1. No category

Vitulano et al., Int J Cardiovasc Res 2015, 4:1
http://dx.doi.org/10.4172/2324-8602.1000195
International Journal of
Cardiovascular Research
Research Article
A SCITECHNOL JOURNAL
Should every Patient with Heart
Failure be Investigated for Sleep
Apnea Syndrome?
Nicola Vitulano*, Francesco Perna, Gianluigi Bencardino, Pio
Cialdella, Maria Lucia Narducci, Daniela Pedicino, Gemma
Pelargonio and Fulvio Bellocci
Department of Cardiovascular Sciences, Catholic University of the Sacred Heart,
Rome, Italy.
*Corresponding author: Nicola Vitulano, Parco dei Cedri 46, 71043 Manfredonia
(FG), Italy, Tel: +39.884.532763; E-mail: nicola.vitulano@gmail.com
Rec date: Jun 21, 2014 Acc date: Aug 24, 2014 Pub date: Aug 26, 2015
of SAS in order to obtain an adequate response to other cardiovascular
treatments.
Normal Sleep, Heart and Respiration
Sleep encompasses about a third of one’s life. The reasons for this
are mostly linked to its effects on the respiratory and cardiovascular
system. During the sleep there are physiological changes in the human
body that conduce to a state of quiescence involving the
cardiovascular, respiratory and metabolic system: the increase of
parasympathetic tone leads to a reduction of blood pressure, mean
heart rate, cardiac output and systemic vascular resistances.
Respiration gets more regular. The respiratory activity regulation
becomes predominantly metabolic and at the same time the
respiratory system operates with a higher trigger threshold.
Heart Failure
Abstract
The increasing interest in the field of sleep medicine during the
whole twentieth century is principally due to the involvement of
sleep-related disordered breathing (SDB) in cardiovascular
disease. Disorders of a physiological phenomenon such as
sleep lead to important changes in state of quiescence of the
cardiovascular, respiratory and metabolic systems during the
night. Consequences of SDB (microawakening, sleep
fragmentation, hypoxemia) represent important harmful triggers
on the cardiovascular system, above all in patients suffering by
inability of the heart to provide an adequate output such as for
heart failure (HF) patients. SDB and HF may be related to each
other in a bidirectional way from epidemiologic and
physiopathologic point of view.
Keywords: Sleep apnea syndrome; Heart failure; Continuous
positive airway pressure (CPAP); Ventricular arrhythmias
Introduction
Questions like “why do we spend so much time sleeping?” and
“what are the mechanisms accountable for sleeping?” accompanied the
research in the area of sleep medicine for the whole 20th century.
Starting from the first definition of sleep as a phenomenon produced
by a tiredness-induced reduction of cerebral activity, the definition of
the sleep was subsequently developed as an actively induced cerebral
condition which is organized in distinct phases. Sleep is a physiologic
phenomenon defined from the behavioral point of view by four
criteria: reduction in motor activity, reduction in response to the
stimulus, presence of stereotyped position, quickly reversible
vegetative status [1]. The importance of sleep in the human life
explains the rising interest about SDB syndromes and their
cardiovascular involvement. Recent studies showed an increased
cardiovascular risk in patients with sleep apnea syndrome (SAS) [2].
The close link between SAS and hypertension is now universally
recognized, as well as its relationship with cardiac arrhythmias,
atherosclerosis, endothelial dysfunction, ischemic heart disease and
HF. Nightly apneic events may also worsen preexisting cardiac
conditions. This review will focus on the impact of SAS on HF,
describing the epidemiology of these two diseases, the difficulties
clinicians can encounter while treating HF patients who are also
affected by SAS, and the importance of an early and effective treatment
Different definitions of HF during the last decades pointed out the
complex and numerous features of this syndrome, being derived from
clinical aspects, hemodynamic traits, oxygen consumption, or exercise
capacity. HF is a syndrome in which symptoms are due to the inability
of the heart to support the normal tissue perfusion because of pump
failure or (less frequently) increased peripheral oxygen demand.
Typical symptoms and signs include shortness of breath at rest or
during exertion, fatigue, fluid retention causing pulmonary congestion
or ankle swelling, and objective evidence of a structural or functional
abnormality of the heart at rest [3,4].
Epidemiology of Heart Failure
Approximately 1–2% of the adult population in developed countries
is affected by HF. Its prevalence rises up to ≥10% among persons ≥70
years old, and is continuously growing due to the ageing of the
population and the advanced treatment of acute cardiac conditions
[4-6] Effective treatment and new therapeutic advances have improved
the prognosis of HF, whose mortality is nevertheless high [7,8], with a
relative reduction in hospitalizations and a smaller but significant
decrease in mortality in the recent years. On the other hand, it is
important to recognize conditions that might underlie HF or influence
its clinical course, in order to improve its outcome. Sleep apnea is
associated with a worse clinical status and is a predictor of poor
prognosis among HF patients; its treatment may positively influence
the global clinical course of HF.
