Obstructive sleep apnea syndrome (OSAS) is a disorder of breathing characterized by repetitive collapse of pharyngeal airway during sleep that leads to sleep fragmentation and oxygen desaturation (1-3). The associated consequences include daytime sleepiness, decreased cognitive performance and quality of life, increased risk of automobile accidents and adverse cardiovascular consequences such as pulmonary and arterial hypertension, myocardial infarction and stroke (4). The mechanisms responsible for upper airway obstruction in OSAS are very complicated and as yet not fully understood (5). Upper airway and craniofacial abnormalities are said to play a role in OSAS together with the neurological dysfunction (6, 7). OSAS occurs in 4 to 9% of middle-aged men and 1 to 2% of middle-aged women. The incidence of this syndrome among morbidly obese patients is 12 to 30 times higher than in general population (8).
Obesity is one of the strongest risk factor for the development of OSAS. Obesity
is present in 60 to 90% of patients diagnosed with apnea (8). OSAS is three
times frequenting among obese than non-obese patients (9). Obesity is associated
with metabolic derangement, including dyslipidemia, hyperinsulinism, impaired
glucose tolerance and hypertension. The presence of these factors is termed
the insulin-resistant syndrome and they predispose obese patients to morbidities
such as
diabetes mellitus and cardiovascular diseases (10). Recent studies
support a correlation between breathing disturbances during sleep and insulin
resistant syndrome, independent of the degree of obesity (10-12). The research
into the genetic basis of obesity may uncover factors linking obesity and OSAS.
The adipose associated hormone - leptin, seems to be responsible for the central
regulation of food intake and energy hemostasis, may play a particularly important
protective role in the regulation of respiration, especially during sleep (13).
The circulating levels of leptin are higher in women than in men because subcutaneous
fat (lower - female body obesity) produces more leptin than visceral (upper
-male body obesity) (14).
The aim of our study was to evaluate the correlation between the Body Mass Index (BMI) and sleep study parameters in overweight and obese patients suffering from breathing disturbances during sleep.
MATERIAL AND METHODS
A total of 106 consecutive obese or overweight patients, represented by 12 women
and 94 men, aged from 24 to 78 were recruited for our study. All patients gave
their consent to participate in the study, which had previously been approved
by the Ethics Committee of the Silesian Medical University. All subjects were
presented to our outpatient clinic between July 1997 and April 2002 with a primary
complaint of snoring or other breathing disturbances during sleep. All of them
were studied during sleep by PolyMESAM (MAP Medizintechnik für artz und patient
GMBH). The following parameters were measured: the snoring level, nasal and
mouth airflow, body position, heart rate frequency, thoracic and abdominal respiratory
movements, oxygen saturation and leg movement activity. On the base of the results
after 7-hour night examination the following indexes were calculated: Respiratory
Disturbance index (RDI), Apnea Index (AI), Desaturation Index (DI) and Average
of Lowest Saturation (LSAT). After the sleep studies our patients were divided
into the habitual snorers (RDI<10) and OSA patients (RDI>10). All the patients
were physically examined (especially status and anatomical abnormalities of
the upper airway). The site of obstruction was identified by means of endoscopic
evaluation. On the basis of the BMI values (assessed from patient's weight and
height) the subjects were divided into three groups according to the severity
of obesity. The first group consisted of subjects with BMI between 25 and 30
kg/m
2 (overweight), the second with BMI between
30 and 35 kg/m
2 and the third with BMI over the
35 kg/m
2.
In these three groups correlations between BMI and sleep study parameters (RDI, AI, DI and LSAT) were examined. The measurements were conducted using the rank correlation Spearman test. The evaluations were performed with the use of the statistical package SPSS and SAS (WIN).
RESULTS
The mean age of the 106 subjects (represented by 12 women and 94 men) was 49.2
± 11.8 (ranged from 24 to 78 years). This group was divided into three subgroups
- overweight (BMI 25-30), obesity class I (BMI 30-35) and obesity class II (BMI
over 35). In the first group there were 55 subjects aged from 24 to 71 (mean
age 50.4 ± 11). The mean BMI in this group was 27.4 ± 1.4 kg/m
2
(ranged from 25 to 29.9). Overnight sleep study revealed that in this group
were 22 habitual snorers (RDI lower than 10) and 33 OSA patients (RDI higher
than 10). The mean value of RDI was 19.8 ± 20.3 (ranged from 0 to 83). Among
the OSA patients, 17 were classified as mild, 10 as moderate and 6 as severe
OSAS (
Table 1).
Table 1.
The results of sleep study in the overweight and obese patients. |
|
The group of class I obesity consisted of 34 patients with BMI between 30 and
35 kg/m
2 aged from 27 to 70 years (mean age 49.1
± 9.4). The mean BMI was 31.7 ± 1.47 kg/m
2 (ranged
from 30 to 34.9). Sleep study divided obesity subjects into 9 habitual snorers
and 25 OSA patients. The mean value of RDI in OSA patients was 30. There were
5 mild, 11 moderate and 9 severe cases of OSAS.
