: 1230–1235.
4Stradling JR, Crosby JH. Predictors and prevalence of
obstructive sleep apnoea and snoring in 1001 middle aged
men. Thorax 1991; 46: 85–90.
5Jennum P, Sjøl A. Epidemiology of snoring and obstructive
sleep apnoea in a Danish population, age 30–60. J Sleep Res
1992; 1: 240–244.
6Dura
´n J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep
apnea–hypopnea and related clinical features in a
population-based sample of subjects aged 30 to 70 yr. Am
J Respir Crit Care Med 2001; 163: 685–689.
7Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A.
Effects of age on sleep apnea in men: I. Prevalence and
severity. Am J Respir Crit Care Med 1998; 157: 144–148.
8Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-
disordered breathing in women: effects of gender. Am J
Respir Crit Care Med 2001; 1623: 608–613.
9Gislason T, Almqvist M, Eriksson G, Taube A, Boman G.
Prevalence of sleep apnea syndrome among Swedish
men – an epidemiological study. J Clin Epidemiol 1988; 41:
571–576.
10 Puvanendran K, Goh KL. From snoring to sleep apnea in a
Singapore population. Sleep Res Online 1999; 2: 11–14.
11 Polysomnography Task Force, American Sleep Disorders
Association Standards of Practice Committee, Practice
parameters for the indications for polysomnography and
related procedures. Sleep 1997; 20: 406–422.
12 American Academy of Sleep Medicine Task Force, Sleep-
related breathing disorders in adults: recommendations for
syndrome definition and measurement techniques in
clinical research. Sleep 1999; 22: 667–689.
13 Rechtschaffen A, Kales S, eds. A Manual of Standardized
Terminology, Techniques and Scoring System for Sleep
Stages of Human Subjects. Bethesda, National Institutes of
Health, 1968.
14 Pepperell JC, Davies RJ, Stradling JR. Sleep studies for
sleep apnoea. Physiol Meas 2002; 23: R39–R74.
15 Ferber R, Millman R, Coppola M, et al. Portable recording
in the assessment of obstructive sleep apnea. ASDA
standards of practice. Sleep 1994; 17: 378–392.
16 Cluydts R, De Valck E, Verstraeten E, Theys P. Daytime
sleepiness and its evaluation. Sleep Med Rev 2002; 6: 83–96.
17 Littner MR, Kushida C, Wise M, et al. Practice parameters
for clinical use of the multiple sleep latency test and the
maintenance of wakefulness test. Sleep 2005; 28: 113–121.
18 Johns MW. A new method for measuring daytime
sleepiness: the Epworth sleepiness scale. Sleep 1991; 14:
540–545.
19 Johns MW. Sleepiness in different situations measured by
the Epworth Sleepiness Scale. Sleep 1994; 17: 703–710.
20 Johns MW. Reliability and factor analysis of the Epworth
Sleepiness Scale. Sleep 1992; 15: 376–381.
21 Reyner LA, Horne JA. Falling asleep whilst driving: are
drivers aware of prior sleepiness? Int J Legal Med 1998; 111:
120–123.
22 Kingshott RN, Sime PJ, Engleman HM, Douglas NJ. Self
assessment of daytime sleepiness: patient versus partner.
Thorax 1995; 50: 994–995.
23 Benbadis SR, Mascha E, Perry MC, Wolgamuth BR,
Smolley LA, Dinner DS. Association between the Epworth
sleepiness scale and the multiple sleep latency test in a
clinical population. Ann Intern Med 1999; 130: 289–292.
24 Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT.
Continuous positive airway pressure therapy for treating
sleepiness in a diverse population with obstructive sleep
apnea: results of a meta-analysis. Arch Intern Med 2003; 163:
565–571.
25 Nguyen AT, Baltzan MA, Small D, Wolkove N, Guillon S,
Palayew M. Clinical reproducibility of the Epworth
Sleepiness Scale. J Clin Sleep Med 2006; 2: 170–174.
26 Saaresranta T, Polo O. Sleep-disordered breathing and
hormones. Eur Respir J 2003; 22: 161–172.