Sleep Apnea Syndrome: Definitions and Diagnosis
Patients with HF frequently have sleep disturbances. Within the
definition of SDB syndrome, several conditions are included, such as
habitual snoring, sleep apnea, Cheyne-Stokes respiration pattern,
sleep-related hypoventilation [9] Apnea is defined as the cessation of
the airflow or a drop in the peak airflow signal excursion by > 90% of
baseline for more than 10 seconds associated with oxygen desaturation
and arousal detected at the electroencephalogram (EEG). Hypopnea is
defined as a 30% or more reduction in breathing amplitude with
respect to the baseline airflow associated to a desaturation of >3% or
an arousal [9]. The consequences of these events are represented by
important modifications in the blood gases concentration and in the
mechanical respiratory work, that makes the body react in the only
possible way, that is, by microawakening, reduction in the sleep
All articles published in International Journal of Cardiovascular Research are the property of SciTechnol and is protected
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Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
intensity, thus sleep fragmentation. The goal of all of these actions is to
restore a normal respiratory rate and blood hemoglobin saturation.
The presence of hypopnea/apnea-related symptoms is crucial for the
diagnosis of SAS. It is possible to distinguish the apnea into
obstructive, when the airflow cessation is accompanied by a thoracicabdominal effort to overcome the collapsed upper airways (figure 1A), central, characterized by the absence of the airflow as well as of the
thoracic-abdominal movements (figure 1-B), and mixed, with a
delayed manifestation of thoracic-abdominal movements, after an
initial central apneic phase (figure 1-C).
Signs and Symptoms of Sleep Disordered Breathing
Habitual snoring (every night) and persistent (from at least 6 months)
Daytime Somnolence
Unrefreshing Sleep
Witnessed Apnea
Awakenings with Choking
Morning Headache
Lack of concentration
Table 1: Signs and Symptoms of Sleep Disordered Breathing
The gold standard for the diagnosis of SAS often requires spending
a night in a sleep laboratory, performing a multiparametric
monitoring and recording physiological variables (polysomnography).
These variables include neurological signs (detected with EEG,
electromyography (EMG), electrooculography (EOG)) and
cardiorespiratory parameters. After an accurate screening for signs
and symptoms, the use of cardiac and respiratory nightly monitoring
only (cardiorespiratory sleep study) could be considered, which
includes the recording of the airway flow, hemoglobin O2 saturation,
electrocardiogram, thoracic-abdominal movements, body position
during the sleep. For the diagnosis of SAS, some indexes are used; the
most widely known is the apnea-hypopnea index (AHI), that indicates
the average number of apneas and hypopneas per hour of sleep. Other
indices include Respiratory Disturbance Index (RDI), that represents
the average number per hour of sleep of apneas, hypopneas, and
respiratory effort-related arousals (RERAs), and oxygen desaturation
index (ODI), indicating the average number of significant oxygen
desaturations per hour of sleep. The diagnosis of SAS can be
established with an AHI≥5/hour associated to typical symptoms. The
SAS is defined mild, moderate or severe when this value is respectively
between 5 and 15, between 15 e 30 and over 30 events per hour [9].
Obstructive Sleep Apnea in Heart Failure Patients
Figure 1: examples of a cardiorespiratory sleep study. Sleep apnea
episodes are classified into obstructive (A), central (B) or mixed
(C). The criterion differentiating between obstructive and central is
the concomitant presence or absence of breathing efforts
respectively, evidenced by the registration of thorax and abdominal
movements. Mixed sleep apneas are characterized by an initial
central sleep apnea followed by an obstructive component
The diagnosis of SAS should not be made without an instrumental
evaluation encompassing the whole night. Before starting a diagnostic
work-up for a patient with suspected SAS, typical signs and symptoms
should be investigated in order to enhance the accuracy of the
screening Table 1.
Volume 4 • Issue 1 • 1000195
Several studies have shown a strong relationship between
obstructive sleep apnea syndrome (OSAS) and HF. Patients affected by
both these pathologies often present some specific features. In fact,
narrow pharynx related to fat accumulation in the neck and anatomic
abnormalities of the upper airways in addition to a loss of tone of the
pharyngeal dilator muscle during the sleep can cause pharyngeal
collapse and obstructive apneas. During apneic events, hypoxia and
hypercapnia trigger the respiratory drive with subsequent arousals
from sleep in order to terminate the apneic events. The
pathophysiologic bases of this phenomenon are quite complex. The
loss of lung volume due to fluid retention and congestive edema
reduces the longitudinal traction forces on the upper airways, thus
rendering them more collapsible. Furthermore, despite the typical
caudal fluid displacement in HF patients related to leg edema and
sedentary living, this pattern experiences a different distribution
during the night due to a rostral shift from the legs, contributing to a
higher severity of OSAS; in fact, fluid accumulation in the neck soft
tissues contributes in this way to increase their collapsibility during the
sleep by a worsening of the constriction of the pharynx [10] From a
mechanical point of view, the main negative influence of OSAS on HF
is given by an exaggerated negative intrathoracic pressure that creates
• Page 2 of 7 •
Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
an increase in left ventricular transmural pressure. In addition,
recurrent apneas trigger on one hand the activation of the sympathetic
system and on the other hand an increased release of vasoactive and
inflammatory agents. The above mentioned mechanisms provoke the
progression of the underlying cardiovascular disease because of poorly
controlled hypertension and endothelial dysfunction, which are major
risk factors for ischemic heart disease, that is in turn the most frequent
and important substrate of HF. Such detrimental triggers on the
cardiovascular system can also contribute to the development or
worsening of arrhythmias, stroke, renal failure, which are often part of
the clinical scenario of HF [3,11].
