From the Sleep Disorders Laboratory, Department of Veterans Affairs
Medical Center, and the Department of Medicine, University of Cincinnati
College of Medicine, Cincinnati, Ohio.
Methods and Results—This article reports the results of a
prospective study of 81 of 92 eligible patients with heart failure and
a left ventricular ejection fraction <45%. There were 40
patients without (hourly rate of apnea/hypopnea, 4±4; group 1) and 41
patients with (51% of all patients; hourly rate of apnea/hypopnea,
44±19; group 2) sleep apnea. Sleep disruption and arterial
oxyhemoglobin desaturation were significantly more severe and the
prevalence of atrial fibrillation (22% versus 5%) and
ventricular arrhythmias were greater in group 2 than in
group 1. Forty percent of all patients had central sleep apnea, and
11% had obstructive sleep apnea. The latter patients had significantly
greater mean body weight (112±30 versus 75±16 kg) and prevalence of
habitual snoring (78% versus 28%). However, the hourly rate of
episodes of apnea and hypopnea (36±10 versus 47±21), episodes of
arousal (20±14 versus 23±11), and desaturation (lowest saturation,
72±11% versus 78±12%) were similar in patients with these different
types of apnea.
Conclusions—Fifty-one percent of male patients with stable heart
failure suffer from sleep-related breathing disorders: 40% from
central and 11% from obstructive sleep apnea. Both obstructive and
central types of sleep apnea result in sleep disruption and
arterial oxyhemoglobin desaturation. Patients with sleep
apnea have a high prevalence of atrial fibrillation and
ventricular arrhythmias.
However, few systematic studies of sleep apnea in heart failure have
been reported, and large-scale studies with detailed historical and
physical findings and laboratory examinations are needed. We studied 81
ambulatory male patients with stable heart failure without major
comorbid disorders to determine (1) sleep characteristics and the
prevalence of atrial and ventricular arrhythmias in
heart failure patients with and without sleep apnea, (2) the prevalence
of the two major forms of sleep apnea (obstructive and central) in the
ambulatory heart failure population, (3) their clinical features, and
(4) polysomnographic consequences.
The etiologies of heart failure were ischemic
cardiomyopathy (30 patients without sleep apnea,
group 1, and 31 patients with sleep apnea, group 2), idiopathic
cardiomyopathy (7 patients in group 1 and 9 in
group 2), and presumed alcoholic cardiomyopathy (3
patients in group 1 and 1 in group 2).
Exclusion criteria included unstable angina; unstable heart failure;
acute pulmonary edema; congenital heart disease; intrinsic
pulmonary diseases, including interstitial lung
disease and obstructive lung defect (ratio of percent predicted forced
expiratory volume to forced vital capacity <68%); intrinsic renal and
liver disorders; kyphoscoliosis; untreated hypothyroidism; and use of
morphine derivatives, benzodiazepines, or theophylline. For uniformity,
only male patients were studied, because female patients are seldom
referred to this center (therefore, we acknowledge that our results
cannot necessarily be extrapolated to women).
Of the 92 eligible patients, 81 (88% recruitment) agreed to
participate. The main reasons for refusal were unwillingness to stay in
the hospital for sleep studies or unwillingness to travel to the
hospital because of distance. The mean left ventricular
ejection fraction of 6 of these patients for whom data were available
was 18±6%.
At the time of the recruitment, no information was sought about
symptoms or risk factors for sleep apnea. The patients were admitted to
the hospital for 2 consecutive nights. Caffeinated products were
avoided during hospitalization. On the first day, a detailed history
was obtained and physical examination was performed. The following
tests were also obtained: complete blood count, serum electrolytes,
blood urea nitrogen, serum creatinine, thyroxine and
digoxin levels, radionuclide ventriculography, arterial
blood gases and pH, pulmonary function, and polysomnography
with nocturnal Holter monitoring.
Polysomnography
Standard definitions were used for sleep-related disordered breathing.
