Basic and Clinical

March, April 2018, Volume 9, Number 2

Research Paper: Sleep Architecture in Patients With Prima-

ry Snoring and Obstructive Sleep Apnea
Kaveh Shahveisi1, Amir Jalali2,3, Mohammad Raman Moloudi4, Shahla Moradi1, Azad Maroufi4, Habibolah Khazaie1*

1. Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
2. Department of Psychiatric Nursing, Faculty of Nursing & Midwifery, Kermanshah University of Medical Sciences, Kermanshah, Iran.
3. Substance Abuse Prevention Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
4. Neurosciences Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.

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Citation: Shahveisi, K., Jalali, A., Moloudi, M. R., Moradi, Sh., Maroufi, A., & Khazaie, H. (2018). Sleep Architecture
in Patients With Primary Snoring and Obstructive Sleep Apnea. Basic and Clinical Neuroscience, 9(2), 147-156. https://doi.
org/10.29252/NIRP.BCN.9.2.147
: : https://doi.org/10.29252/NIRP.BCN.9.2.147

Article info: AB STRACT

Received: 10 September 2017
First Revision: 04 October 2017 Introduction: This study aimed to investigate sleep architecture in patients with primary snoring
Accepted: 12 November 2017 and obstructive sleep apnea.
Methods: In this study, we analyzed polysomnographic data of 391 clients who referred to Sleep
Disorders Research Center (SDRS). These people were classified into three groups based on
their Apnea-Hypopnea Index (AHI) and snoring; control, Primary Snoring (PS), and Obstructive
Sleep Apnea (OSA) group. Sleep architecture variables were then assessed in all groups.
Results: The results of this study indicated a decrease in deep sleep or Slow Waves Sleep (SWS)
and increase in light sleep or stage 1 of non-REM sleep (N1) in OSA patients compared with the
control and PS groups. After controlling the effects of confounding factors, i.e. age and Body Mass
Index (BMI) (which was performed through multiple regression analysis) significant differences
were observed among the three groups with regard to N1. However, with regard to SWS, after
controlling confounding variables (age and BMI), no significant difference was found among the
groups.
Key Words: Conclusion: The results indicated that OSA, regardless of age and BMI, may increase light
Obstructive sleep (N1) sleep possibly via a decline in blood oxygen saturation (SpO2). Such increase in N1 may
apnea, Primary snoring, be responsible for brain arousal. In addition, by controlling confounding factors (age and BMI),
Sleep architecture, OSA did not affect SWS in OSA patients. However, further research is necessary to determine
Polysomnography sleep architecture in more detail in the patients with OSA.

O
1. Introduction increase in the prevalence of obesity (Khazaie et al.,
2011; Punjabi, 2008). Based on recent studies on general
bstructive Sleep Apnea (OSA) is the population, the prevalence of OSA is 3%-7% in adult
most common type of sleep disorder men and 2%-5% in adult women (Punjabi, 2008).
which has increased over the last few
decades in developed countries due to Sleep-Disordered Breathing (SDB) is recognized as a
the changes in lifestyle along with an group of sleep disorders, ranging from Primary Snoring

* Corresponding Author:
Habibolah Khazaie, MD
Address: Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Tel: +98 (31) 8260700
E-mail: [email protected]

147
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March, April 2018, Volume 9, Number 2