Central Sleep Apnea in Heart Failure Patients
Patients with HF present increased filling pressures leading to
pulmonary congestion and an imbalance in gas exchange; during the
night there is indeed a progressive reduction in PaO2 below the
threshold of the physiological 4-10 mmHg reduction, and an increase
in PaCO2 above the 3-7 mmHg usually observed during a normal
sleep [12]. These conditions, combined with the stretching of
pulmonary J receptors due to increased transthoracic pressure,
provoke the beginning of hyperventilation and a subsequent drop of
PaCO2 below the so-called apnea threshold. The consequent
hypocapnia causes suppression of the respiratory muscles by the
central nervous system, thus causing phases of apnea. During the
apnea, decreased PaO2 and increased PaCO2 again stimulate the
central nervous system that increases the ventilation rate and provoke
arousal with sleep fragmentation. In this way, this vicious circle starts
over Figure 2.
Further pathophysiologic mechanisms linking CSA and HF include
chemoreflex receptors, pulmonary congestion, autonomic imbalance
with increased sympathetic tone, thus rendering the overall process
rather complex [13-15].
Sleep Apnea
Epidemiology
Syndrome
and
Heart
Failure:
Moderate to severe SDB affects 39% of the general population, with
an increased prevalence in male and older subjects [16], but its
prevalence in HF patients is much higher. Among HF patients
undergoing a polysomnography, the reported prevalence of OSAS is
between 12% and 53% [17-19]. On the other hand, more than 55% of
patients with OSAS have diastolic dysfunction [20]. Many studies have
detected such high prevalence of SDB in the HF setting, reporting a
wide distribution range mainly because of the choice of different AHI
cutoffs for the definition of SDB, different HF severity, different mean
ejection fraction (EF) values (systolic and diastolic dysfunction), and
differences in the presence of other comorbidities or risk factors. The
same studies have also detected a higher prevalence of CSA in patients
with chronic HF. Studies reporting the prevalence of obstructive sleep
apnea syndrome (OSAS) and central sleep apnea (CSA) are reported
in Table 2 [17-27].
The results of the studies reported in Table 2 point out not only the
importance of SDB in the setting of HF, but also the disparity of its
prevalence among different studies. This highlights the importance of
standardizing the cutoff values for the diagnosis of sleep apnea, the
patient populations taken in exam while investigating SDB, and the
classification of different types of SDB. Moreover poor sleep, including
insomnia [28], is common among HF patients; these features could
make more difficult the realization and assessment of sleep study.
Indeed HF patients perceived insomnia as having a negative impact on
quality and duration of sleep and on daytime function [29], have a
longer sleep-onset latencies, sleep less one hour and half than patients
without HF (due to diuretics therapies, nycturia, symptoms,
paroxysmal nocturnal dyspnea), some positions are obliged to avoid
discomfort and dyspnea (preference of right side regard left one as a
sort of autoprotective mechanisms to increase cardiac output in the
sleep right side position) [30-31]. Besides, the selection of severity of
HF in the study population might play an important role since the
prevalence of CSA seems to increase in patients with more advanced
HF. With the advances in therapies for the HF population, more
specific investigation is warranted to further understand the
relationship between CSA and HF
Figure 2: Pathophysiologic Mechanisms Linking CSA and HF
Study
Patients
Gender
(n)
MF (n)
Age
(Years
mean ±
SD)
Mean
LVEF
NYHA
Functional
Class
AHI
Cutoff
(eventshour)
OSA + CSA
>50
||-|||
>10
(%)
OSA
Prevelance
(%)
CSA
55
35
20
Prevelance
(%)
Prevelance
(%)
Chan, 1997
20
7/13
65+6
Javaheri, 1998
81
81/0
64
10,5
±
25
|-|||
≥15
51
11
40
Sin, 1999
450
382/68
60
13,6
±
27,3
||-|V
≥10
70
37
33
Volume 4 • Issue 1 • 1000195
• Page 3 of 7 •
Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
Femier, 2005
53
41/12
60,1
9,8
Javaheri, 2006
100
100/0
Vazi, 2007
55
Wang, 2007
±
34
|-||
≥10
68
53
15
64 ± 10
24
|-|||
≥15
49
12
37
55/0
61 ± 12
30,6
||
≥15
53
15
28
218
120/44
55
11,7
±
25
||-|V
≥15
47
26
21
Oldenburg,
2007
700
561/139
64,5
10,4
±
28,3
||-|V
≥5
76
36
40
Yum ino, 2009
218
≤45
||-|V
≥15
29
21
Henecher, 2011
71
60/11
61.4
9.5
±
29,6
||-|V
≥5
81
49
32
Aslan, 2013
80
65/15
44,1
9,4
±
66
|
≥15
46
46
.