Apnea was defined as cessation of inspiratory airflow for
Other Studies
Classification of Patients
Statistical Analysis
For group 1 compared with group 2 patients, there were no significant
differences in demographics, historical data, and physical examination
findings (Table 1
There were remarkable differences in the severity of various disordered
breathing events between the two groups (Table 2
Left ventricular ejection fraction was significantly lower
(22±8% versus 27±9%, P=0.01) and the prevalence of
atrial fibrillation (22% versus 5%, P=0.026) and nocturnal
ventricular tachycardia (51% versus 37%,
P=0.23) were higher in patients with sleep apnea than in
those without. Similarly, during sleep the mean values for premature
ventricular depolarizations (178±272 versus 34±58 per
hour, P=0.0002), couplets (15±43 versus 0.4±1.4 per hour,
P=0.0001), and ventricular
tachycardias (1.3±3.8 versus 0.1±0.2 per hour,
P=0.07) were higher in patients with sleep apnea than in
those without. There were significant correlations between
apnea-hypopnea index and premature ventricular
depolarizations (r=0.42), couplets (r=0.58),
ventricular tachycardias (r=0.26),
and left ventricular ejection fraction
(r=-.35). The arrhythmias occurred randomly
throughout the night. There was no significant difference in right
ventricular ejection fraction between groups 1 and 2
(44±16% versus 47±13%, P=0.51).
Group 2 patients were further subdivided (Figures 2
Periodic Breathing and Sleep Characteristics
Periodic Breathing, Oxyhemoglobin Desaturation, and Cardiac
Dysfunction
We emphasize that these data do not permit us to determine whether
sleep-disordered breathing exacerbates left ventricular
dysfunction or alternatively, that patients with more impaired cardiac
function were more likely to have excessive sleep-disordered breathing.
However, we speculate that the interaction between sleep-disordered
breathing and left ventricular
dysfunction3 could result in a vicious circle,
further increasing morbidity and mortality in patients with heart
failure.
Periodic Breathing and Central and Obstructive Sleep Apnea
In summary, the present study shows that 51% of patients with
stable heart failure due to systolic dysfunction suffer from a
moderate to severe degree of sleep-disordered breathing. Patients with
heart failure and sleep apnea have a higher prevalence of atrial
fibrillation, ventricular arrhythmias, and lower left
ventricular ejection fraction than do heart failure
patients without sleep apnea. Central sleep apnea accounted for 40%
and obstructive sleep apnea for 11%. Heart failure patients with
obstructive sleep apnea were typically obese and had a history of
habitual snoring, features that were relatively scarce in patients with
central sleep apnea. Both central and obstructive sleep apnea may
result in recurrent episodes of arousal and arterial
oxyhemoglobin desaturation. The pathophysiological
consequences of sleep apnea may ultimately affect the morbidity and
mortality of patients with heart failure.
Received November 20, 1997;
revision received January 23, 1998;
accepted January 28, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Sleep Apnea in 81 Ambulatory Male Patients With Stable Heart Failure
Types and Their Prevalences, Consequences, and Presentations
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Heart failure is a highly
prevalent disorder that continues to be associated with repeated
hospitalizations, high morbidity, and high mortality. Sleep-related
breathing disorders with repetitive episodes of asphyxia may adversely
affect heart function. The main aims of this study were to determine
the prevalence, consequences, and differences in various sleep-related
breathing disorders in ambulatory male patients with stable heart
failure.
Key Words: lung • pulmonary heart disease • oxygen • arrhythmia
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
In spite of recent
advances in the management of heart failure,1 it remains
highly prevalent and is associated with excess morbidity and mortality.
Sleep-related periodic breathing with recurrent episodes of apnea
(cessation of breathing) and hypopnea (decrease in breathing) is known
to occur in patients with heart failure.2 3 4 5
These breathing disorders may be associated with arterial
oxyhemoglobin desaturation (impairment of myocardial
O2 demand/supply balance) and excessive arousals,
resulting in sympathetic activation.6 7 These and
other pathophysiological consequences of sleep
apnea and hypopnea could further contribute to the morbidity and
mortality of heart failure patients.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Eighty-one ambulatory male patients (including the 41 patients
reported earlier in Reference 22 ) with stable heart failure due to
systolic dysfunction (left ventricular ejection
fraction <45%) took part in the study. Details have been published
previously.2 8 Most of the patients were
recruited within 4 years from primary care and
cardiology clinics. Patients who met exclusion criteria
(see below) were not studied any further. The primary investigator or
the cardiologist coinvestigator evaluated all patients to confirm that
they were clinically stable and on standard therapy, with no change in
signs or symptoms of heart failure within the previous 4 weeks.
