Download Left Ventricular Hypertrophy Is a Common Echocardiographic

Left Ventricular Hypertrophy Is a
Common Echocardiographic
Abnormality in Severe Obstructive Sleep
Apnea and Reverses With Nasal
Continuous Positive Airway Pressure*
Tom V. Cloward, MD, FCCP; James M. Walker, PhD;
Robert J. Farney, MD, FCCP; and Jeffrey L. Anderson, MD
Study objectives: To determine cardiac structural abnormalities by echocardiography in subjects
with severe obstructive sleep apnea (OSA), and to determine the long-term effects of nasal
continuous positive airway pressure (CPAP) on such abnormalities.
Design: Polysomnography was conducted on oximetry-screened patients who showed a desaturation index > 40/h and > 20% cumulative time spent below 90%. From these, 25 patients with
severe OSA but without daytime hypoxemia underwent echocardiography prior to, then 1 month
and 6 months following initiation of CPAP treatment.
Setting: Outpatient sleep disorders center.
Results: Of the 25 patients, 13 patients (52%) had hypertension by history or on physical
examination. Baseline echocardiograms showed that severe OSA was associated with numerous
cardiovascular abnormalities, including left ventricular hypertrophy (LVH) [88%], left atrial
enlargement (LAE) [64%], right atrial enlargement (RAE) [48%], and right ventricular hypertrophy (16%). In all patients (intent to treat) as well as those patients compliant with CPAP therapy
(84% > 3 h nightly), there was a significant reduction in LVH after 6 months of CPAP therapy as
measured by interventricular septal distance (baseline diastolic mean, 13.0 mm; 6-month mean
after CPAP, 12.3 mm; p < 0.02). RAE and LAE were unchanged after CPAP therapy.
Conclusions: LVH was present in high frequency in subjects with severe OSA and regressed after
6 months of nasal CPAP therapy.
(CHEST 2003; 124:594 – 601)
Key words: echocardiography; hypertension; left ventricular hypertrophy; nasal continuous positive airway pressure;
obstructive sleep apnea; right ventricular hypertrophy
Abbreviations: AHI ⫽ apnea/hypopnea index; BMI ⫽ body mass index; CPAP ⫽ continuous positive airway pressure;
IVSD ⫽ interventricular septal distance; LAE ⫽ left atrial enlargement; LVH ⫽ left ventricular hypertrophy;
LVPWT ⫽ left ventricular posterior wall thickness; OSA ⫽ obstructive sleep apnea; RAE ⫽ right atrial enlargement;
RDI ⫽ respiratory disturbance index; RVH ⫽ right ventricular hypertrophy; Sao2 ⫽ arterial oxygen saturation
hypertrophy (LVH) is a leading
L eftcauseventricular
of morbidity and mortality. An increase in
left ventricular mass predicts a higher incidence of
clinical events, including death, attributable to cardiac disease.1– 6 A report7 from the Framingham
Heart Study found that the presence of LVH re*From the Intermountain Sleep Disorders Center (Drs. Cloward,
Walker, and Farney), LDS Hospital; and Division of Cardiology
(Dr. Anderson), University of Utah, Salt Lake City, UT.
Financial support was provided by Deseret Foundation, LDS
Hospital.
Manuscript received April 9, 2002; revision accepted February
27, 2003.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:
[email protected]).
Correspondence to: Tom V. Cloward, MD, FCCP, Intermountain
Sleep Disorders Center, LDS Hospital, Eighth Ave and C St, Salt
Lake City, UT 84143; e-mail: [email protected]
sulted in a twofold greater risk of sudden death
compared to those without LVH. The adverse cardiac consequences from LVH are likely ultimately
related to coronary ischemia, with increased muscle
mass that is inadequately perfused, and which may
compress endocardial capillaries.5,8,9 LVH may also
cause electrophysiologic changes that predispose the
heart to arrhythmias and sudden death.10 –13
Obstructive sleep apnea (OSA) is now recognized
as an independent risk factor for hypertension14 –19
and imposes several adverse effects on the heart.
During an obstructive apnea, large negative intrathoracic pressures are generated during inspiratory efforts, which increases transmural pressures across
the myocardium, thus increasing afterload. An increase in preload and pulmonary congestion may also
occur due to increased venous return. Secondly, the
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Clinical Investigations
presence of hypoxemia decreases oxygen delivery to
the myocardium, which may promote angina or
arrhythmias. Lastly, frequent arousals from sleep
due to respiratory events lead to increased sympathetic nervous system activity, with subsequent elevation in urinary and plasma catecholamines levels.