Table 2: Prevalence of obstructive sleep apnea syndrome (OSAS) and central sleep apnea
Sleep Apnea Syndrome and Heart Failure: Ventricular
Arrhythmias
The presence of SDB provokes a mechanical stress in the chest
which can be detrimental, in patients with severe OSAS, even in the
absence of any cardiac disease. Therefore, the same mechanical stress
might be much more hazardous in the presence of HF [32].
Myocardial stretch induced by OSAS may trigger both atrial and
ventricular arrhythmias [33]. Many patients with HF die suddenly
because of ventricular arrhythmias [34]. It has been demonstrated that
in patients with HF there is a different daily pattern of ventricular
ectopies during the sleep depending on the presence of either OSAS or
CSA: in patients with OSAS, ventricular premature beats (VPBs) occur
more frequently during apnea phases than in CSA patients, who have
instead more frequent VPBs during phases of hyperpnea. These
dissimilar patterns are probably caused by slower blood circulation in
patient with CSA, which causes a time shift of the arrhythmogenic
trigger later after the apnea compared with patients with OSAS, in
whom such trigger is fairly coincident with apnea termination [35].
Despite numerous studies and reports about ventricular arrhythmias
in SDB patients, there are so far no conclusive data to demonstrate a
primary etiologic role of OSAS and CSA. However, the Sleep Heart
Health Study (SHHS) suggested a strict link between SDB and
nocturnal ventricular arrhythmias [36]. Furthermore, a recent study
including 472 patients with congestive HF underlined that in these
patients CSA and OSAS are independently associated with an
increased risk of ventricular arrhythmias and appropriate therapy of
implantable cardioverter-defibrillator (ICD) [37]. The various
mechanisms by which SDB provokes ventricular arrhythmias are not
completely known. Shepard et al. in their study showed that when the
level of oxygen saturation decreases below 60% there is increased
ventricular irritability evidenced by a higher burden of VPBs. Hypoxia
and the sympathetic trigger induced by apneic events; cooperate to
trigger ventricular arrhythmias in the presence of an important
substrate such as HF [38]. A recent study including 10,701 consecutive
adults undergoing their first diagnostic polysomnogram assessed the
incidence of resuscitated or fatal sudden cardiac death (SCD) in
relationship to the presence of OSAS; during an average follow-up of
5.3 years, the multivariate analysis identified independent risk factors
for SCD, including lowest nocturnal oxygen saturation, which is an
Volume 4 • Issue 1 • 1000195
important consequence of OSAS. In particular, SCD was best
predicted by age >60 years (HR 5.53), AHI >20 (HR 1.60), mean
nocturnal O2sat <93% (HR 2.93), and lowest nocturnal O2sat <78%.
The authors concluded that the presence of OSAS predicts incident
SCD, and the magnitude of the risk is predicted by multiple
parameters characterizing OSAS severity, therefore OSAS should be
considered as a novel risk factor for SCD [39]. Sano et al. recently
demonstrated, in patients admitted for worsening HF and undergoing
cardiorespiratory study and Holter ECG, that the severity of CSA and
C-reactive protein levels are independently associated with the
prevalence and complexity of cardiac arrhythmias [40].
It is known that apneic events are highly prevalent and associated
with neurohormonal and electrophysiological abnormalities that may
increase the risk of sudden death from cardiac causes, especially
during sleep. In the general population it is described a peak of the risk
of sudden death from 6 a.m. to noon and has a nadir from midnight to
6 a.m., but at the same time it is showed by Gami et al. that patients
affected by obstructive sleep apnea have a peak in sudden death from
cardiac causes during the sleeping hours, contrasting with the nadir of
sudden death from cardiac causes during this period in people without
obstructive sleep apnea and in the general population [41]. Regard
increased prevalence of HF, in the last decade also atrial fibrillation
(AF) has become one of the most public health problem; AF and HF
coexist in a large percentage of patients (22%-42%) and share risk
factors; each of these conditions strongly predisposes to the other. In
HF patients the occurrence of new AF is associated with a two-fold
higher risk of death in comparison with those without AF [42-44]. In
the aforementioned SHHS compared with those without sleepdisordered breathing and adjusting for age, sex, body mass index and
prevalent coronary heart disease, patients with SDB had four times the
odds of atrial fibrillation [36]. Recent findings show and high
prevalence of OSAS among patients with AF and at the same time in a
close relationship patients suffering of OSAS present a high incidence
of AF [45-46]. Sano et al. revealed that index of central sleep apnea was
associated with prevalence of AF in a group of patients with worsening
HF and CSA [40].
