Original article 120

The effect of continuous positive airway pressure on

dyslipidemia in patients with obstructive sleep apnea
Walid Abdelmohsen Shehab-Eldina, Mahmoud Elhabashyb

Background Obstructive sleep apnea (OSA) is a prevalent month without more improvement after 3 months. Low-
disease associated with increased risk of cardiovascular density lipoprotein-cholesterol and total-C did not change
mortality. However, the exact causal relationship is not clear. after 1 month with significant reduction after 3 months.
One of the proposed mechanisms is dyslipidemia.
Conclusion Treatment with CPAP improves lipid profile in
Aim To study the effect of continuous positive airway patients with OSA.
pressure (CPAP) on dyslipidemia in patients with OSA. Egypt J Bronchol 2019 13:120–124
© 2019 Egyptian Journal of Bronchology
Patients and methods Forty obese patients with OSA were
recruited. All patients were subjected to history taking, Egyptian Journal of Bronchology 2019 13:120–124
physical examination, and polysomnography. Fasting blood Keywords: continuous positive airway pressure, dyslipidemia, obstructive
sugar, liver function, kidney function, and lipid profile were sleep apnea
measured after fasting for 14 h. Apnea/hypopnea index and
Departments of, aInternal Medicine, bChest, Faculty of Medicine, Menoufia
BMI were calculated. The patients then received CPAP University, Menoufia, Egypt
treatment during night for 3 months. Polysomnography and
Correspondence to Walid Abdelmohsen Shehab-Eldin, MD, Department of
laboratory parameters were remeasured after 1 and 3 months Internal Medicine, Diabetes & Endocrinology Unit, Menoufia University,
of treatment. Menoufia, 32951, Egypt. Tel: +20 101 660 6390; fax: +2048 5752777;
e-mail: [email protected]
Results The natural correlation between body weight and
lipid profile is lost. Apnea/hypopnea index and high-density Received 29 July 2018 Accepted 31 October 2018
lipoprotein improved significantly after 1 month and more
significantly after 3 months. Triglycerides were lowered after 1

Introduction conjecture that dyslipidemia is a nontraditional risk

Obstructive sleep apnea (OSA) syndrome is a factor increasing the incidence of CVD in patients with
condition characterized by complete or partial OSA [9].
interruption of respiration during sleep leading to
awakening from sleep, bouts of hypoxia, and Continuous positive airway pressure (CPAP) is the
hemodynamic changes [1]. main line of treatment of OSA with documented
improvement of respiratory function. Moreover, it
The global prevalence of OSA is estimated at one may improve the CVD outcome in those patients
billion people in 2018 [2]. Thirty percent of adult [10]. However, the mechanism of this improvement
Egyptians have OSA [3]. The association between is not clear. Improvement of dyslipidemia may be
OSA and cardiovascular disease (CVD) is very among the factors that could improve the CVD
strong [4]; 61.9% of patients with cerebrovascular outcome in this population. The effect of CPAP on
disease have OSA [5]. There are several mechanisms dyslipidemia is not established and gave conflicting
that may lead to the development of CVD in patients data [11,12].
with OSA. These mechanisms include and are not
limited to intermittent hypoxia, hypercapnia, sleep
disruption, and intrathoracic pressure oscillations [6]. Aim
To study the effect of CPAP on dyslipidemia in
Dyslipidemia as evidenced by low high-density patients with OSA.
lipoprotein-cholesterol (HDL-C), hypertriglyceri-
demia, high low-density lipoprotein-cholesterol
Patients and methods
(LDL-C), and high total-C is a major CVD risk
The present study is a prospective, interventional trial
factor [7]. The causative relationship between OSA
carried out on 40 obese patients diagnosed as OSA
and dyslipidemia is yet to be established. However,
there is cumulative evidence that OSA is independently
associated with dyslipidemia via the production of This is an open access journal, and articles are distributed under the terms
of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0
stearoyl-coenzyme A desaturase-1 and reactive License, which allows others to remix, tweak, and build upon the work
oxygen species, peroxidation of lipids, and non-commercially, as long as appropriate credit is given and the new
sympathetic system derangement [8]. So, there is a creations are licensed under the identical terms.