Consequently, the adverse consequences of repetitive episodes of increased afterload on the heart
during sleep may persist into the daytime. In this
context, it would be expected that OSA may contribute to LVH, but results are equivocal.20 –29
Nasal continuous positive airway pressure (CPAP)
has been shown to reduce BP in subjects with
OSA.30 –34 Classic studies from the hypertension
literature show that treatment of hypertension with
medications (compared to no treatment) over a 3- to
5-year period prevents progression to severe hypertension, reduces LVH, and reduces congestive heart
failure.35 Furthermore, regression of LVH (as measured by ECG or echocardiography) has favorable
prognostic implications for reduction of cardiovascular
events.36 –38 For these reasons, it is important to achieve
a better understanding of the relationship of LVH to
OSA and the possible effects of CPAP therapy.
The purposes of this study were as follows: (1) to
determine the incidence of LVH as well as other
cardiac structural abnormalities in patients with severe OSA and nocturnal hypoxemia without daytime
hypoxemia, and (2) to determine if changes in LVH
occurred after 6 months of CPAP therapy. The rationale was that LVH, if present, would be accentuated in
patients with severe OSA associated with nocturnal
hypoxemia, and that LVH regression with CPAP therapy might be more evident in such a population.
Materials and Methods
Design and Setting
All patients were evaluated at the Intermountain Sleep Disorders Center at LDS Hospital in Salt Lake City, UT (elevation
1,371 m). The Institutional Review Board approved the design
and methods of this study. All patients referred for evaluation of
OSA were initially screened by overnight pulse oximetry (Nonin
8500M; Nonin Medical; Plymouth, MN) [sampling rate, once
every 4 s]. All patients with a desaturation index of ⬎ 40/h (based
on a 3% drop in saturation) and ⱖ 20% cumulative time spent
with arterial oxygen saturation (Sao2) ⬍ 90% (Profox version
PFD 06/97; PROFOX Associates; Escondido, CA) were targeted
as possible study subjects. The intent of performing screening
oximetry was to readily and inexpensively identify subjects with a
high likelihood of having severe sleep apnea. Patients were
excluded if daytime hypoxemia was present (defined at this
elevation as resting Sao2 ⬍ 88% or Pao2 ⬍ 55 mm Hg).39
Patients with known valvular heart disease or congestive heart
failure were also excluded. The first 25 patients who met the
criteria as outlined above, and who agreed to participate, were
enrolled for study. All patients who were enrolled then underwent a full night of diagnostic polysomnography, baseline echo-
cardiography, followed by a full night of polysomnography with
nasal CPAP titration. Echocardiography and compliance checks
were then performed at 1 month and 6 months after CPAP was
initiated, during routine clinic follow-up visits (Table 1).
Polysomnography
All patients underwent an entire night of diagnostic polysomnography while breathing room air, followed by a second night of
polysomnography with nasal CPAP titration. Attended polysomnography was conducted measuring the following: central (C3/A2
or C4/A1) and occipital (O1/A2 or O2/A1) EEG; right and left
electrooculography; submentalis electromyography; ECG; anterior tibialis electromyography; airflow, by oronasal pressure
transducers; and respiratory effort, determined by measurement
of chest and abdominal motion using piezo electric bands and
pulse oximetry. Data were acquired on either a CNS Sleep Lab
2000 (CNS; Minneapolis, MN) or an Aequitron 1000P
(Aequitron-Medical; Plymouth, MN) using Matrix software
(Jaeger-Toennies; Hoechberg, Germany). Sleep was manually
scored page by page in 30-s epochs for sleep stages using
standard criteria of Rechtschaffen and Kales.40 Apneas and
hypopneas were manually scored. Apneas were defined as an
absence (⬍ 20% baseline) of airflow for ⱖ 10 s. Hypopneas were
defined as a reduction in airflow (20 to 50% baseline), associated
with a desaturation of ⱖ 3%. Obstructive and mixed events are
defined by the presence of respiratory effort and/or characteristic
changes of the inspiratory flow pattern. Central apneas lacked
respiratory effort and airflow. The apnea/hypopnea index (AHI)
was computed as the total of all respiratory events divided by the
total sleep time in hours. Patients were then prescribed nasal
CPAP (Resmed Elite V; ResMed Corporation; Poway, CA),
including use of a heated humidifier. The CPAP machines were
equipped with compliance monitors that measured CPAP use, in
order to observe CPAP usage/compliance at home.