Seventy-three patients were on an ACE inhibitor, 5 on
hydralazine, 61 on digoxin, 34 on isosorbide dinitrate, and 69
on diuretics. Medication dosages had been adjusted on the basis
of the hemodynamic and clinical status of each patient
and had not been changed within the previous 4 weeks. The calculated
average daily dosage of heart failure medications was 88 mg for
captopril, 15 mg for lisinopril, 22 mg for enalapril, 137
mg for hydralazine, 82 mg for isosorbide dinitrate, 0.21 mg for
digoxin, and 80 mg for furosemide.
On the first night, the patients slept in the sleep laboratory
after the electrodes had been placed, with the intention of
familiarizing the patients with the environment of the sleep
laboratory. On the second night, polysomnography was performed by use
of standard techniques as detailed
previously.2 8 9 10 For staging sleep, we
recorded the electroencephalogram, chin electromyogram, and
electro-oculogram. Thoracoabdominal excursions and naso-oral airflow
(by use of a thermocouple or a CO2
analyzer) were measured qualitatively, and arterial
blood oxyhemoglobin saturation was recorded with a pulse oximeter.
These variables were recorded on a multichannel polygraph
(model 78D; Grass Instrument Co).2 8 9 10 
10 seconds.
Obstructive apnea was defined as the absence of airflow in the presence
of rib cage and abdominal excursions. Central apnea was defined as the
absence of rib cage and abdominal excursions with an absence of airflow
(for further details, see References 2 and 82 8 through 10). Hypopnea was
defined as a reduction of airflow (or thoracoabdominal excursions)
lasting 10 seconds or more and associated with at least a 4% drop in
arterial oxyhemoglobin saturation or an arousal. An arousal
was defined as the appearance of µ waves on the electroencephalogram
for at least 3 seconds.11 The number of episodes
of apnea and hypopnea per hour is referred to as the apnea-hypopnea
index. Polysomnograms were scored in a blinded manner.
To determine the prevalence of arrhythmias, Holter
monitoring was performed during polysomnography as detailed
previously.2 Ventricular
tachycardia was defined as the presence of three
ventricular premature beats in a row. Right and left
ventricular ejection fractions were calculated from gated
first-pass and multigated radionuclide ventriculograms, respectively,
by standard techniques. Pulmonary function tests and
arterial blood samples were obtained according to strict
criteria as detailed previously.12 13
Different thresholds have been used to define the prevalence of
sleep apnea. In patients with heart failure, several
studies14 15 have used an apnea-hypopnea index of
10 per hour. In a previous study,2 we used an
apnea-hypopnea index of 20 per hour. However, like
others,14 15 we have encountered patients with an
index below this level with significant arterial
oxyhemoglobin desaturation. Therefore, for the purpose of this study,
an index 15 per hour was used. Group 1 consisted of patients without
sleep apnea (defined polysomnographically by using an apnea-hypopnea
index of <15 per hour). Group 2 patients had sleep apnea, defined by
an apnea-hypopnea index 15 per hour. Group 2 patients were further
subdivided into those with obstructive sleep apnea (obstructive
apnea-hypopnea index >15 per hour) and those with central sleep apnea
(all of these patients had an obstructive apnea-hypopnea index <10 per
hour). In all patients classified as having obstructive or central
sleep apnea, that breathing disorder was the predominant pattern.
We used the Wilcoxon rank-sum test to assess significant
differences between group 1 and group 2, since the data were not
normally distributed. 