(PS) to Obstructive Sleep Apnea (OSA) (Nisbet, Yial- Several studies have indicated that age strongly influ-
lourou, Walter, & Horne, 2014). PS is a condition with ences sleep architecture (Ayalon, Ancoli-Israel, & Drum-
snoring (repetitive sounds due to vibration of upper air- mond, 2010; Dorffner, Vitr, & Anderer, 2015; Punjabi,
way structures) during sleep without apnea or hypopnea 2008). In general, there is a tendency to increase in light
(Zhu et al., 2014). OSA is defined as repeated periods sleep and a decrease in deep sleep with increasing age
of breathing cessation, called apnea or partial obstruc- (Ohayon, Carskadon, Guilleminault, & Vitiello, 2004;
tions in the upper airway, hypopnea, lasting 10 seconds Redline et al., 2004; Smagula et al., 2015). Also, there is
for the either one (Malhotra & White, 2002). The Ap- strong evidence that increased body mass index (BMI)
nea-Hypopnea Index (AHI) is defined as the number of may lead to changes in sleep structure. As previously re-
apnea and hypopnea events per hour of sleep. An AHI ported, there is a reverse correlation between BMI and
greater than 5 can be diagnosed as OSA (Moon, Punjabi, SWS (Rao et al., 2009). There is always a concern in
& Aurora, 2015). studies that examine the sleep architecture in people with
OSA, because the confounding factors, age and BMI,
Sleep architecture refers to circular pattern of sleep can affect the accuracy of results.
which changes among different sleep stages, such as
non-Rapid Eye Movement (non-REM) and rapid eye Because of limited information on sleep architecture
movement (Alabi et al., 2012) which normally starts in the patients with PS and OSA, further investigations
with lighter sleep stages, stage 1 non-REM (N1) and are needed to clarify precise sleep architecture in these
gradually shift to non-REM stages of sleep, each deeper people. This study aimed to investigate the sleep archi-
than previous, until it reaches the final stage, Slow Waves tecture by controlling age and BMI among the people
Sleep (SWS) stage (Hirshkowitz, 2004). Each sleep cy- with OSA, PS and those lacking sleep respiratory disor-
cle eventually leads to REM sleep stage. This non-REM/ der. We hypothesized that sleep architecture features are
REM cycle repeats several times until the person wakes different among these three groups.
up (Smagula et al., 2015).
2. Methods
The most common symptoms of sleep apnea include
excessive daytime sleepiness, fatigue, restless sleep, and 2.1. Study patients
morning headache. Among these, excessive daytime
sleepiness, due to an increased risk of accidents is very The polysomnographic data used in this study were
serious (Khazaie & Maroufi, 2014). However, daytime obtained from 391 clients (from Jan 2012 to Apr 2015)
sleepiness is absent in 40%-50% of OSA patients (Kapur, who referred to sleep disorder research center (Kerman-
Baldwin, Resnick, Gottlieb, & Nieto, 2005; Roure et al., shah, Iran). We excluded those people who suffered from
2008). Therefore, this disorder goes undetected and left diabetes, pulmonary disorders, mental disorders, cardio-
untreated. On the other hand, OSA accounts as an alarm vascular and neuromuscular diseases, drug users, ciga-
for many severe diseases, including hypertension (Tor- rette smokers and people who had been taking medica-
res, Sanchez-de-la-Torre, & Barbe, 2015), cardiovascu- tions affecting sleeping. Subjects were divided into three
lar diseases (De Torres-Alba et al., 2013; Devulapally, groups based on their AHI and snoring index: normal
Pongonis, & Khayat, 2009), stroke (Barone & Krieger, group with an AHI<5 without snoring; primary snoring
2013), and even diabetes (Cass, Alonso, Islam, & Weller, group with AHI<5 with snoring, and, OSA group with
2013; Tasali, Mokhlesi, & Van Cauter, 2008). For these AHI ≥5 with or without snoring.
reasons, diagnosis and treatment of OSA is necessary.
2.2. Study procedures
Today, Polysomnography (PSG) is considered as the
most accurate method for diagnosing of OSA (Kapoor AHI and snoring index was derived from polysomnog-
& Greenough, 2015). Polysomnography is composed raphy taken from subjects. After explaining the proce-
of several different leads to record physiological signals dure and providing sufficient time for them to familiar-
such as Electroencephalogram (EEG), Electroocculo- ize with the environment, all subjects underwent a full
gram (EOG), airflow, oxygen saturation, respiratory ef- overnight polysomnography. We analyzed some sleep
fort, heart rate and chin electromyogram. Continuous parameters of sleep architecture such as Total Sleep
Positive Airway Pressure therapy (CPAP) is the best Time (TST) which is defined as the period of time spent
known and the gold standard treatment for OSA (Spicuz- sleeping except wakefulness intervals, the percentage of
za, Caruso, & Di Maria, 2015; Vlachantoni et al., 2013). total sleep time spent in stage 1 of non-REM sleep, the
percentage of sleep time spent in stage 2 of non-REM