© 2019 Egyptian Journal of Bronchology | Published by Wolters Kluwer - Medknow DOI: 10.4103/ejb.ejb_57_18
 CPAP improves OSA induced dyslipidemia Shehab-Eldin and Elhabashy 121

[apnea/hypopnea index (AHI>15)] [13] referred to arousal [13]. However, it is acceptable for hypopnea to
the Sleep Laboratory Unit in Chest Department at be associated with more than or equal to 4% oxygen
Menoufia University Hospital. Ethics committee desaturation from pre-event baseline.
approval was obtained before the beginning of the
study. Polysomonography was done on room air followed by
follow-up after 1 and 3 months of CPAP treatment.
All patients referred to our center over the year 2017
and diagnosed with OSA were included in the study. AHI is calculated by the number of apnea and
The patients were excluded if they were diabetic or hypopnea events divided by the number of hours of
hypertensive or receiving any treatment affecting the sleep [13,14].
lipid profile. After taking an informed written consent,
the following data were obtained from every patient: Fasting blood sugar and cholesterol profile were
measured after overnight fasting at baseline without
(1) Personal history included (age, sex, and smoking). CPAP. Reevaluation was done after 1 month and after
(2) Clinical examination findings with special 3 months of CPAP treatment during sleep.
attention to body weight (kg), height (cm),
BMI, and neck circumference (cm(. Statistical analysis
(3) Epworth Sleepiness Scale: The Epworth The statistical analysis of data was done using the
Sleepiness Scale final score was categorized into statistical package for the social sciences, version 22
less than 11 (low risk for sleepiness) and more than (SPSS Inc., Chicago, Illinois, USA). The quantitative
or equal to 11 (high risk for sleepiness). variables were described as mean±SD and range as
(4) Routine laboratory investigations included (fasting appropriate. Qualitative variables were described as
blood sugar, triglycerides, total-C, LDL-C, and number or frequency. Paired t test was used to
HDL-C). indicate collectively the presence of any significant
difference between two groups for a normally
AHI was estimated three times: at baseline, after 1 distributed quantitative variable. χ 2 test was used to
month, and after 3 months. Overnight compare two groups as regards qualitative variables.
polysomonography on room air was done using
EMBLA S 4000 system (Biomed, Reykjavik,
Iceland). It was conducted in the Sleep Laboratory Results
Unit, Chest Department, Menoufia University The present study is a prospective interventional study
Hospital over a whole night (at least 8 h sleep). on 62 patients (32 men and 30 women). All patients
Factors that affect sleep rhythm such as xanthines, were instructed to use CPAP for 6–8 h per night with a
hypnotics, and central nervous system stimulants pressure ranging from 8 to 12 cm H2O at least 5 days
were stopped at least one night before the session. per week. Only 40 (22 men and 18 women) (64%) were
ECG electrodes were fixed one below the clavicle in the compliant and fulfilled the criteria till the end of the
mid-clavicular line and the second was fixed at the apex study, while 22 (36%) patients dropped out.
of the heart; the abdominal belt was fitted at the level of
umbilicus; the thoracic belt was fitted at the level of the The included patients were overweight or obese
nipples; the body position sensor was fixed between the (BMI=36.01±4.25) and have OSA (AHI=44.00
two belts; oronasal thermistor transducer was fitted in ±11.96). The fasting blood sugar ranged from 78 to
the nostrils to measure changes in inhalation and 99 mg/dl. Their basal lipid profiles were as follows:
exhalation and the rate of breathing. Pulse oximeter total-C=255.90±40.18 mg/dl, LDL-C=166.90
was placed on a patient’s finger to detect blood oxygen ±40.13 mg/dl, HDL-C=30.45±5.73 mg/dl, and
saturation levels and the sound probe was placed over triglycerides=292.75±64.99 mg/dl. Other baseline
the trachea or on the side of the neck. criteria are presented in Table 1.

