Introduction
Obstructive sleep apnea (OSA) is a condition that is
commonly encountered in clinical practice but may be
underestimated. The importance of OSA is that it has a high
prevalence rate and is related to major cardiovascular diseases.
The prevalence of OSA may be as high as 37% in males and 50% in
females (1), and up to 67.5% in
smokers (2). OSA has been reported
to be related to hypertension, hypertensive crisis, impaired left
ventricular ejection fraction and peripheral artery disease
(3-7).
The presence of OSA alongside these diseases has also been
indicated to produce unfavorable cardiovascular disease
outcomes.
Left ventricular hypertrophy (LVH) is a crucial
predictor of cardiovascular diseases and mortality (8,9). A
previous study indicated that LVH increased the risk of
cardiovascular disease and coronary heart disease by 62 and 56%,
respectively (8). LVH in
hypertensive patients was also determined to be related to
mortality [adjusted odds ratio (OR): 1.40; 95% confidence interval
(CI): 1.08-1.81] (10).
As both OSA and LVH have been associated with major
cardiovascular diseases, it may be worthwhile to evaluate LVH in
patients with OSA (3-5,8).
Previous studies have indicated that, compared with non-OSA, OSA is
related to LVH with an OR of 1.70 (95% CI: 1.44-2.00), particularly
in patients with coronary artery disease (11-15).
According to one meta-analysis, the severity of OSA is
significantly associated with the left ventricular mass compared to
controls (15). However, there is
limited data on the risk factors of LVH in patients with OSA. The
present study aimed to evaluate the prevalence and clinical factors
that are predictive of LVH in patients with OSA.
Patients and methods
Patients
The present study was a retrospective, analytical
study conducted at Srinagarind Hospital, a university hospital of
Khon Kaen University (Khon Kaen, Thailand). The inclusion criteria
were adult patients with a diagnosis of OSA who had undergone an
echocardiogram. Pregnant patients were excluded from the study.
Those patients diagnosed with OSA between January 2011 and 2017
were included in the study. OSA was diagnosed by evidence of an
apnea-hypopnea index of five events/hour or more by polysomnography
type 3. The type 3 polysomnography was comprised of at least three
channels of recording: Airflow, respiratory effort and blood
oxygenation (16,17). This study was a part of an OSA and
cardiovascular consequences project (7).
Eligible patients were reviewed for baseline
characteristics, physical signs and laboratory results, including
echocardiography. Patients were categorized into two groups by LVH.
LVH was defined by using left ventricular mass index (LMVI)
calculated by the Cube formula 2D linear method:
LVMI={0.8x1.04x[(IVS + LVID + PWT)3-LVID3] +
0.6}/body surface area, with an LVH cut-off point of >115
g/m2 and 95 g/m2 in males and females,
respectively (18). IVS is the
interventricular septum; LVID the LV internal diameter and PWT the
inferolateral wall thickness.
Statistical analysis
All cardiovascular events were reported as the
prevalence. Patients with or without LVH were compared regarding
basic characteristics, symptoms and signs of OSA, polysomnography,
comorbidities, cardiovascular events, current medications,
laboratory findings and echocardiography. For numerical factors,
the Wilcoxon rank-sum or Student's t-test was used to analyze
differences between the LVH and non-LVH groups. The categorical
factors of these two groups were compared by either Fisher's exact
test or the Chi-square test where appropriate. In the first step of
the logistic regression analysis, a univariate logistic regression
analysis was applied to determine an unadjusted OR for each factor
for evidence of LVH. Factors that either had a P-value of <0.20
according to univariate logistic regression analysis or were
clinically significant were selected for the subsequent
multivariate, binary logistic regression analysis. Results were
presented as unadjusted OR and adjusted OR with 95% CI. The final
predictive model was evaluated by the Hosmer-Lemeshow test.
Statistical analyses were performed using STATA software, version
10.1 (StataCorp LP).
Results
Patient characteristics
A total of 130 patients were enrolled in the present
study. Of these, 36 patients had LVH (27.69%). There were four
significantly different factors between those patients with and
without LVH in terms of baseline characteristics (Table I). The LVH group had an older age
(56 years vs. 48 years), a larger proportion of female patients
(69.4% vs. 38.3%), fewer patients with unrefreshed sleep (61.5% vs.