148 Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156.
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March, April 2018, Volume 9, Number 2

sleep, the percentage of sleep time spent in slow waves (P>0.05). However, marital status among the groups had
sleep (stages 3 and 4) of non-REM sleep, and lastly the a different and significant distribution (P=0.004) as 69.1
percentage of sleep time spent in REM sleep. The mini- % of the OSA subjects were married (Table 1).
mal arterial oxygen saturation (minimal SpO2), wake in-
dex (total number of awakenings per hour of sleep), and With regard to the PSG data (Table 2), the total sleep
brain arousals (total number of brain arousals in the total time in the three groups was more than 6 h (maximum 6.5
sleep time) also were evaluated in the groups. h in the OSA group and minimum 6.07 h in the normal
group) and no significant difference was found among
2.3. Statistical analyses the groups (P=0.688). Sleep Efficiency (SE) in all three
groups was more than 80% and no significant difference
The obtained data were initially assessed for normality was observed among these groups (P=0.647). However,
using Kolmogorov-Smirnov test. Afterwards, the mean N1 showed a significant difference between the OSA and
(SD) values were used for normally distributed data, two other groups; the highest percentage (48.57%) was
median (interquartile range) values for non-normally dis- observed in the OSA group (P<0.001) (Table 2 and Fig-
tributed data, and frequency percentage for categorical ure 2). With regard to N2, no significant difference was
data. The Chi-square test was used to determine the dif- observed among the groups. However, Slow Wave Sleep
ferences among the three groups. The differences among (SWS) (N3 and N4 stages of non-REM sleep) revealed a
the obtained means were analyzed using 1-way ANOVA significant difference among the groups (P<0.001) as the
followed by Tukey test and the differences among the lowest SWS (17%) was observed in the OSA group and
medians were analyzed using Kruskal-Wallis test fol- the highest SWS in the normal group (29.1%) (Table 2
lowed by Dunn’s test. Multiple linear regression analy- and Figure 2). As demonstrated in Table 2 and Figure 2,
sis was used to adjust confounding variables (BMI and the percentage of REM sleep of TST showed a similar
age). All study data were analyzed using SPSS 18 and P distribution among three groups (minimum 9.6% in the
values<0.05 was considered statistically significant. normal group and maximum 10.65% in the OSA group)
and there was no significant difference (P=0.721). As
3. Results shown in Table 2, minimal SpO2 in the OSA group with
a mean (SD) of 84(11) indicated a significant reduction
Table 1 presents the demographic data of 391 study compared to those of the other two groups with a mean
subjects. The mean (SD) age and BMI values (46±14 y of 90% (P<0.001). Brain arousal (in TST) showed a
and 28.67±4.2 kg/m2, respectively) of the subjects of the significant increase (with a mean [SD] of 27.14 [8.29])
OSA group were significantly higher than those of the in the OSA group in comparison with the other groups
PS and control groups (P<0.001). Therefore, multiple re- (P<0.001). Wake index in the three groups showed no
gression analysis was used to control the effects of these significant difference among the groups (Table 2).
two confounding variables (Table 3).
Because age and BMI confounding factors were sig-
The results showed an uneven distribution with regard nificantly different among the groups (Table 1 and Fig-
to gender among the groups (P=0.01). The distribution ure 3), we used multiple regression analysis to control
of other variables, such as job and educational status, did their effects (Table 3). It should be noted that only those
not show any significant difference among the groups

Figure 1. The effects of OSA on sleep architecture

↑: Increase; ↓: Decrease; -: No effect; OSA: Obstructive Sleep Apnea; N1: Stage 1 of Non-REM sleep; N2: Stage 2 of Non-REM
sleep; SWS: Slow-Wave Sleep; REM: Rapid Eye Movement; Minimal SpO2: Minimal oxygen saturation

Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156. 149
 Basic and Clinical
March, April 2018, Volume 9, Number 2

Table 1. Demographic data

Normal PS OSA P

Age, y 36.21a±14.03 38.82a±17.42 46.23b±13.9 <0.001‡

AHI 1.9a(2.75) 2.3a(2) 15.7b(20.35) <0.001†

BMI, kg/m2 24.3a±3.81 25.39a±4.85 28.69b±4.78 <0.001‡

Female 24(17.9) 41(30.6) 69(51.5)

Gender
0.01§
n (%)
Male 27(10.5) 60(23.3) 170(66.1)

Unemployment 22(19.1) 36(31.3) 57(49.6)

Employment 23(11.3) 48(23.6) 132(65.0)

Job
0.077#
n (%)
Driver 6(10.3) 14(24.1) 38(65.5)

Shift worker 0(0.0) 3(20.0) 12(80.0)

Illiterate 2(5.7) 9(25.7) 24(68.6)

Primary 13(14.8) 27(30.7) 48(54.5)

Educational status
0.32§
n (%)
High school & diploma 20(15.0) 26(19.5) 87(65.4)