27 Jennum P, Sjøl A. Self-assessed cognitive function in
snorers and sleep apneics. An epidemiological study of
1,504 females and males aged 30–60 years: the Dan-
MONICA II Study. Eur Neurol 1994; 34: 204–208.
28 Launois SH, Pe
´pin JL, Le
´vy P, Sleep apnea in the elderly: a
specific entity? Sleep Med Rev 2007; 11: 87–97.
29 Lavie P, Herer P, Lavie L. Mortality risk factors in sleep
apnoea: a matched case–control study. J Sleep Res 2007; 16:
128–134.
30 Lavie L, Lavie P. Smoking interacts with sleep apnea to
increase cardiovascular risk. Sleep Med 2008; 9: 247–253.
31 Jennum P, Hein HO, Suadicani P, Sorensen H,
Gyntelberg F. Snoring, family history, and genetic markers
in men. The Copenhagen Male Study. Chest 1995; 107:
1289–1293.
32 Carmelli D, Bliwise DL, Swan GE, Reed T. Genetic factors
in self-reported snoring and excessive daytime sleepiness:
a twin study. Am J Respir Crit Care Med 2001; 164: 949–952.
33 Ovchinsky A, Rao M, Lotwin I, Goldstein NA. The familial
aggregation of pediatric obstructive sleep apnea syn-
drome. Arch Otolaryngol Head Neck Surg 2002; 128: 815–818.
34 Riha RL, Gislasson T, Diefenbach K. The phenotype,
genotype of adult obstructive sleep apnoea/hypopnoea
syndrome. Eur Respir J 2009; 33: 646–655.
35 Grunstein RR, Stenlof K, Hedner JA, Peltonen M,
Karason K, Sjostrom L. Two year reduction in sleep apnea
symptoms and associated diabetes incidence after weight
loss in severe obesity. Sleep 2007; 30: 703–710.
36 Newman AB, Foster G, Givelber R, Nieto FJ, Redline S,
Young T. Progression and regression of sleep-disordered
breathing with changes in weight: the Sleep Heart Health
Study. Arch Intern Med 2005; 165: 2408–2413.
37 Spivak H, Hewitt MF, Onn A, Half EE. Weight loss and
improvement of obesity-related illness in 500 U.S. patients
following laparoscopic adjustable gastric banding proce-
dure. Am J Surg 2005; 189: 27–32.
38 Fogel RB, Malhotra A, Pillar G, Pittman SD, Dunaif A,
White DP. Increased prevalence of obstructive sleep apnea
syndrome in obese women with polycystic ovary syn-
drome. J Clin Endocrinol Metab 2001; 86: 1175–1180.
39 Vgontzas AN, Legro RS, Bixler EO, Grayev A, Kales A,
Chrousos GP. Polycystic ovary syndrome is associated
with obstructive sleep apnea and daytime sleepiness: role
of insulin resistance. J Clin Endocrinol Metab 2001; 86:
517–520.
40 McNicholas WT, Bonsigore MR. Sleep apnoea as an
independent risk factor for cardiovascular disease: current
EPIDEMIOLOGY OF SLEEP APNOEA P. JENNUM AND R.L. RIHA
912 VOLUME 33 NUMBER 4 EUROPEAN RESPIRATORY JOURNAL
evidence, basic mechanisms and research priorities. Eur
Respir J 2007; 29: 156–178.
41 Blankfield RP, Hudgel DW, Tapolyai AA, Zyzanski SJ.
Bilateral leg edema, obesity, pulmonary hypertension, and
obstructive sleep apnea. Arch Intern Med 2000; 160:
2357–2362.
42 Sajkov D, Wang T, Saunders NA, Bune AJ, Mcevoy RD.
Continuous positive airway pressure treatment improves
pulmonary hemodynamics in patients with obstructive
sleep apnea. Am J Respir Crit Care Med 2002; 165: 152–158.
43 McArdle N, Riha RL, Vennelle M, et al. Sleep-disordered
breathing as a risk factor for cerebrovascular disease: a
case–control study in patients with transient ischemic
attacks. Stroke 2003; 34: 2916–2921.