Echocardiography
On enrollment, an echocardiogram (HP Sonos 5500, using
version B.2.1 software; Philips Sonos; Andover, MA) was obtained on each patient prior to initiation of nasal CPAP, in the
Cardiology Laboratory at LDS Hospital. Patients were imaged
from standard transthoracic windows using two-dimensional,
M-mode, and Doppler echocardiographic techniques. Echocardiographic images were obtained in the parasternal long and
short axis, apical two-chamber, four-chamber, and subcostal
views. The left ventricular internal dimension was obtained at
both end-diastole and systole. The chamber size and wall thickness were measured manually by technicians who were blind to
Table 1—Study Design
Time of Test
Tests Performed
Prescreening
Baseline
Overnight oximetry
Echocardiography
BP measurement
Diagnostic polysomnography
Polysomnography with nasal CPAP titration
Echocardiography
BP measurement
Nasal CPAP compliance check
Echocardiography
BP measurement
Nasal CPAP compliance check
1 mo
6 mo
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CHEST / 124 / 2 / AUGUST, 2003
595
the purpose of the study, and formally reviewed by cardiologists
blinded to the patients involved with this study. Left ventricular
size was determined by measuring diastolic interventricular
septal distances (IVSDs), and left ventricular posterior wall
thickness (LVPWT). Left atrial enlargement (LAE) was defined
as left atrial diameter of ⬎ 4.5 cm on parasternal short-axis or
long-axis views. Right atrial enlargement (RAE) was defined as
right atrial diameter ⬎ 2.5 cm on short-axis view. Right ventricular
hypertrophy (RVH) was defined as a right ventricular free-wall
diastolic thickness ⬎ 5 mm.41
Protocol
Echocardiograms were obtained following the diagnosis of
OSA and prior to initiation of CPAP, and again at 1 month and 6
months. During 1-month and 6-month follow-up visits, compliance data were downloaded (Resmed Autoscan Version 3.0;
ResMed Corporation), and echocardiography was repeated. BP
measurements were obtained at each follow-up visit. Routine
troubleshooting took place in an effort to maximize compliance
with nasal CPAP. Patients were considered to be CPAP compliant if they used CPAP an average ⬎ 3 h per night at the 6-month
follow-up.
Hypertension was defined as the presence of an office sphygmomanometer systolic BP ⬎ 140 mm Hg, diastolic BP ⬎ 90 mm
Hg, or if the subject was receiving antihypertensive medications.
Twenty-four– hour BP measurements were not obtained.
Statistical Analysis
A t test for related measurements (two tailed) was used to
compare primary outcome variables of LVH (IVSD and
LVPWT), at baseline, 1 month, and 6 months. Comparisons were
considered significant with a p ⬍ 0.05 (Bonferroni correction,
%:0.05/2 measures of LVH ⫽ 0.025).
Results
Echocardiographic Data
The 25 subjects were predominantly men (23 of 25
subjects), and ages ranged from 31 to 68 years. All
subjects were obese (mean BMI, 38.1 ⫾ 10.7), with
normal awake oxygenation by arterial blood gas
(mean Pao2, 66 mm Hg; mean Sao2, 92%). Polysomnography revealed severe OSA, with a mean AHI of
81/h, associated with significant nocturnal hypoxemia
(mean time spent with Sao2 ⬍ 90% equaled 64% of
recording time) [Table 2].
Of the 25 subjects, 23 subject (92%) had structural
abnormalities on echocardiography (Fig 1). LVH was
the most common finding (present in 22 of 25
subjects) and occurred in those both with and without hypertension. Hypertension was present in 13 of
25 subjects (52%). All 13 subjects with hypertension
had LVH. Of the 12 subjects without hypertension,
10 subject had LVH. LVH was defined as an IVSD
or LVPWT ⬎ 12 mm. There were 16 subjects who
had LAE (64%), 13 subjects who had RAE (48%),
and 4 subjects who had RVH (16%). Only 2 of the 25
subjects had completely normal echocardiographic
Table 2—Demographic Characteristics of OSA
Subjects Referred to the Sleep Clinic*
Variables
Age, yr
Education, yr
Male gender, No. (%)
Weight, kg
Height, m
BMI
Hypertension, No. (%)
Awake supine Pao2, mm Hg, by arterial
blood gas
Awake supine Sao2, mm Hg, by arterial
blood gas
AHI, by polysomnography
Desaturation index from nocturnal
oximetry, based on 3% drop from
baseline
Percentage of time spent with Sao2 ⬍ 90%
on nocturnal oximetry
Data
(n ⫽ 25)
49.6 (31–68)
14.1 (11–18)
23 (92)
116.1 ⫾ 22.7
1.75 ⫾ 0.08
38.1 ⫾ 10.7
13 (52)
66.0 ⫾ 7.5
91.9 ⫾ 3.0
81.1 ⫾ 25.1
68.1 ⫾ 25.4
64.1 ⫾ 27.9
*Data are presented as mean (range) or mean ⫾ SD unless otherwise
indicated.