Academic 16(11.9) 39(28.9) 80(59.3)

Single 18(22.2) 31(38.3) 32(39.5)

Marriage statues
Married 27(9.7) 59(21.2) 192(69.1) 0.004#
n (%)
Widow or divorced 6(18.8) 11(34.4) 15(46.9)

PS: Primary Snoring; OSA: Obstructive Sleep Apnea; BMI: Body Mass Index; AHI: Apnea–Hypopnea Index
Mean±SD, median (interquartile range), and percentage (%) are presented for parametric, nonparametric, and categorical data,
respectively. Means or median with same superscript letters are not significantly different (P>0.05).
†: Kruskal-Wallis test followed by Dunn’s multiple comparisons test was used.
‡: One-way ANOVA test followed by Tukey test was used.
§: The Chi-square test was used.
#: Monte Carlo Chi-square was used.

variables which were statistically significant in Table 2 of 25-44 age range, BMI indicated a significant increase
(N1 and SWS), were reanalyzed and presented in Table in the OSA group compared to the two other groups
3 to control the effects of the confounding factors. The (P=0.002). On the other hand, minimal SpO2 showed
analysis indicated a significant difference in observed a significant decrease in OSA compared to the others
N1 among the three groups (95%CI=0.42-5.6) (Table 3). (P<0.001). Brain arousals showed a significant increase
In the case of SWS, no significant difference was found in the OSA group as compared with the PS but with the
among the groups (95%CI=-4.6-0.5) (Table 3). control group (P=0.001).

PSG data were also examined in the age ranges of 15- The results obtained from PSG data of 45-64 and
24, 25-44, 45-64, and 65-84 years. As illustrated in Table 65-84 years age groups are presented in Table 5. Ac-
4, BMI showed a significant increase in the age range cording to the results, BMI in the age range of 45-64
of 15-24 years of the OSA group as compared with the years, showed a significant increase in the OSA group
same age range of the PS (P=0.022) group. In addition, compared with the same age range of the control and
in this age range, minimal SpO2 demonstrated a signifi- PS groups (P=0.002). OSA had a significant increase
cant decrease in the OSA group compared with the con- (P=0.003) in N1 and a significant decrease (P=0.021)
trol group (P=0.014). As shown in Table 4, in the case in SWS at the age range of 45-64 years as compared

150 Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156.
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Table 2. Polysomno graphic data

Normal (n=51) PS (n=101) OSA (n=239) P

TST (h) 6.72a(1.14) 6.89a(1.26) 6.605a(1.25) 0.688†

SE 88.1a(13.37) 89.5a(13.2) 87.3a(13.68) 0.647†

N1 (%TST) 40.24a±16.86 38.15a±17.84 48.57b±17.81 <0.001‡

N2 (%TST) 18.5a(15.08) 20.8a(23.75) 18.9a(15.3) 0.37†

SWS (%TST) 29.1b(21.53) 23.3b(25.2) 17a(20.5) <0.001†

REM (%TST) 5.5a(11.7) 7.3a(10.5) 7.2a(10.8) 0.721†

Minimal SpO2 90b(4) 90b(5) 84a(11) <0.001†

Brain arousals (in TST) 23.97a±6.38 23.91a±7.32 27.14b±8.29 <0.001‡

Wake index 4.2a(4.55) 3.1a(5.5) 3.6a(4.6) 0.834†

PS: Primary Snoring; OSA: Obstructive Sleep Apnea; TST: Total Sleep Time; SE: Sleep Efficiency; N1, stage 1 of non-REM sleep;
N2, stage 2 of non-REM sleep; SWS: Slow-Wave Sleep; REM: Rapid Eye Movement; Minimal SpO2, minimal oxygen saturation
Mean±SD, median (interquartile range), and percentage (%) are presented for parametric, nonparametric, and categorical data,
respectively. Means or median with same superscript letters are not significantly different (P>0.05).
†: Kruskal-Wallis test followed by Dunn’s multiple comparisons test was used.
‡: One-way ANOVA test followed by Tukey’s test was used.