44 Neau JP, Paquereau J, Meurice JC, Chavagnat JJ, Gil R.
Stroke and sleep apnoea: cause or consequence? Sleep Med
Rev 2002; 6: 457–469.
45 Valham F, Mooe T, Rabben T, Stenlund H, Wiklund U,
Franklin KA. Increased risk of stroke in patients with
coronary artery disease and sleep apnea: a 10-year follow-
up. Circulation 2008; 118: 955–960.
46 Hsu CY, Vennelle M, Li HY, Engleman HM, Dennis MS,
Douglas NJ. Sleep-disordered breathing after stroke: a
randomised controlled trial of continuous positive airway
pressure. J Neurol Neurosurg Psychiatry 2006; 77: 1143–1149.
47 de Miguel J, Cabello J, Sa
´nchez-Alarcos JM, Alvarez-Sala R,
Espino
´s D, Alvarez-Sala JL. Long-term effects of treatment
with nasal continuous positive airway pressure on lung
function in patients with overlap syndrome. Sleep Breath
2002; 6: 3–10.
48 Mansfield D, Naughton MT. Effects of continuous positive
airway pressure on lung function in patients with chronic
obstructive pulmonary disease and sleep disordered
breathing. Respirology 1999; 4: 365–370.
49 Chan CS, Woolcock AJ, Sullivan CE. Nocturnal asthma:
role of snoring and obstructive sleep apnea. Am Rev Respir
Dis 1988; 137: 1502–1504.
50 Engleman HM, Kingshott RN, Martin SE, Douglas NJ.
Cognitive function in the sleep apnea/hypopnea syn-
drome (SAHS). Sleep 2000; 23: Suppl. 4, S102–S108.
51 Engleman HM, Hirst WS, Douglas NJ. Under reporting of
sleepiness and driving impairment in patients with sleep
apnoea/hypopnoea syndrome. J Sleep Res 1997; 6: 272–275.
52 Tera
´n-Santos J, Jime
´nez-Go
´mez A, Cordero-Guevara J. The
association between sleep apnea and the risk of traffic
accidents. Cooperative Group Burgos-Santander. N Engl J
Med 1999; 340: 847–851.
53 Barbe
´, Perica
´s J, Mun
˜oz A, Findley L, Anto
´JM, Agustı
´AG.
Automobile accidents in patients with sleep apnea
syndrome. An epidemiological and mechanistic study.
Am J Respir Crit Care Med 1998; 158: 18–22.
54 George CF, Smiley A. Sleep apnea and automobile crashes.
Sleep 1999; 22: 790–795.
55 Ulfberg J, Carter N, Edling C. Sleep-disordered breathing
and occupational accidents. Scand J Work Environ Health
2000; 26: 237–242.
56 Lindberg E, Carter N, Gislason T, Janson C. Role of snoring
and daytime sleepiness in occupational accidents. Am J
Respir Crit Care Med 2001; 164: 2031–2035.
57 Koskenvuo M, Partinen M, Kaprio J. Snoring and disease.
Ann Clin Res 1985; 17: 247–251.
58 Jennum P, Hein HO, Suadicani P, Gyntelberg F.
Cardiovascular risk factors in snorers. A cross-sectional
study of 3,323 men aged 54 to 74 years: the Copenhagen
Male Study. Chest 1992; 102: 1371–1376.
59 Jennum P, Sjøl A. Snoring, sleep apnoea and cardiovas-
cular risk factors: the MONICA II Study. Int J Epidemiol
1993; 22: 439–444.
60 Davies DP, Rodgers H, Walshaw D, James OF, Gibson GJ.
Snoring, daytime sleepiness and stroke: a case-control
study of first-ever stroke. J Sleep Res 2003; 12: 313–318.
61 Mohsenin V. Sleep-related breathing disorders and risk of
stroke. Stroke 2001; 32: 1271–1278.