• Page 4 of 7 •
Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
Sleep Apnea Syndrome and
Hospitalization and Mortality
Heart
Failure:
HF affects about 2-3% of the population and accounts for most
hospitalizations in industrialized countries [4]. Despite the advances in
medical and interventional treatments, its outcome has not improved
as expected; therefore poor prognosis and poor quality of life are still a
major trait of this disease. HF is the cause of 5% of acute hospital
admissions, affects 10% of patients recovered in hospital, and accounts
for 2% of national health expenditure in the United Kingdom, mostly
due to the cost of hospital admissions [47].
The overall life expectancy is pessimistic; in fact about 50% of
patients die within 4 years from the diagnosis and 40% of patients die
or are re-hospitalized within 1 year after hospital admission for
worsening HF [4]. Besides the different etiologies of HF, it is necessary
to consider also the co-pathologies that may worsen or precipitate it,
such as SDB.
Several studies showed how SAS is related to hospitalizations, rehospitalizations and mortality, and how its treatment can reduce these
phenomena. Some studies report statistically significant differences in
the mortality rate for patients with OSAS compared to those with mild
or no sleep apnea [23]. The impact of nocturnal breathing patterns in
chronic HF has been evaluated by Damy et al. enrolling 384 patients
with HF and LVEF ≤45% (mean LVEF 29 ± 9%) assessed by
polygraphy; combined endpoints were death, heart transplant, and
implant of a ventricular assist device. The authors found that patients
with OSAS with an AHI 5-20/h and that one with an AHI ≥20/h or
CSA had a poorer prognosis compared with patients without SDB.
Moreover, patients treated with nocturnal ventilation had a
better outcome than untreated ones [48].
Treatment of Sleep Apnea Syndrome in the Setting of
Heart Failure
To understand the importance and the complexity of HF, from the
clinical aspects to therapeutic and economical resources to invest, it is
necessary to consider that chronic HF causes twice deaths as compared
with tumoral diseases such as breast and bladder cancer and about the
same number of deaths as colon cancer. In spite of the improvement of
therapeutic approaches, patients with HF continue to have a poor
prognosis. Worsening symptoms require continuous therapy
adjustments. The therapeutic options include both pharmacological
treatment and invasive procedures: beta-blocking agents, reninangiotensin-aldosteron system antagonists and diuretics, cardiac
resynchronization therapy and implantable cardioverter-defibrillator
implantation.
It is equally important to detect and treat all the associate
conditions that might contribute to worsen the HF. In such context it
is necessary to promptly diagnose SAS for the considerable positive
impact on HF derived by its treatment. The therapeutic strategies
involve first of all lifestyle changes such as weight loss, avoidance of
hearty meals, alcohol and sedative hypnotics intake before sleep,
avoidance of the supine position during sleep. However, the main
choice in the treatment of SAS is represented by the nightly use of
continuous positive air pressure ventilatory support, such as
Automatic Positive Airway Pressure (APAP), Automatic Continuous
Airway Pressure (CPAP), bilevel Positive Airway Pressure (bi-PAP), or
adaptive servo-ventilation. The choice of the right ventilation mode
depends on the type and number of apneic events and underlying
Volume 4 • Issue 1 • 1000195
cardiac and respiratory conditions. Several studies have shown the
advantages of this therapeutic option for HF patients with sleep apnea
in terms of blood pressure [49,50], insulin sensitivity [51] and LVEF
improvement [52,53]. Although the main results of the CANPAP trial
had shown no effect of CPAP on heart transplant-free survival, on the
other hand a post-hoc analysis found that if CSA is suppressed soon
after starting the CPAP treatment, the nightly ventilatory support
might improve both LVEF and heart trasplant-free survival [54].
In patients with chronic HF the co-existence of OSAS and CSA is
often seen; in a small study it has been shown that adaptive servoventilation is effective in reducing all forms of SDB with improvement
of LVEF at six-month follow-up [55]. At the same time, the abolition
of OSAS by CPAP resulted in a reduction of ventricular premature
beats during the sleep in patients with systolic dysfunction and OSAS
[56,57]
Conclusion
Nowadays several data suggest that SDB should be included among
cardiovascular risk factors. Due to the high prevalence of SAS in HF
patients, the worsened quality of sleep and life and the poorer outcome
resulting from the combination of these two conditions, and above all
the potential beneficial effects of nightly ventilatory support on the
prognosis of HF patients, physicians should be aware of typical
symptoms and signs of SAS. Even the sole presence of a sleeping
history suggestive for sleep disturbances or typical anthropometric
features of SAS in the setting of HF should raise the suspicion of SAS
and lead the physician to prescribe further investigation in order to
obtain a early diagnosis and treatment. A nightly cardiorespiratory
monitoring could be effectively used in selected cases as an initial
screening tool, but the portable monitor is not appropriate for the
diagnosis of SAS in patients with significant comorbid medical
conditions (including, but not limited to, moderate to severe
pulmonary disease, neuromuscular disease, or congestive HF).