Any breathing irregularities, mainly apneas and All patients received CPAP as the main line of
hypopneas, were recorded. Apnea means a complete treatment and were reevaluated after 1 month.
or near-complete interruption of airflow for at least Paired sample t test showed significant improvement
10 s, while hypopnea means reduction of airflow more of AHI, significant reduction of triglycerides, and
than or equal to 30% of pre-event baseline for at least elevation of HDL-C. On the other hand, no
10 s associated with 3% oxygen desaturation from pre- significant changes were noticed as regards total-C
event baseline and/or the event is associated with an and LDL-C (Table 3, Figs 1 and 2).
122 Egyptian Journal of Bronchology, Vol. 13 No. 1, January-March 2019

After 3 months of CPAP, there was a significant Discussion

reduction of AHI, total-C, LDL-C, and The present study is a prospective interventional study
triglycerides while HDL-C was elevated to show the effect of CPAP on dyslipidemia in patients
as compared with the baseline levels (Table 2, with OSA. The natural correlation between body
Fig. 1). weight and all basal lipid profile parameters were
lost in this study (Table 2). This reflects the effect
Comparison of lipid profile after 1 month and after 3 of OSA on lipid profile [15,16]. The association
months of CPAP therapy showed a significant between OSA and dyslipidemia is explained on the
reduction of total-C and LDL-C, there was more basis of excessive adipose tissue lipolysis during sleep
significant elevation in HDL-C while there were no leading to an increase in plasma-free fatty acids. This
significant changes in triglyceride levels (Table 3, systemic lipotoxicity may be one of the causes of
Figs 1 and 2). increased CVD risk in patients with OSA [17,18].
The activated lipolysis is thought to be through
Table 1 Descriptive statistics of the studied group (N=40) sympathetic and adrenocortical activation due to
Minimum Maximum Mean SD stress at night [19].
Age (years) 38.00 70.00 56.45 8.941
Sex (male/female) 22/18 After 1 month of therapy with CPAP, and as expected,
Weight (kg) 70.00 140.00 96.20 19.975 there was marked improvement of AHI. This was in
Height (cm) 150.00 191.00 163.20 12.463 agreement with other studies which confirmed the
BMI (kg/m2) 27.00 42.00 36.01 4.251 improvement of AHI with CPAP therapy [20–22].
Neck circumference 35.00 46.00 43.65 2.560
Other studies failed to reach the same conclusion and
(cm)
Apnea/hypopnea index 15.90 65.70 44.00 11.962
the researchers explained the results by lack of
Fasting blood sugar 78.00 99.00 93.65 5.999 adherence to therapy [23].
(mg/dl)
AST (U/l) 20.00 42.00 31.70 6.814 Triglycerides were lowered significantly very early after
ALT (U/l) 19.00 40.00 29.20 6.685 1 month of CPAP therapy. This is in accordance with
Creatinine (mg/dl) 0.70 1.20 0.91 0.146
Drager et al. [24] who recently arrived at the same
Total-C (mg/dl) 200.00 320.00 255.90 40.176
LDL-C (mg/dl) 108.00 237.00 166.90 40.133
conclusion. This improvement is through
HDL-C (mg/dl) 21.00 39.00 30.45 5.725 reinstatement of lipolysis rate of triglyceride-rich
Triglycerides (mg/dl) 150.00 380.00 292.75 64.999 lipoproteins and accelerating the removal of remnant
ALT, alanine aminotransferase; AST, aspartate aminotransferase; particles. Of interest, these changes have been reversed
HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density again after stoppage of CPAP therapy [19]. In our
lipoprotein-cholesterol.
study, there was no further improvement in the level of
triglycerides after 3 months of CPAP therapy.
Table 2 Pearson’s correlation between BMI and basal lipid
profile and apnea/hypopnea index As regards HDL-C level, there was a significant
r P value increase in its level after 1 month which continued
Total- C (mg/dl) −0.090 0.705 to rise significantly after 3 months of CPAP therapy.
LDL-C (mg/dl) −0.143 0.547 This finding is in agreement with Chin et al. [25] who
HDL-C (mg/dl) −0.112 0.639 found a significant increase in HDL-C after 8 months
Triglycerides (mg/dl) 0.212 0.369
of CPAP therapy regardless of the changes in body
Apnea/hypopnea index 0.077 0.748
weight. Borgel et al. [26] also demonstrated a
HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density
lipoprotein-cholesterol.
significant increase in HDL-C (P<0.013) after 6
months of CPAP therapy in 127 patients with