with the PS; however, it did not demonstrate any sig- 4. Discussion
nificant difference in these variables when compared
with the control group. Minimal SpO2 in the OSA The study findings show that people with OSA experi-
group was significantly (P<0.001) lower than the other ence more light sleep and less deep sleep as compared
groups. Lastly, brain arousals showed a significant in- with the people without apnea and even people who are
crease in the OSA group as compared with merely the having snoring without apnea (primary snorer). Further-
control (P=0.02). Finally, as it has been presented in more, the obtained data indicate that the OSA groups
Table 5, in the 65-84 years age group, only wake index also have a lower minimal SpO2 in comparison with the
revealed a significant increase in the OSA group com- control group. Finally, we found no significant differ-
pared with the PS group (P=0.001). It should be noted ences in total sleep time and Sleep Efficacy (SE) among
that no subject of this age range (65-84) was in the the groups studied.
control group. In brief, as illustrated in Figure 1, OSA
increased N1 and brain arousals and decreased SWS The study results also show that gender is not equally
and minimal SpO2; however, it did not have any effect distributed in study groups, so that most people who were
on N2 or REM stages. diagnosed with OSA were men but women constituted a
higher percentage in PS group (P=0.01). Many studies

Table 3. Multiple regression model

Outcome Variable Predictor Variable B 95%CI SE P

Age 0.24 (0.16-0.41) 0.062 <0.001
N1 (%TST) BMI 0.108 (0.004-0.78) 0.199 0.048
Category 0.117 (0.42-5.6) 1.31 0.023
Age -0.131 (-0.27- -0.33) 0.061 0.013
SWS (%TST) BMI -0.252 (-1.3- -0.54) 0.196 <0.001
Category -0.081 (-4.6-0.5) 1.29 0.114

Multiple regression model was used to adjust confounding variables (age and BMI) to determine the significant differences
in sleep stages (N1 and SWS) among the groups. Abbreviations: Category, study groups; CI: Confidence Interval; TST: Total
Sleep Time; BMI: Body Mass Index; SWS: Slow Wave Sleep; BMI: Body Mass Index

Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156. 151
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Table 4. Age classification of variables

15-24 Year 25-44 Year

Normal PS OSA P Normal PS OSA P

AHI 1.3a±0.92 2.2a±1.16 13.86b±18.72 0.011‡ 2.3a(3.3) 2a(2.32) 13.6b(14.8) <0.001†

BMI 21.63a±3.46 21.93ab±2.34 24.95b±3.92 0.022‡ 24.99a±3.28 25.96ab±3.76 27.73b±3.79 0.002‡

TST (h) 6.97±0.56 7.12±0.67 6.97±0.99 0.849‡ 6.60±.84 6.42±1.56 6.88±.71 0.072‡

SE 91.67±5.70 91.87±5.29 91.52±9.10 0.992‡ 86.5(21.6) 89.6(12.65) 90.9(11.6) 0.206†

N1 (%TST) 35.19±12.05 32.85±8.76 36.54±10.09 0.640‡ 40.03±17.26 39.98±17.15 44.03±15.13 0.329‡

N2 (%TST) 15.53±8.45 22.35±13.93 22.72±7.15 0.149‡ 22.22±15.08 24.59±13.02 23.74±12.25 0.774‡

SWS (%TST) 38.36±15.87 33.63±18.09 32.47±14.39 0.621‡ 27.98±15.08 24.36±19.06 22.37±15.22 0.355‡

REM (%TST) 10.92±18.27 7.69±8.70 8.28±11.44 0.810‡ 7.1(14.4) 7.85(11.63) 7.3(10.6) 0.922†

Minimal SpO2 91.92b±1.51 90.31ab±3.52 88.87a±2.17 0.014‡ 91b(4) 91b(3) 87a(6) <0.001†

Brain arousals (in TST) 25.50±4.17 27.45±5.01 25.80±5.99 0.594‡ 24.85ab±5.38 22.73a±7.73 27.88b±7.87 0.001‡

WI 3.62±2.02 2.20±1.79 2.76±2.97 0.333‡ 4.3(7) 3.3(5.8) 3.1(3.1) 0.305†

Abbreviations: PS, primary snoring; OSA, obstructive sleep apnea; AHI, apnea–hypopnea index; BMI, body mass index; TST,
total sleep time; SE, sleep efficiency; N1, stage 1 of non-REM sleep; N2, stage 2 of non-REM sleep; SWS, slow-wave sleep; REM,
rapid eye movement; Minimal SpO2, minimal oxygen saturation. Mean±SD, median(interquartile range), and percentage(%)
are presented for parametric, nonparametric, and categorical data, respectively. Means or median with same superscript letters
are not significantly different(P>0.05).
† Kruskal-Wallis test followed by Dunn’s multiple comparisons test was used.
‡ One-way ANOVA test followed by Tukey test was used.
§ Independent Samples t test was used.