Polysomnography, which is currently considered as the gold standard
investigation in this field, is almost invariably effective to reach the
correct diagnosis, although the optimal screening tools for SDB in
patients with HF have been not established yet. The treatment of SAS
certainly plays an important role in the therapeutic plan of HF. This
field of interest needs further knowledge in order to understand the
precise role played by SDB in HF patients: a risk factor, an important
comorbidity or a precipitating factor that potentially hastens the
progression of the disease or causes sudden death. In this perspective,
its treatment is crucial in order to optimize the treatment of HF and
might improve the clinical response to other pharmacological and
interventional treatments.
References
1.
2.
3.
4.
Rechtshaffen A, Siegel J (2003) Sleep and dreaming principles of
Neural Science. (3rdedn),New York, McGraw-Hill.
Dong JY, Zhang YH, Qin LQ (2013) Obstructive sleep apnea and
cardiovascular risk: meta-analysis of prospective cohort studies.
Atherosclerosis 229: 489-495.
Naughton MT, Lorenzi-Filho G (2009) Sleep in heart failure.
Prog Cardiovasc Dis 51: 339-349.
McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M,
et al. (2012) ESC Guidelines for the diagnosis and treatment of
acute and chronic heart failure 2012: The Task Force for the
Diagnosis and Treatment of Acute and Chronic Heart Failure
• Page 5 of 7 •
Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
2012 of the European Society of Cardiology. Developed in
collaboration with the Heart Failure Association (HFA) of the
ESC. Eur Heart J 33: 1787-847.
Murdoch DR, Love MP, Robb SD, McDonagh TA, Davie AP, et
al. (1998) Importance of heart failure as a cause of death.
Changing contribution to overall mortality and coronary heart
disease mortality in Scotland 1979-1992. Eur Heart J 19:
1829-1835.
Senni M, Tribouilloy CM, Rodeheffer RJ, Jacobsen SJ, Evans JM,
et al. (1999) Congestive heart failure in the community: trends in
incidence and survival in a 10-year period. Arch Intern Med 159:
29-34.
Redfield MM, Jacobsen SJ, Burnett JC Jr, Mahoney DW, Bailey
KR, et al. (2003) Burden of systolic and diastolic ventricular
dysfunction in the community: appreciating the scope of the
heart failure epidemic. JAMA 289: 194-202.
Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, et al.
(2002) Long-term trends in the incidence of and survival with
heart failure. N Engl J Med 347: 1397-1402.
Berry RB, Budhiraja R, Gottlieb DJ, Gozal D, Iber C, et al. (2012)
Rules for scoring respiratory events in sleep: update of the 2007
AASM Manual for the Scoring of Sleep and Associated Events.
Deliberations of the Sleep Apnea Definitions Task Force of the
American Academy of Sleep Medicine. J Clin Sleep Med 8:
597-619.
Yumino D, Redolfi S, Ruttanaumpawan P, Su MC, Smith S, et al.
(2010) Nocturnal rostral fluid shift: a unifying concept for the
pathogenesis of obstructive and central sleep apnea in men with
heart failure. Circulation 121: 1598-1605.
Kasai T, Bradley TD (2011) Obstructive sleep apnea and heart
failure: pathophysiologic and therapeutic implications. J Am Coll
Cardiol 57: 119-127.
Nava S, Fanfulla F. Basi (2010) Rrational of ventilatory during
sleep Ventilazione meccanica non invasiva. (1stedn), Luogo,
Casa Editrice.
Müller M, de Jong M, Jaarsma T, Koops A, Voors AA, et al.
(2010) Central sleep apnoea syndrome in chronic heart failure:
an underestimated and treatable comorbidity. Neth Heart J 18:
260-263.
CROWELL JW, GUYTON AC, MOORE JW (1956) Basic
oscillating mechanism of Cheyne-Stokes breathing. Am J Physiol
187: 395-398.
Javaheri S (2005) Central sleep apnea in congestive heart failure:
prevalence, mechanisms, impact, and therapeutic options. Semin
Respir Crit Care Med 26: 44-55.
Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, et al.
(2013) Increased prevalence of sleep-disordered breathing in
adults. Am J Epidemiol 177: 1006-1014.
Yumino D, Wang H, Floras JS, Newton GE, Mak S, et al. (2009)
Prevalence and physiological predictors of sleep apnea in patients
with heart failure and systolic dysfunction. J Card Fail 15:
279-285.