The group of class II obesity consisted of 17 patients with BMI over 35 kg/m
2.
The mean age of this group was 45.1 ± 8.1 (ranged from 36 to 63). The mean BMI
was 38.8 ± 3.2 kg/m
2 (ranged from 35 to 45.3).
After the sleep study these patients were divided on 4 habitual snorers, 4 moderate
and 9 severe OSAS. The mean RDI in this group was 49.
The measurements of relationship between the BMI and sleep study parameters
were conducted using the Rang Spearman correlation test. The results of this
test were showed in the
Table 2, 3 and
4. We found no statistically
significant correlation between BMI and sleep study parameters in the overweight
patients. In the obesity class I this correlation were statistically significant
positive when we compared BMI and RDI and significant negative in comparison
of BMI and LSAT. In the obesity class II we found statistically significant
positive correlation when we compared BMI with RDI and AI.
Table 2.
The results of correlation test between BMI and sleep study parameters
in overweight patients |
|
* BMI - Body
Mass Index
RDI - Respiratory Disturbance Index
AI - Apnea Index
DI - Desaturation Index
LSAT - Lowest Saturation |
Table 3.
The results of correlation test between BMI and sleep study parameters in obese class I patients (BMI 30-35) |
|
* BMI - Body
Mass Index
RDI - Respiratory Disturbance Index
AI - Apnea Index
DI - Desaturation Index
LSAT - Lowest Saturation |
Table 4.
The results of correlation test between BMI and sleep study parameters in obese class II patients (BMI over 35) |
|
* BMI - Body
Mass Index
RDI - Respiratory Disturbance Index
AI - Apnea Index
DI - Desaturation Index
LSAT - Lowest Saturation |
DISCUSSION
Obesity is probably the most important among the risk factors for OSAS (15, 16). Significant sleep apnea is present in approximately 40% of obese individuals and 70% of OSAS patients are obese. Weight loss in OSAS patients led to a significant decrease in apnea frequency (17-19). An increase in BMI of 1 SD is associated with a fourfold increase in risk for OSA. The neck circumference was the most powerful predictor of OSA among all anthropometric variables. This fact suggested that upper body or central obesity may be important for the development of OSAS (3, 20).
The exact mechanisms underlying the effects of obesity on the risk of OSA are still unclear. It may be the results of fat deposition on upper airway wall or changes in upper airway function (19). The modification in central mechanisms regulating airway tone or ventilatory control stability caused by obesity may also be implicated. Leptin is a circulating hormone expressed, synthesized and released in adipose tissue. Plasma leptin concentrations are increased in people with obesity in direct proportion to body fat mass (3). Leptin has important effect on regulation of chemoreflex function and hence breathing control (19).
It has been recognized that not only increased body weight, but also the type of regional fat distribution (abdominal-visceral vs. gluteal-femoral) plays an important role in the development of OSAS. Central (visceral) obesity is associated more often with OSAS than other forms of obesity. The fat deposition in the neck region, especially in the parapharyngeal region plays an important role in the development of OSAS (3). Fat deposits in the upper airway and pharyngeal walls of obese patients can lead to narrowing of the pharyngeal space (9). Fat infiltration of the upper airway and parapharyngeal region may soften the soft palate, tongue, epiglottis and pharyngeal walls, predisposing to upper airway narrowing or obstruction during sleep (21).
Several studies of obese patients have shown that the relationship between the
measures of obesity and severity of OSAS is only moderate and varies widely.
Increased BMI has been found to be an unfavourable prognostic factor for the
success of surgical treatment for OSAS (22). Akita
et al. observed no
significant correlation between BMI and either AHI or desaturation rate in obese
patients. There was only a tendency for the increase of AHI together with the
increase in BMI (23). Vgontzas found in a group of 250 obese men and women that
only 50% of men and 8.5% of women had AHI more than 30 during the night. There
was no difference in mean BMI in the group with and without apnea (24). Similarly,
Rajala found no difference in mean BMI in a group of morbidly obese patients
with and without apnea during sleep (25). Fogel observed no relationship between
obesity (weight or BMI) and apnea severity (RDI) in the group of 14 morbidly
obese patients (4). Dixon studied the predicting factors of OSA in the severely
obese patients. He found that four clinical and two biochemical factors independently
predicted AHI: observed sleep apnea, male sex, higher BMI, age, fasting insulin
and glycosylated hemoglobin A. The increasing of BMI was associated with reduced
sleep efficiency and a reduction in the proportion of REM sleep (26). Pillar
observed in the large population of patients referred to sleep laboratory the
significant correlation between BMI and AHI. This correlation was moderate and
weakened when the group was restricted to cases with only overweight (27).
Our results were very similar. We observed no significant relationship between
the obesity measurement (BMI) and sleep study parameters (RDI, AI, HI and DI)
in overweight patients (BMI 25-30 kg/m
2) but in
obese patients (class I and II) there were a significant correlation between
increasing BMI and RDI was found. The mean RDI progressively increased with
the increasing of obesity measurement (BMI).
We conclude that BMI is a simple, yet important predictor of the OSAS in the group of obese patients.
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