have confirmed our findings about ‌a higher prevalence any significant difference in sleep architecture of snor-
of OSA in men (Chan, Wong, Tang, & Ng, 2012; Pami- ers and non-snoring subjects (Fuentes-Pradera et al.,
di, Knutson, Ghods, & Mokhlesi, 2011; Punjabi, 2008; 2003; Hoffstein, Mateika, & Mateika, 1991). Hoffman
Quintana-Gallego et al., 2004; Redline, Kump, Tishler, investigated the sleep architecture of heavy snoring and
Browner, & Ferrette, 1994). However, contrary to our light snoring subjects without any difference in their
findings that demonstrated a higher prevalence of snor- age, BMI and AHI and didn’t find any significant differ-
ing in women, other studies reported that snoring was ence in sleep architecture between these groups (Hoffs-
more prevalent in men (Alabi et al., 2012; Bouscoulet tein et al., 1991).
et al., 2008; Chan et al., 2012). Based on the obtained
data from clients who were referred to the sleep center, The results of our study agree with the previous investi-
these results cannot be a good representation of the com- gation concerning the effect of age and BMI variables on
munity. In this regard, Zhan and colleagues in a system- the sleep architecture. Our findings also show a positive
atic review published in 2012 about gender difference in correlation between age and the risk of OSA. Thus, peo-
snoring, reported that a selection bias existed in studies ple with OSA have a higher average age compared with
intended to examine the effects of gender in snoring and people without OSA, as previous studies have reported
therefore their results were overshadowed by this issue (Jennum & Riha, 2009; Punjabi, 2008). In this study,
(Chan et al., 2012). we used relevant statistical analysis methods to control
age and BMI. In addition, the clients were classified into
Furthermore, there was no significant difference be- four age ranges and PSG data in these age ranges were
tween normal and PS group with regard to sleep archi- reanalyzed.
tecture. In this regard, previous studies have not found

152 Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156.
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Table 5. Age classification of variables

45-64 Year 65-84 Year

Normal PS OSA P Normal PS OSA P

AHI 2.25a(3.15) 2.5a(1.4) 20.1b(27.4) <0.001† - 2.21±1.43 21.24±14.37 <0.001§

BMI, kg/m2 25.71a±3.69 28.14ab±5.31 29.99b±4.93 0.002‡ - 25.59±4.25 27.68±4.61 0.312§

TST (h) 6.8(1.13) 6.47(1.45) 6.47(1.31) 0.593† - 5.87±.68 6.27±.61 0.164§

SE 88.1(11.52) 84.9(15.4) 84.5(16.2) 0.37† - 76.49±8.99 83.11±8.73 0.108§

N1 (%TST) 45.65ab(18.25) 40.8a(29.9) 53b(26.35) 0.003† - 56.83±22.99 54.54±18.46 0.799§

N2 (%TST) 21.7(17.95) 21.8(25.5) 17.6(13.3) 0.246† - 11.10±9.05 14.11±7.23 0.398§

SWS (%TST) 21.55ab(28.55) 22.2b(18.7) 14a(18.75) 0.021† - 24.09±22.95 20±15.95 0.621§

REM (%TST) 5.4(9.53) 7.9(11.6) 7.2(11.5) 0.836† - 7.97±9.44 11.33±13.93 0.567§

Minimal SpO2 89b(4) 87b(6) 82a(12) <0.001† - 89±2 77±15 0.53§

Brain arousals (in TST) 21.57a±8.60 22.99ab±6.65 26.64b±8.87 0.02‡ - 27.11±10.46 28.62±7.84 0.702§

WI 5.05(4.47) 4.3(7.7) 4.3(5.75) 0.832† - 9.89±4.23 4.75±2.21 0.001§

Abbreviations: PS: Primary Snoring; OSA: Obstructive Sleep Apnea; AHI: Apnea–Hypopnea Index; BMI: Body Mass Index;
TST: Total Sleep Time; SE: Sleep Efficiency; N1: stage 1 of Non-REM sleep; N2: stage 2 of Non-REM sleep; SWS: Slow-Wave
Sleep; REM: Rapid Eye Movement; Minimal SpO2: Minimal Oxygen Saturation
Mean±SD, median (interquartile range), and percentage (%) are presented for parametric, nonparametric, and categorical data,
respectively. Means or median with same superscript letters are not significantly different (P>0.05).
†: Kruskal-Wallis test followed by Dunn’s multiple comparisons test was used.
‡: One-way ANOVA test followed by Tukey test was used.
§: Independent Samples t test was used.