findings, and their results are included within the
final analyses. All of the patients had a normal
ejection fraction, which did not change during the
course of therapy (Fig 2).
Compliance
Of the 25 subjects, 20 subject were compliant with
CPAP therapy, which we defined as ⱖ 3 h of nightly
use. The five patients who were noncompliant with
nasal CPAP still completed participation in the
study, including follow-up echocardiography and BP
measurements. Subjects who were compliant with
therapy averaged 5.9 h of CPAP usage per night, as
determined by a compliance monitor within the
CPAP machine. Subjects who were noncompliant
used CPAP for 0.8 h per night. The major reasons for
noncompliance were mask discomfort or pressure
intolerance. All subjects were offered heated humidity, and efforts were made in all subjects to improve
comfort and compliance with therapy. There was no
change from baseline after 6 months in either weight
or BP. Only two subjects had their BP regimen
altered: one subject had the diuretic dose halved,
and the other had the diuretic dose doubled.
Changes in average CPAP pressure after 6 months of
therapy did not change from the initial CPAP pressure that was prescribed (Table 3).
LVH Regression
The primary measures of LVH obtained from echocardiograms, IVSD, and LVPWT showed regression
after 6 months of CPAP therapy. Table 4 depicts IVSD
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Clinical Investigations
Figure 1. Echocardiographic measurements at baseline in 25 subjects with severe OSA. In solid bars,
the frequency of each structural abnormality is depicted. In hatched bars, the frequency of
hypertension (HTN) in each subgroup is shown. The coexistence of hypertension was present in 13 of
the 23 subjects with LVH.
and LVPWT values at baseline, and after 1 month and
6 months of CPAP use, respectively. Using an intentto-treat analysis, IVSD was significantly reduced after 6
months (p ⬍ 0.02). Reduction in LVPWT approached,
but did not reach, statistical significance after 6 months
(p ⬍ 0.08). Further analysis of compliant vs noncompliant subjects reveals that reduction in IVSD and
LVPWT occurred in those who were compliant with
nasal CPAP. Noncompliant subjects showed no reduction in either parameter (Table 4).
LAE and RAE did not change during the course of
therapy (data not shown). RVH was present in four
patients (16%). The effect of CPAP on RVH was not
analyzed due to the low number of subjects with RVH.
Discussion
This investigation further confirms that multiple
cardiac structural abnormalities are associated with
Figure 2. Ejection fraction determined by echocardiography in 25 patients with severe OSA. Normal
systolic function was present at baseline, and did not significantly change after 1 month and 6 months
of CPAP use, respectively.
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Table 3—Comparison of Compliant and Noncompliant Subjects at Baseline and After 6 Months of CPAP Usage*
Variables
AHI
Baseline
6 mo
Baseline
6 mo
Baseline
6 mo
Compliance,
hours per
night
Compliant
(n ⫽ 20)
Noncompliant
(n ⫽ 5)
84.4 ⫾ 24.4
120.1 ⫾ 25.2
119.7 ⫾ 26.9
130/82 ⫾ 14/9
133/82 ⫾ 13/11
11.1 ⫾ 2.5
11.2 ⫾ 2.5
5.9 ⫾ 2.3
68.0 ⫾ 24.3
111.1 ⫾ 11.1
110.6 ⫾ 8.9
140/83 ⫾ 13/10
132/83 ⫾ 20/11
9.8 ⫾ 3.3
Weight, kg
BP, mm Hg
CPAP, cm H2O
0.8 ⫾ 0.9
*Data are presented as mean ⫾ SD.
severe OSA. Only 8% of our subjects had normal
echocardiographic findings. In contrast, 88% of subjects had LVH. The second-most-common structural
abnormality was LAE (present in 64% of patients),
followed by RAE (48% of subjects), and RVH (16%
of subjects). Ejection fraction was normal in all
subjects.