2 was used for
comparison of proportions. Similar tests were used to compare
significant differences between patients with obstructive and those
with central sleep apnea. Spearman correlation coefficients were used
to compute correlations between apnea-hypopnea index and certain
pathophysiologically related variables. A
value of P<0.05 was considered significant. Values are
reported as mean±SD. Calculations were done with SAS
software.16
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The frequency distribution of the apnea-hypopnea index in 10-unit
intervals for the 81 heart failure patients is depicted in Figure 1
. According to our defined thresholds,
there were 40 patients (group 1, 49% of all patients) who did not have
sleep apnea, and the mean (±SD) of the apnea-hypopnea index was 4±4
per hour. In the remaining 41 patients (group 2, 51% of all patients),
the mean apnea-hypopnea index was 44±19 per hour.
View larger version (16K):
[in a new window]
Figure 1. Frequency distribution of apnea-hypopnea index in
10 unit-intervals in 81 male patients with stable, compensated heart
failure. ). In 
15% of
patients in each group, crackles and third or fourth heart sounds were
heard. Mean values of laboratory tests, including serum electrolytes,
creatinine (124±53 versus 124±51 µmol/L),
hemoglobin (15±2 versus 14±2 g/dL), hematocrit (.43±.05 versus
.42±.05), and digoxin (0.9±0.5 versus 1.3±0.6 nmol/L) in group 1 and
group 2 patients, respectively, were similar. Thyroid function tests
were normal in both groups. There were no significant differences when
mean values of forced vital capacity, functional residual capacity,
total lung capacity, and diffusion for CO were compared (data not
shown). However, the mean value of forced expiratory volume in 1 second
over forced vital capacity ratio was slightly but significantly lower
in group 1 (91±12% predicted) than in group 2 (99±10% predicted),
although we had excluded patients with major obstructive airway
defects.
View this table:
[in a new window]
Table 1. Demographics, Historical Data, and Physical
Examination Findings in 81 Male Heart Failure Patients Without (Group
1) or With (Group 2) Sleep-Disordered Breathing ). Consequently,
patients with sleep apnea developed relatively severe oxyhemoglobin
desaturation, despite a higher daytime
PaO[R]2 (Table 2), and
significant sleep disruption (Table 3).
In this regard, the mean values of arousal index (number of arousals
per hour), stage 1 (light) sleep as a percentage of total sleep time,
and wakefulness after sleep onset (Table 3) were significantly greater
and total rapid eye movement sleep significantly less in heart failure
patients with sleep apnea (group 2) than in those without (group
1).
View this table:
[in a new window]
Table 2. Awake Arterial Blood Gases,
Sleep-Disordered Breathing Episodes, and Arterial
Oxyhemoglobin Saturation in 81 Male Heart Failure Patients Without
(Group 1) or With (Group 2) Sleep-Disordered Breathing
View this table:
[in a new window]
Table 3. Sleep Characteristics in 81 Male Heart Failure
Patients Without (Group 1) or With (Group 2) Sleep-Disordered
Breathing and 3)
into those with central sleep apnea (n=32, 40% of all patients) and
those with obstructive sleep apnea (n=9, 11% of all patients) as
defined previously. There were no significant differences in height
(172±7 versus 174±5 cm); age (66±9 versus 63±10 years); left
ventricular ejection fraction (21±8% versus 26±6%); and
hourly episodes of premature ventricular contractions
(202±298 versus 89±182), couplets (10±18 versus 31±87), or
ventricular tachycardias (1.0±2.3 versus
2.3±6.6) during sleep. However, the prevalence of loud snoring and the
mean values for body mass index and diastolic blood
pressure were significantly lower in patients with central than in
those with obstructive sleep apnea (Figure 2). As expected, the mean
values of central (45±22 versus 7±7 per hour, P=0.0001)
and obstructive (1±2 versus 28±8 per hour, P=0.0001)
sleep-disordered breathing events were significantly different, but the
overall mean values for apnea-hypopnea index (47±21 versus 36±10 per
hour) and lowest saturation (78±12% versus 72±11%) did not differ
significantly. Furthermore, the mean values for total dark time
(394±15 versus 388±28 minutes), total sleep time (264±51 versus
265±45 minutes), sleep efficiency (67±13% versus 69±14%), and
arousal index (29±18 versus 44±29 per hour) did not differ
significantly when patients with central and obstructive sleep apnea
were compared.