Ferrier K, Campbell A, Yee B, Richards M, O'Meeghan T, et al.
(2005) Sleep-disordered breathing occurs frequently in stable
outpatients with congestive heart failure. Chest 128: 2116-2122.
Vazir A, Hastings PC, Dayer M, McIntyre HF, Henein MY, et al.
(2007) A high prevalence of sleep disordered breathing in men
with mild symptomatic chronic heart failure due to left
ventricular systolic dysfunction. Eur J Heart Fail 9: 243-250.
Volume 4 • Issue 1 • 1000195
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
Chan J, Sanderson J, Chan W, Lai C, Choy D, et al. (1997)
Prevalence of sleep-disordered breathing in diastolic heart
failure. Chest 111: 1488-1493.
Javaheri S, Parker TJ, Liming JD, Corbett WS, Nishiyama H, et
al. (1998) Sleep apnea in 81 ambulatory male patients with stable
heart failure. Types and their prevalences, consequences, and
presentations. Circulation 97: 2154-2159.
Javaheri S (2006) Sleep disorders in systolic heart failure: a
prospective study of 100 male patients. The final report. Int J
Cardiol 106: 21-28.
Wang H, Parker JD, Newton GE, Floras JS, Mak S, et al. (2007)
Influence of obstructive sleep apnea on mortality in patients with
heart failure. J Am Coll Cardiol 49: 1625-1631.
Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, et al.
(1999) Risk factors for central and obstructive sleep apnea in 450
men and women with congestive heart failure. Am J Respir Crit
Care Med 160: 1101-1106.
Oldenburg O, Lamp B, Faber L, Teschler H, Horstkotte D, et al.
(2007) Sleep-disordered breathing in patients with symptomatic
heart failure: a contemporary study of prevalence in and
characteristics of 700 patients. Eur J Heart Fail 9: 251-257.
Aslan K, Deniz A, Cayli M, Bozdemir H, Sarica Y, et al. (2013)
Early left ventricular functional alterations in patients with
obstructive sleep apnea syndrome. Cardiol J 20: 519-525.
Herrscher TE, Akre H, Øverland B, Sandvik L, Westheim AS
(2011) High prevalence of sleep apnea in heart failure
outpatients: even in patients with preserved systolic function. J
Card Fail 17: 420-425.
Laugsand LE, Strand LB, Platou C, Vatten LJ, Janszky I (2014)
Insomnia and the risk of incident heart failure: a population
study. Eur Heart J 35: 1382-1393.
Andrews LK, Coviello J, Hurley E, Rose L, Redeker NS (2013)
"I'd eat a bucket of nails if you told me it would help me sleep:"
perceptions of insomnia and its treatment in patients with stable
heart failure. Heart Lung 42: 339-345.
Arzt M, Young T, Finn L, Skatrud JB, Ryan CM, et al. (2006)
Sleepiness and sleep in patients with both systolic heart failure
and obstructive sleep apnea. Arch Intern Med 166: 1716-1722.
Ozeke O, Ertan C, Demir AD (2012) Sleep apnea, heart failure,
and sleep position. Sleep Breath 16: 933-935.
Shivalkar B, Van de Heyning C, Kerremans M, Rinkevich D,
Verbraecken J, et al. (2006) Obstructive sleep apnea syndrome:
more insights on structural and functional cardiac alterations,
and the effects of treatment with continuous positive airway
pressure. J Am Coll Cardiol 47: 1433-1439.
Franz MR, Cima R, Wang D, Profitt D, Kurz R (1992)
Electrophysiological effects of myocardial stretch and mechanical
determinants of stretch-activated arrhythmias. Circulation 86:
968-978.
Chakko CS, Gheorghiade M (1985) Ventricular arrhythmias in
severe heart failure: incidence, significance, and effectiveness of
antiarrhythmic therapy. Am Heart J 109: 497-504.
Ryan CM, Juvet S, Leung R, Bradley TD (2008) Timing of
nocturnal ventricular ectopy in heart failure patients with sleep
apnea. Chest 133: 934-940.
Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, et al.
(2006) Association of nocturnal arrhythmias with sleepdisordered breathing: The Sleep Heart Health Study. Am J Respir
Crit Care Med 173: 910-916.
• Page 6 of 7 •
Citation:
Vitulano N, Perna F, Bencardino G, Cialdella P, Narducci ML, et al. (2015) Should every Patient with Heart Failure be Investigated for Sleep
Apnea Syndrome?. Int J Cardiovasc Res 4:1.
doi:http://dx.doi.org/10.4172/2324-8602.1000195
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
Bitter T, Westerheide N, Prinz C, Hossain MS, Vogt J, et al.
(2011) Cheyne-Stokes respiration and obstructive sleep apnoea
are independent risk factors for malignant ventricular
arrhythmias requiring appropriate cardioverter-defibrillator
therapies in patients with congestive heart failure. Eur Heart J 32:
61-74.