Hypertension was present in only 52% of the
subjects, so daytime hypertension alone does not
account for the high prevalence of LVH observed in
this study. Ten of 12 normotensive subjects had
LVH. This suggests that the nocturnal consequences
of OSA, including increased transmural pressure due
to respiratory effort during an apneic event, hypoxemia, and increased sympathetic neural activity, may
account for the development of LVH in patients with
OSA. An alternative explanation is that our subjects
may have had a higher incidence of hypertension if
measured by 24-h ambulatory monitoring. There is
evidence that LVH may precede the presence of
hypertension.42
Other investigators have characterized cardiac
structure and function in OSA.20 –29 Hedner et al20
compared 61 men with OSA to 61 control subjects,
and reported that left ventricular mass and left
ventricular mass index were significantly higher
among the OSA patients. Left ventricular mass index
was approximately 15% higher in the normotensive
OSAS patients compared to normotensive control
Table 4 —Measures of LVH at Baseline, and After
Nasal CPAP Therapy*
Variables
Overall (n ⫽ 25)
IVSD
LVPWT
Compliant (n ⫽ 20)
IVSD
LVPWT
Noncompliant (n ⫽ 5)
IVSD
LVPWT
Baseline
1 mo
6 mo
p Value†
13.0 (1.6) 12.7 (2.5) 12.3 (1.6)
12.8 (2.0) 12.2 (2.0) 12.2 (1.6)
0.011
0.084
13.1 (1.8) 12.9 (2.6) 12.3 (1.7)
13.0 (2.1) 12.3 (2.1) 12.3 (1.6)
0.018
0.039
12.8 (0.4) 12.0 (1.7) 12.4 (1.5)
12.2 (1.1) 11.8 (1.7) 12.4 (2.6)
0.476
0.875
*Data are presented as mean (SD).
†Difference between baseline and 6-month values.
subjects. The study was limited by lack of polysomnography data in both groups. Noda et al22 examined
51 subjects with hypertension, and reported LVH in
50% of those with an AHI ⬎ 20/h, compared to
21.4% in those with an AHI ⬍ 20/h. LVH and RVH
were more likely in the presence of high AHI,
sustained hypoxemia, and obesity. Davies et al23 did
not find any significant difference in left ventricular
mass between 19 subjects with OSA, 19 nonapneic
snorers, and 38 control subjects matched for age, sex,
BMI, and tobacco and alcohol use. Niroumand and
coworkers25 studied 533 subjects in a clinic population and found that OSA does not independently
increase left ventricular mass or impair left ventricular diastolic filling. Although left ventricular mass
was higher in OSA subjects, it was predominantly
related to coexisting obesity, in addition to the
effects of aging and presence of hypertension.
Kraiczi et al26 studied 81 subjects and examined the
relationship of OSA with hypertension and left ventricular thickness after adjusting for age, gender, use
of antihypertensives, smoking, BMI, coronary artery
disease, hyperlipidemia, and circulating c-peptide
concentrations. OSA severity and left ventricular
muscle thickness were primarily linked via the presence of coexisting increased BP. Alchanatis et al27
studied 15 OSA subjects (mean AHI, 52/h) and
found left ventricular diastolic dysfunction and increased diastolic BP, each of which improved following 12 to 14 weeks of nasal CPAP therapy. Fung
et al28 reported that severe OSA (in 68 patients) was
associated with left ventricular diastolic dysfunction.
Amin et al29 found that OSA in children is associated
with increased left ventricular mass.
The Framingham Heart Study43 showed that obesity is significantly correlated with left ventricular
mass, even after controlling for age and BP. The
increase in left ventricular mass associated with
increased body weight reflects both left ventricular
wall thickness and left ventricular internal dimension. This association is present even in those with
mild-to-moderate obesity. The presence or absence
of OSA in obese subjects was not considered as a
potential confounding variable that may contribute
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Clinical Investigations
to LVH in this population-based epidemiologic
study. In fact, Narkiewicz and colleagues44 have
shown that obesity alone, in the absence of OSA, is
not accompanied by increased sympathetic activity to
muscle blood vessels. MacMahon and colleagues45
demonstrated that weight loss in overweight, hypertensive subjects reduced left ventricular mass and
posterior wall thickness. Patients in our investigation
were obese (mean BMI, 38). The effects of obesity
alone in our study population cannot be discounted
as a potential confounding contributor to underlying
LVH; however, the fact that there was a significant
regression of LVH over a 6-month period following
CPAP therapy, without concomitant weight loss,
strongly suggests that OSA was at least a contributory
factor.