View larger version (28K):
[in a new window]
Figure 2. Demographics, historical data, and physical
examination findings in male heart failure patients with either central
(CSA) or obstructive (OSA) sleep apnea. Wt indicates weight; BMI, body
mass index; EDS, excessive daytime sleepiness; SBP, systolic
blood pressure; and DBP, diastolic blood pressure.
View larger version (23K):
[in a new window]
Figure 3. Polysomnographic findings in male heart failure
patients with either central (CSA) or obstructive (OSA) sleep apnea.
CAI indicates central apnea index; OAHI, obstructive
apnea-hypo- pnea index; AHI, apnea-hypopnea index; ArI, arousal
index; and SaO2, arterial
oxyhemoglobin saturation.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
This report represents the only large-scale, systematic
study of heart failure with well-defined criteria in patients who have
undergone sleep studies and other detailed laboratory tests to
determine the prevalence, consequences, and factors associated with
various forms of sleep-related breathing disorders in this population.
The results show that (1) 51% of the patients have relatively severe
periodic breathing during sleep, with an average apnea-hypopnea index
of 44 per hour; (2) central sleep apnea occurs in 40% and
obstructive sleep apnea in 11% of the patients; (3) both central and
obstructive forms of sleep apnea result in sleep disruption and
arterial oxyhemoglobin desaturation; and (4) three factors
associated with sleep apnea in heart failure are atrial fibrillation,
ventricular arrhythmias, and low left
ventricular ejection fraction.
Owing to the small number of patients in our initial
report,2 there were no significant differences in
most sleep parameters of patients with and those without
sleep apnea. However, the present data (Table 3
) show that heart
failure patients with sleep apnea slept significantly less and had a
significantly greater proportion of stage 1 (light) sleep and less
rapid eye movement sleep than did heart failure patients without sleep
apnea. These abnormalities in sleep characteristics may result in
daytime fatigue and sleepiness when measured
quantitatively,17 and we found a tendency for a
greater prevalence of subjective excessive daytime sleepiness in
patients with sleep-disordered breathing (Table 1).
Periodic breathing also resulted in severe arterial
oxyhemoglobin desaturation, with an average low level of 76±12% and
the patients' spending 19% of their total sleep time at or below a
saturation of 90% (Table 2). Nocturnal arterial
oxyhemoglobin desaturation occurred despite a normal baseline
PaO2 (Table 2). Periodic breathing
also resulted in an excessive number of arousals in patients with sleep
apnea, with an average of 20 per hour compared with 3 per hour in
patients without sleep apnea (Table 2). Recurrent episodes of nocturnal
oxyhemoglobin desaturation, arousals, and changes in intrathoracic
pressure due to periodic breathing while
asleep,18 as well as daytime dips in
saturation,19 could adversely affect cardiac
function by a variety of mechanisms,6 7 20 21 22 23 24
eventually resulting in an imbalance between myocardial oxygen delivery
and consumption.3 In this context, left
ventricular ejection fraction was significantly lower in
patients with sleep apnea (group 2) than in patients without, thus
confirming our previous findings.2 Furthermore,
the new observation is the increased prevalence of atrial fibrillation,
which was approximately 4 times higher in heart failure patients with
sleep apnea than in those without. Atrial fibrillation might have been
caused in part by the increased right heart afterload due to hypoxic
vasoconstriction and pulmonary
hypertension.24 These data suggest that atrial
fibrillation in particular should serve as a clinical marker for
development of periodic breathing during sleep.
We found that there was a surprisingly high prevalence (51% of
patients) of sleep-disordered breathing, which in our population would
not have been suspected clinically (Table 1). This observation is in
contrast with the obstructive sleep apnea–hypopnea
syndrome.25 The prevalence of habitual snoring
and daytime sleepiness, major symptoms of the obstructive sleep
apnea–hypopnea syndrome, did not differ significantly between the two
groups (Table 1), and there were no distinguishing features during the
general physical examination (eg, hypertension, obesity, etc; Table 1).