The results showed that by controlling the age and BMI to the potent effects of confounding variables. Rao et al.
effects on the sleep architecture, the percentage of N1 in (2009) showed a negative correlation between BMI and
OSA group was significantly higher than the other two SWS (Rao et al., 2009). Moreover, some studies have
groups. As it was revealed by 1‐way ANOVA with Tukey also shown that SWS decreases with increasing age
post hoc test, this significant difference was observed (Ohayon et al., 2004; Redline et al., 2004). Therefore,
only in 45-65 years age group. This finding is consistent the effect of confounding factors such as age and BMI
with the results of an epidemiological study indicating could reduce SWS in OSA patients (Ohayon et al., 2004;
the majority of OSA patients to be in 50-59 years age Rao et al., 2009; Redline et al., 2004; Zhu et al., 2014).
range and that a reduction in the risk of OSA is observed In other words, the effect of OSA on reducing SWS may
after the age 60 (Gislason, Almqvist, Eriksson, Taube, & be due to age and BMI variables on sleep architecture.
Boman, 1988). In this regard, other studies have reported
an increase in the risk of OSA until the age 60 and a re- Also in this study, demographic variables such as em-
duction thereafter (Bixler, Vgontzas, TenHave, Tyson, & ployment status, education, and marital status were eval-
Kales, 1998; Cass et al., 2013). Therefore, these studies uated. With regard to employment status and education,
support the validity of our results. no statistically significant difference was found among
three groups. Regarding marital status of the subjects,
With regard to slow-wave sleep, the initial tests showed most people with OSA were married and such difference
a significant difference among three groups. However by can, at least be due to sampling of this study, as the ma-
controlling age and BMI, as confounding factors, SWS jority of the OSA married subjects were forced by their
showed no significant difference among the groups. It is spouses to refer to our research center.
difficult to explain these results, but it might be related

Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156. 153
 Basic and Clinical
March, April 2018, Volume 9, Number 2

A B
100
50
80
45 60

N1 (%TST)

N2 (%TST)
40 40

20
35
0
Normal PS OSA Normal PS OSA
C D
100
60
80

REM (%TST)
60 40
SWS (%TST)

40
20
20

0 0
Normal PS OSA Normal PS OSA

Figure 2. The effect of PS and OSA on sleep architecture (sleep stages)

N1 stage showed a significant increase induced by OSA (A) and SWS showed a significant decline induced by OSA (C). N2 (B)
and REM (D) stages did not show any difference among the groups. The data of N1 was normally distributed and analyzed us-
ing One-way ANOVA test followed by Tukey’s test; but, the data of N2, SWS, and, REM stages were non-normally distributed
and analyzed using Kruskal-Wallis test followed by Dunn’s multiple comparisons test.
TST: Total Sleep Time; N1, stage 1 of non-REM sleep; N2, stage 2 of non-REM sleep; SWS: Slow-Wave Sleep; REM: Rapid Eye
Movement.

A B
100 R2 Liner= 0.061
100 R2 Liner= 9.196E-5

80 80
N1 (%TST)

N2 (%TST)

60 60

40 40

20 20

0 0
10 20 30 40 50 10 20 30 40 50
C BMI D BMI
R2 Liner= 0.112
100 R2 Liner= 0.022

60
80
REM (%TST)
SWS (%TST)

60 40

40
20
20

0 0
10 20 30 40 50 10 20 30 40 50
BMI BMI

Figure 3. Correlation between BMI and sleep architecture (sleep stages)

N1 showed a positive correlation with BMI (A) and SWS showed a negative correlation with BMI (C). N2 (B) and REM (D)
did not have any significant correlation with BMI.
BMI: Body Mass Index; TST: Total Sleep Time; N1, stage 1 of non-REM sleep; N2, stage 2 of non-REM sleep; SWS: Slow-Wave
Sleep; REM: Rapid Eye Movement

154 Shahveisi, K., et al. (2018). Sleep Architecture in Primary Snoring and OSA. BCN, 9(2), 147-156.
Basic and Clinical
March, April 2018, Volume 9, Number 2

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