The second important finding in this study was the
finding of LVH regression after initiation of nasal
CPAP. After 1 month of nasal CPAP, regression of
LVH was not significant. After 6 months of nasal
CPAP, IVSD was significantly reduced. LVPWT also
decreased after 6 months of therapy and approached, but did not reach, statistical significance.
It is unknown if extending duration of therapy would
have resulted in further improvement in either index
of LVH. Another possibility is that nasal CPAP, by
itself, may improve LVH, irrespective of amelioration of OSA. This seems less likely, as those subjects
who were noncompliant with CPAP in this study did
not have LVH regression. A control group of nonOSA patients with LVH treated with CPAP would be
necessary to establish such a relationship
The presence of LVH is important because of an
increased association with heart failure, ventricular
arrhythmias, death following myocardial infarction,
and sudden cardiac death. Koren et al2 followed up
253 hypertensive patients with and without LVH
over the course of 10 years, and found that cardiac
events were more frequent (26% vs 12%) and cardiovascular deaths were higher (14% vs 0.5%) if
LVH was present. Liao et al6 followed up 988
patients over 7 years. The presence of LVH was
associated with a threefold greater risk of death
compared to those without LVH. This was present in
patients with and without coronary artery disease.
The Framingham study7 followed up 3,661 subjects
with LVH over 14 years. The risk factor adjusted
hazard ratio for sudden death was 2.16.
Regression of LVH occurs with the use of antihypertensive medications, with improvements observed relatively quickly (15 to 30 weeks). Further
resolution of LVH occurs relatively slowly (ⱖ 3
years) and may reverse completely if BP is controlled. The present study shows regression of LVH
by CPAP somewhere between the range of that
demonstrated by angiotensin-converting enzyme in-
hibitors and calcium-channel blockers, but better
than diuretics and beta-blockers.46 The difference,
however, is that in patients with OSA, CPAP alters
potential underlying causative factors by reducing
cardiac afterload associated with apneas, maintaining
normal oxygenation, and reducing repetitive sympathetic activity across the night.
The primary aims of this study were to document
the frequency of LVH in patients with severe OSA
and to determine if changes occurred with CPAP.
Other echocardiographic structural abnormalities,
such as bilateral atrial enlargement, were not ameliorated with CPAP therapy. There were no significant changes observed in LAE or RAE following 6
months of treatment with nasal CPAP, following an
intent-to-treat analysis. Of the four subjects with
RVH, three subjects were compliant with nasal
CPAP; in those three patients, regression of RVH
was noted. This is observational information only, as
the low numbers preclude meaningful statistical
analysis. Reduction in RVH with CPAP therapy is
consistent with a previous report.47 Daytime hypoxemia, postulated by some48,49 to be a prerequisite for
RVH, was not present in our patients.
This study, as well as others that have shown either
LVH or RVH, could be criticized on the basis of
biased sampling by recruiting patients referred for
sleep apnea. To circumvent sampling bias, Guidry et
al50 matched subjects in a population-based study
with high respiratory disturbance index (RDI) [90th
percentile] with low RDI (below 50th percentile)
and found that the right ventricle was significantly
thicker in the high RDI group but there were no
differences in left ventricular thickness.
The sample in the present study was unique from
other studies for both the frequency of respiratory
disturbances (mean AHI, 80/h) and the degree of
nocturnal hypoxemia (64% of testing time spent with
Sao2 ⬍ 90%). These factors possibly accentuated
cardiac abnormalities that otherwise might not be
evident in less severe OSA without a larger sample
size. Further studies are necessary to determine
which factors are necessary for the development of
LVH in patients with OSA. A larger population of
study subjects would be helpful to determine the
relative importance of such factors as obesity, age,
AHI, degree of hypoxemia, and presence or absence
of 24-h hypertension in relationship to the presence of LVH. It is also important to elucidate the
reverse of this finding: does LVH on echocardiography serve as a marker for sleep-related breathing
disorders?
In conclusion, LVH was by far the most common
echocardiographic abnormality observed in this
group of patients with severe OSA. Application of
nasal CPAP resulted in reduction of LVH after
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599
6 months of therapy. It may be beneficial to administer nasal CPAP in patients with sleep apnea and
LVH, in order to provide the advantages that occur
with LVH regression.
18
19
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