This result confirms our previous observation2 in
a smaller number of patients. In the present study, however, when
heart failure patients with sleep apnea were classified in a blinded
manner (without the investigator's knowledge of their clinical
presentations) according to polysomnographic findings as
those with central sleep apnea (40% of all patients) and those with
obstructive sleep apnea (11% of all patients) (Figure 2), the
prevalence of snoring was significantly greater in the latter group.
Only nine of the 32 patients (28%) with central sleep apnea had
habitual snoring, which was significantly less than the 78% of
patients with heart failure and obstructive sleep apnea. Furthermore,
body weight, body mass index, and the diastolic blood
pressure of patients classified as having obstructive sleep apnea were
significantly greater than those with central sleep apnea (Figure 2).
Therefore, the reason why sleep-disordered breathing in heart failure
remains relatively occult (Table 1) is in part due to the predominance
(40% of the patients) of central sleep apnea. Our data (Figure 2) show
that this disorder is less frequently associated with loud snoring and
excessive body weight, which are the hallmarks of the obstructive sleep
apnea–hypopnea syndrome with or without heart failure. We emphasize,
however, that the severity of arterial oxyhemoglobin
desaturation and the number of arousals were similar in both central
and obstructive sleep apnea patients (Figure 3).
Acknowledgments
This work was supported by Merit Review Grants from the
Department of Veterans Affairs to S. Javaheri, MD.
Footnotes
Reprint requests to S. Javaheri, MD, Professor of Medicine, Pulmonary Section (111F), VA Medical Center, 3200 Vine St, Cincinnati, OH 45220.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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K. A. Franklin Sleep apnoea screening in heart failure? Not until benefit is proven! Eur. Respir. J., June 1, 2007; 29(6): 1073 - 1074. [Full Text] [PDF]
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R. Schulz, A. Blau, J. Borgel, H. W. Duchna, I. Fietze, I. Koper, R. Prenzel, S. Schadlich, J. Schmitt, S. Tasci, et al. Sleep apnoea in heart failure Eur. Respir. J., June 1, 2007; 29(6): 1201 - 1205. [Abstract] [Full Text] [PDF]
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L. A. Smith, M. Vennelle, R. S. Gardner, T. A. McDonagh, M. A. Denvir, N. J. Douglas, and D. E. Newby Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial Eur. Heart J., May 2, 2007; 28(10): 1221 - 1227. [Abstract] [Full Text] [PDF]
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S. Garrigue, J.-L. Pepin, P. Defaye, F. Murgatroyd, Y. Poezevara, J. Clementy, and P. Levy High Prevalence of Sleep Apnea Syndrome in Patients With Long-Term Pacing: The European Multicenter Polysomnographic Study Circulation, April 3, 2007; 115(13): 1703 - 1709. [Abstract] [Full Text] [PDF]
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A. M. Luks and E. R. Swenson Travel to high altitude with pre-existing lung disease Eur. Respir. J., April 1, 2007; 29(4): 770 - 792. [Abstract] [Full Text] [PDF]
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 D. E. Leaf and D. S. Goldfarb Mechanisms of action of acetazolamide in the prophylaxis and treatment of acute mountain sickness J Appl Physiol, April 1, 2007; 102(4): 1313 - 1322. [Abstract] [Full Text] [PDF]
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H. Nakashima, T. Katayama, C. Takagi, K. Amenomori, M. Ishizaki, Y. Honda, and S. Suzuki Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction Eur. Heart J., October 1, 2006; 27(19): 2317 - 2322. [Abstract] [Full Text] [PDF]
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 M. Arzt, T. Young, L. Finn, J. B. Skatrud, C. M. Ryan, G. E. Newton, S. Mak, J. D. Parker, J. S. Floras, and T. D. Bradley Sleepiness and sleep in patients with both systolic heart failure and obstructive sleep apnea. Arch Intern Med, September 18, 2006; 166(16): 1716 - 1722. [Abstract] [Full Text] [PDF]
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S. K. Sharma, S. Kumpawat, A. Banga, and A. Goel Prevalence and risk factors of obstructive sleep apnea syndrome in a population of delhi, India. Chest, July 1, 2006; 130(1): 149 - 156. [Abstract] [Full Text] [PDF]
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