Shepard JW Jr, Garrison MW, Grither DA, Evans R, Schweitzer
PK (1985) Relationship of ventricular ectopy to nocturnal oxygen
desaturation in patients with chronic obstructive pulmonary
disease. Am J Med 78: 28-34.
Gami AS, Olson EJ, Shen WK, Wright RS, Ballman KV, et al.
(2013) Obstructive sleep apnea and the risk of sudden cardiac
death: a longitudinal study of 10,701 adults. J Am Coll Cardiol
62: 610-616.
Sano K, Watanabe E, Hayano J, Mieno Y, Sobue Y, et al. (2013)
Central sleep apnoea and inflammation are independently
associated with arrhythmia in patients with heart failure. Eur J
Heart Fail 15: 1003-1010.
Gami AS, Howard DE, Olson EJ, Somers VK (2005) Day-night
pattern of sudden death in obstructive sleep apnea. N Engl J Med
352: 1206-1214.
Zoni-Berisso M, Lercari F, Carazza T, Domenicucci S (2014)
Epidemiology of atrial fibrillation: European perspective. Clin
Epidemiol 6: 213-220.
Wang TJ, Larson MG, Levy D, Vasan RS, Leip EP, et al. (2003)
Temporal relations of atrial fibrillation and congestive heart
failure and their joint influence on mortality: the Framingham
Heart Study. Circulation 107: 2920-2925.
Chamberlain AM, Redfield MM, Alonso A, Weston SA, Roger
VL (2011) Atrial fibrillation and mortality in heart failure: a
community study. Circ Heart Fail 4: 740-746.
Hohl M, Linz B, Böhm M, Linz D1 (2014) Obstructive sleep
apnea and atrial arrhythmogenesis. Curr Cardiol Rev 10:
362-368.
Oza N, Baveja S, Khayat R, Houmsse M (2014) Obstructive sleep
apnea and atrial fibrillation: understanding the connection.
Expert Rev Cardiovasc Ther 12: 613-621.
Stewart S, Jenkins A, Buchan S, McGuire A, Capewell S, et al.
(2002) The current cost of heart failure to the National Health
Service in the UK. Eur J Heart Fail 4: 361-371.
Damy T, Margarit L, Noroc A, Bodez D, Guendouz S, et al.
(2012) Prognostic impact of sleep-disordered breathing and its
Volume 4 • Issue 1 • 1000195
49.
50.
51.
52.
53.
54.
55.
56.
57.
treatment with nocturnal ventilation for chronic heart failure.
Eur J Heart Fail 14: 1009-1019.
Faccenda JF, Mackay TW, Boon NA, Douglas NJ (2001)
Randomized placebo-controlled trial of continuous positive
airway pressure on blood pressure in the sleep apnea-hypopnea
syndrome. Am J Respir Crit Care Med 163: 344-348.
Wilcox I, Grunstein RR, Hedner JA, Doyle J, Collins FL, et al.
(1993) Effect of nasal continuous positive airway pressure during
sleep on 24-hour blood pressure in obstructive sleep apnea. Sleep
16: 539-544.
Harsch IA, Schahin SP, Radespiel-Tröger M, Weintz O, Jahreiss
H, et al. (2004) Continuous positive airway pressure treatment
rapidly improves insulin sensitivity in patients with obstructive
sleep apnea syndrome. Am J Respir Crit Care Med 169: 156-162.
Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, et al. (2003)
Cardiovascular effects of continuous positive airway pressure in
patients with heart failure and obstructive sleep apnea. N Engl J
Med 348: 1233-1241.
Malone S, Liu PP, Holloway R, Rutherford R, Xie A, et al. (1991)
Obstructive sleep apnoea in patients with dilated
cardiomyopathy: effects of continuous positive airway pressure.
Lancet 338: 1480-1484.
Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, et al. (2007)
Suppression of central sleep apnea by continuous positive airway
pressure and transplant-free survival in heart failure: a post hoc
analysis of the Canadian Continuous Positive Airway Pressure
for Patients with Central Sleep Apnea and Heart Failure Trial
(CANPAP). Circulation 115: 3173-3180.
Hastings PC, Vazir A, Meadows GE, Dayer M, Poole-Wilson PA,
et al. (2010) Adaptive servo-ventilation in heart failure patients
with sleep apnea: a real world study. Int J Cardiol 139: 17-24.
Vitulano N, Giubilato G, Santangeli P, Ierardi C, Pieroni M, et al.
(2013) Continuous positive airway pressure treatment in
addition to optimal medical therapy for ventricular ectopy in a
patient with heart failure and sleep-related breathing disorder. J
Cardiovasc Med 14: 673-676.
Ryan CM, Usui K, Floras JS, Bradley TD (2005) Effect of
continuous positive airway pressure on ventricular ectopy in
heart failure patients with obstructive sleep apnoea. Thorax 60:
781-785.
• Page 7 of 7 •