62 Bassetti CL, Milanova M, Gugger M. Sleep-disordered
breathing and acute ischemic stroke: diagnosis, risk
factors, treatment, evolution, and long-term clinical out-
come. Stroke 2006; 37: 967–972.
63 Ellen RL, Marshall SC, Palayew M, Molnar FJ, Wilson KG,
Man-Son-Hing M. Systematic review of motor vehicle
crash risk in persons with sleep apnea. J Clin Sleep Med
2006; 2: 193–200.
64 Tan MC, Ayas NT, Mulgrew A, et al. Cost-effectiveness of
continuous positive airway pressure therapy in patients
with obstructive sleep apnea–hypopnea in British
Columbia. Can Respir J 2008; 15: 159–165.
65 Pack AI, Pien GW. How much do crashes related to
obstructive sleep apnea cost? Sleep 2004; 27: 369–370.
66 Gurubhagavatula I, Nkwuo JE, Maislin G, Pack AI.
Estimated cost of crashes in commercial drivers supports
screening and treatment of obstructive sleep apnea. Accid
Anal Prev 2008; 40: 104–115.
67 Tarasiuk A, Greenberg-Dotan S, Simon T, Tal A,
Oksenberg A, Reuveni H. Low socioeconomic status is a
risk factor for cardiovascular disease among adult obstruc-
tive sleep apnea syndrome patients requiring treatment.
Chest 2006; 130: 766–773.
68 Li X, Sundquist K, Sundquist J. Socioeconomic status and
occupation as risk factors for obstructive sleep apnea in
Sweden: a population-based study. Sleep Med 2008; 9:
129–136.
69 McDaid C, Griffin S, Weatherley H. The continuous positive
airway pressure for the treatment of obstructive sleep
apnoea–hypopnoea syndrome: a systematic review and
economic analysis. Health Technol Assess 2009; 13: 1–142.
70 Douglas NJ, George CF. Treating sleep apnoea is cost
effective. Thorax 2002; 57: 93.
71 Peker Y, Hedner J, Johansson A, Bende M. Reduced
hospitalization with cardiovascular and pulmonary dis-
ease in obstructive sleep apnea patients on nasal CPAP
treatment. Sleep 1997; 20: 645–653.
72 Mar J, Rueda JR, Dura
´n-Cantolla J, Schechter C, Chilcott J.
The cost-effectiveness of nCPAP treatment in patients with
moderate-to-severe obstructive sleep apnoea. Eur Respir J
2003; 21: 515–522.
73 Albarrak M, Banno K, Sabbagh AA, et al. Utilization of
healthcare resources in obstructive sleep apnea syndrome:
a 5-year follow-up study in men using CPAP. Sleep 2005;
28: 1306–1311.
74 Bing MH, Moller LA, Jennum P, Mortensen S, Skovgaard LT,
Lose G. Prevalence and bother of nocturia, and causes of
sleep interruption in a Danish population of men and
women aged 60–80 years. BJU Int 2006; 98: 599–604.
P. JENNUM AND R.L. RIHA EPIDEMIOLOGY OF SLEEP APNOEA
c
EUROPEAN RESPIRATORY JOURNAL VOLUME 33 NUMBER 4 913
75 Epstein LJ, Dorlac GR. Cost-effectiveness analysis of
nocturnal oximetry as a method of screening for sleep
apnea–hypopnea syndrome. Chest 1998; 113: 97–103.
76 Collop NA, Anderson WM, Boehlecke B, et al. Clinical
guidelines for the use of unattended portable monitors in
the diagnosis of obstructive sleep apnea in adult patients.
Portable Monitoring Task Force of the American Academy
of Sleep Medicine. J Clin Sleep Med 2007; 3: 737–747.
77 Jennum P, Santamaria J. Report of an EFNS task force on
management of sleep disorders in neurologic disease
(degenerative neurologic disorders and stroke). Eur J
Neurol 2007; 14: 1189–1200.
EPIDEMIOLOGY OF SLEEP APNOEA P. JENNUM AND R.L. RIHA
914 VOLUME 33 NUMBER 4 EUROPEAN RESPIRATORY JOURNAL