86.8%) and more patients with heart failure (13.9% vs. 3.2%) than
the non-LVH group. The LVH group also had higher proportions of
patients with consequences of OSA. A total of 63 patients (48.46%)
were treated with a continuous positive airway pressure machine
(CPAP) with a slightly higher proportion of CPAP treatment in the
LVH group than the non-LVH group (55.6% vs. 45.7%; P=0.334).
 | Table IBaseline characteristics of patients
with OSA categorized by presence of LVH. |
Table I
Baseline characteristics of patients
with OSA categorized by presence of LVH.
| Factors | No LVH (n=94) | LVH (n=36) | P-value |
|---|
| Age, years | 48 (35-56) | 56 (41-65) | 0.005 |
| Female sex | 36 (38.3) | 25 (69.4) | 0.001 |
| OSA symptoms | | | |
|
Snoring | 62 (96.9) | 21 (95.5) | 0.754 |
|
Duration of
snoring, years | 8 (3-10) | 10 (4-19) | 0.372 |
|
Witnessed
apnea | 29 (72.5) | 13 (81.3) | 0.495 |
|
Nocturia,
times/night | 2 (1-3) | 2 (1-3) | 0.375 |
|
Morning
headache | 22 (53.7) | 9 (60.0) | 0.672 |
|
Unrefreshed
sleep | 33 (86.8) | 8 (61.5) | 0.047 |
|
EDS | 51 (85.0) | 14 (87.5) | 0.801 |
| Lifestyle habits | | | |
|
Previous
alcohol drinking | 14 (31.8) | 6 (31.6) | 0.985 |
|
Current
alcohol drinking | 6 (13.6) | 6 (31.6) | 0.096 |
|
Previous
smoking | 9 (20.0) | 4 (22.2) | 0.844 |
|
Current
smoking | 4 (8.9) | 0 (0) | 0.204 |
| Comorbid
diseases | | | |
|
DM | 25 (26.6) | 11 (30.6) | 0.652 |
|
GERD | 34 (41.0) | 14 (46.7) | 0.588 |
|
Allergic
rhinitis | 19 (44.2) | 10 (62.5) | 0.211 |
| OSA consequences | | | |
|
Hypertension | 74 (78.7) | 31 (86.1) | 0.339 |
|
Stroke | 5 (5.3) | 5 (13.9) | 0.101 |
|
Coronary
artery disease | 5 (5.3) | 4 (11.1) | 0.244 |
|
Heart
failure | 3 (3.2) | 5 (13.9) | 0.023 |
|
Atrial
fibrillation | 1 (1.1) | 0 (0) | 0.534 |
|
Other
arrhythmias | 5 (5.3) | 0 (0) | 0.158 |
|
CPAP
treatment | 43 (45.7) | 20 (55.6) | 0.334 |
Predictive factors for LVH
Regarding physical signs and laboratory results
(Tables II and III), there were no significant
differences between the two groups, even for the apnea-hypopnea
index (20 events/h vs. 18.5 events/h; P=0.405). A total of six
factors were identified using the final, multivariate predictive
model of LVH (Table IV). Age was
the only independent factor associated with LVH, with an adjusted
OR of 1.048 (95% CI: 1.002-1.096). The predictive model had a
strong goodness of fit, as the Hosmer-Lemeshow χ2 value was 4.97
(P=0.761). A cutoff of 40 years of age or more gave sensitivity of
80.56% and specificity of 34.04%.
| Table IIPhysical signs of patients with
obstructive sleep apnea categorized by presence of LVH. |
Table II
Physical signs of patients with
obstructive sleep apnea categorized by presence of LVH.