Table 3 Paired t test of the lipid profile before, 1, and 3 months after continuous positive airway pressure
Basal (mean±SD) 1 month (mean±SD) 3 months (mean±SD) P1 P2 P3
Total-C (mg/dl) 255.90±40.18 257.15±46.56 234.91±44.62 0.771 0.000 0.000
LDL-C (mg/dl) 166.90±40.13 165.60±44.71 142.52±45.09 0.781 0.000 0.000
HDL-C (mg/dl) 30.45±5.73 35.70±5.47 37.45±4.02 0.00 0.000 0.018
Triglycerides (mg/dl) 292.75±64.99 279.25±60.46 274.65±54.39 0.028 0.002 0.208
Apnea/hypopnea index 44.00±11.99 10.15±2.68 4.75±0.97 0.000 0.000 0.000
HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density lipoprotein-cholesterol. P1, comparison between the basal levels and after
1 month of therapy. P2, comparison between the basal levels and after 3 months of therapy. P3, comparison between the levels and after
1 month and levels after 3 months of therapy.
 CPAP improves OSA induced dyslipidemia Shehab-Eldin and Elhabashy 123

OSA. On the other hand, Davies et al. [27] did not find control trials confirmed the reduction of the total-C
any significant changes in HDL-C or other lipid but not triglycerides, HDL, or LDL-C. They
parameters after 3 months of CPAP therapy in two underestimated the clinical importance of CPAP on
groups of patients: snorers and OSA. Their results are lipid profile [12]. In general, meta-analysis trials gain
inconvenient as they did paired sample t test only on 10 its power from the large number of patients included in
patients. Similarly, Lattimore et al. [28] showed a the study; however; it lacks the homogeneity of the
nonsignificant change in HDL-C after 3 months of patients included.
CPAP therapy. Again, it was a small study on only 10
patients.As regards total-C and LDL-C, no changes The beneficial effect of CPAP on lipid profile was
happened after the first month of therapy. However, a confirmed again in a large meta-analysis study of six
significant reduction in both parameters had occurred randomized control studies on 699 patients with OSA
after 3 months of therapy. This result matches with the [30]. These conflicts in the literature are mainly due to
results of Kumor et al. [29] who confirmed the the difference in sample size, duration of CPAP
reduction of both total-C and LDL-C after 3 therapy, and adherence to therapy. Improvement of
months of CPAP therapy of 75 patients with OSA. chronic intermittent hypoxia and sympathetic
Xu and colleagues in a meta-analysis on six randomized hyperactivity are the main mechanisms that correct

Figure 1

Comparison of basal lipid profile and after 1 and 3 months of CPAP therapy. CPAP, continuous positive airway pressure.

Figure 2

Comparison of basal apnea/hypopnea index after 1 and 3 months of CPAP therapy. CPAP, continuous positive airway pressure.
124 Egyptian Journal of Bronchology, Vol. 13 No. 1, January-March 2019

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