| Factor | No LVH (n=94) | LVH (n=36) | P-value |
|---|
| BMI,
kg/mm2 | 28.49
(24.89-35.59) | 30.0
(26.60-34.36) | 0.405 |
| SBP, mmHg | 141 (130-153) | 141 (130-151) | 0.924 |
| DBP, mmHg | 86 (79-95) | 82.5 (76-90) | 0.103 |
| Torus
palatinus | 8 (25.8) | 2 (25.0) | 0.963 |
| Torus
mandibularis | 5 (16.7) | 3 (37.5) | 0.199 |
| Tonsil
enlargement | 10(27) | 0 (0) | 0.064 |
| Tonsillectomy | 1 (3.4) | 0 (0) | 0.594 |
| Retrognathia | 5 (18.5) | 3 (37.5) | 0.261 |
| Mallampati
class | | | 0.615 |
|
1 | 3 (4.9) | 1 (3.8) | |
|
2 | 23 (37.7) | 7 (26.9) | |
|
3 | 27 (44.3) | 12 (46.1) | |
|
4 | 8 (13.1) | 6 (23.1) | |
| Macroglossia | 31 (75.6) | 12 (75.0) | 0.962 |
| Dentures | 2 (3.4) | 1 (4.8) | 0.787 |
| Neck circumference,
cm | 42 (38-45.5) | 39 (37-42) | 0.113 |
| Table IIILaboratory results of patients with
obstructive sleep apnea categorized by presence of LVH. |
Table III
Laboratory results of patients with
obstructive sleep apnea categorized by presence of LVH.
| Factor | No LVH (n=94) | LVH (n=36) | P-value |
|---|
| AHI, events/h | 18.5 (10-39) | 20 (14-34) | 0.405 |
| HbA1c, % | 6.2 (5.8-7.1) | 6.1 (5.4-7) | 0.201 |
| BUN, mg/dl | 12.6 (9.7-16) | 14 (9.4-16.2) | 0.671 |
| Cr, mg/dl | 0.9 (0.7-1.1) | 0.8 (0.7-1.0) | 0.483 |
| UACR, mg/d | 11.5 (5-53) | 25 (4-102) | 0.614 |
| Cholesterol,
mg/dl | 198 (171-230) | 178 (152-192) | 0.090 |
| TAG, mg/dl | 126 (101-172) | 110 (93-148) | 0.299 |
| HDL, mg/dl | 49.5 (41-57) | 46 (40-54) | 0.206 |
| LDL, mg/dl | 130 (104-163) | 114.5
(106-150.5) | 0.626 |
| EF (Teichholz) | 67.45
(65.59-72.0) | 66.45
(62.84-72.49) | 0.195 |
| Table IVFactors associated with left
ventricular hypertrophy in patients with obstructive sleep apnea by
logistic regression analysis. |
Table IV
Factors associated with left
ventricular hypertrophy in patients with obstructive sleep apnea by
logistic regression analysis.
| Factors | Unadjusted OR (95%
CI) | P-value | Adjusted OR (95%
CI) | P-value |
|---|
| Age (increment by 1
year of age) | 1.045
(1.012-1.078) | 0.007 | 1.048
(1.002-1.096) | 0.037 |
| Female sex | 3.662
(1.609-8.331) | 0.002 | 2.544
(0.837-7.731) | 0.100 |
| Unrefreshed
sleep | 0.528
(0.216-1.289) | 0.161 | 0.502
(0.166-1.519) | 0.223 |
| Body mass index
(increment by 1 kg/m2) | 1.017
(0.976-1.059) | 0.407 | 1.055
(0.987-1.127) | 0.111 |
| Systolic blood
pressure (increment by 1 mmHg) | 1.000
(0.982-1.020) | 0.923 | 1.004
(0.979-1.030) | 0.741 |
| Apnea-hypopnea
index (increment by 1 event/h) | 0.993
(0.975-1.012) | 0.493 | 0.991
(0.965-1.016) | 0.492 |
| Snoring | 0.722 (0.328,
1.589) | 0.419 | Not included | |
| Morning
headache | 1.295 (0.389,
4.307) | 0.673 | Not included | |
| Hypertension | 1.675 (0.577,
4.865) | 0.343 | Not included | |
| Macroglossia | 0.967 (0.254,
3.686) | 0.962 | Not included | |
Discussion
In the cohort of the present study >1/4 of
patients with OSA had LVH. Elderly patients with OSA were at risk
for LVH.
The prevalence of LVH in patients with OSA in the
present study was lower than that in previous reports. Previous
studies determined that the prevalence of LVH in patients was OSA
was 59-88% (12-14).
The different prevalence rate of LVH in the present study was due
to its different study population. The present study enrolled
consecutive patients with OSA, while the other three were performed
in specific OSA populations, including middle-aged males with
hypertension (59%), patients with coronary artery disease (86%) and
patients with severe OSA (88%). The results of the present study
may provide data for a more general population.
Even though previous studies identified predictors
for LVH in patients with OSA (13,14,19,20),
the present study added that age was another factor related to LVH
in patients with OSA after adjusting for severity, gender, OSA
symptoms and systolic blood pressure. There are several proposed
mechanisms by which LVH affects OSA: Ventricular pressure overload,
increasing sympathetic drives, loss of vagal heart rate regulation
and systemic vasculature remodeling (13,21).
Increasing age is a risk factor for both OSA and LVH, regardless of
blood pressure level (22,23). In addition, up to 80% of individuals
with OSA have been indicated to go undiagnosed for a decade
(24,25). These factors may result in an
increased risk of LVH and cardiovascular consequences in elderly
patients, regardless of systolic blood pressure level or other
factors. Even though sex was a significant factor according to
univariate logistic regression analysis, it was not significant in
the multivariate analysis. These findings indicate that sex was not
an independent predictor. It may be that certain confounders such
as hypertension, which may influence both OSA and LVH or sex, was
not strong enough to be significant compared to other factors. As
the present study considered clinical factors that are predictive
of LVH in patients with OSA, the results may be applied in
resource-limited facilities, where clinicians may use these
predictors to evaluate high-risk patients for further referral.
There are certain limitations to this study. First,
the cohort was from a single center in a university hospital
setting. In addition, the sample size was small (n=130).
Furthermore, the present study only enrolled patients who underwent
echocardiography. This may result in selection bias. Other aspects
of OSA (CPAP purchasing, CPAP compliance), other cardiovascular
risk factors (diabetes, hypertension, dyslipidemia, albuminuria,
exercise) and full results of cardiac ultrasound (LV end-diastolic
dimension, interventricular septal thickness at end-diastole,
posterior wall thickness at end-diastole or right ventricular
systolic pressure) were not determined (26-33).
In addition, the present study did not evaluate the physiological
characteristics of patients with OSA, such as upper airway gain or
arousal threshold (34). Finally,
even though echocardiography is not routinely performed in patients
with OSA, the present results had a statistical power of 80.85%.
This was traced back by using a comparison of mean age between both
groups by STATA software. However, further prospective studies may
be required to evaluate the consequences of LVH in patients with
OSA and to confirm the results of the predictive model. A further
prospective study will be conducted to validate this predictive
model. CPAP therapy has demonstrated beneficial outcomes in
reducing LVH and improving LV function (35), but the present study did not
evaluate the effects of CPAP on LVH as it is not the study
objective. However, 48.46% of patients in the present study were
treated with CPAP. Further studies are required to confirm the
results of the present study with a prospective cohort design using
consecutive patients with OSA in a multicenter setting, including
all levels of hospital from primary care hospitals to referral
hospitals.
In conclusion, the prevalence rate of LVH in
patients with OSA in the present study was 27.69%. Older age was
independently related to LVH in patients with OSA.
Acknowledgements
The authors would like to thank Dr Vichai Senthong,
Department of Medicine, Faculty of Medicine, Khon Kaen University
(Khon Kaen, Thailand) for his kind contribution in data
collection.
Funding
Funding: The present study was supported by the Research and
Graduate Studies, Khon Kaen University (Khon Kaen, Thailand; grant
no. 1464/2565), the Fundamental Fund of Khon Kaen University and
the National Science, Research and Innovation Fund (NRSF).
Availability of data and materials
The datasets used and/or analyzed during the present
study are available from the corresponding author upon reasonable
request.
Authors' contributions
SK designed the study, analyzed and interpreted the
data and wrote the manuscript. TS, PL, JC and WB interpreted the
data. SS and KS confirm the authenticity of all the raw data,
participated in data analysis and interpretation and prepared the
manuscript. All authors read and approved the final manuscript.
Ethics approval and consent to
participate
The study protocol was approved by the Khon Kaen
University Ethics Committee for Human Research (approval no.
HE641504).
Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing
interests.
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