Early View

Task Force Report

European Respiratory Society and European

Sleep Research Society Statement on the
treatment of central sleep apnoea with adaptive
servo-ventilation

Winfried J. Randerath, Sophia E. Schiza, Michael Arzt, Maria Rosaria Bonsignore, Raphael Heinzer,
Carolina Lombardi, Robert Lyssens, Gianfranco Parati, Thomas Penzel, Jean Louis Pepin, Dirk
Pevernagie, Silke Ryan, Luca Vignatelli, Esther I. Schwarz

Please cite this article as: Randerath WJ, Schiza SE, Arzt M, et al. European Respiratory
Society and European Sleep Research Society Statement on the treatment of central sleep
apnoea with adaptive servo-ventilation. Eur Respir J 2025; in press
(https://doi.org/10.1183/13993003.00263-2025).

This manuscript has recently been accepted for publication in the European Respiratory Journal. It is
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 European Respiratory Society and European Sleep Research Society Statement
on the treatment of central sleep apnoea with adaptive servo-ventilation

Winfried J. Randerath1, Sophia E. Schiza2, Michael Arzt 3, Maria Rosaria Bonsignore4,

Raphael Heinzer5, Carolina Lombardi6,7, Robert Lyssens8, Gianfranco Parati6,7,
Thomas Penzel9, Jean Louis Pepin10, Dirk Pevernagie11, Silke Ryan12, Luca
Vignatelli13, Esther I. Schwarz14

1
Bethanien Hospital, Clinic of Pneumology and Allergology, Center for Sleep Medicine
and Respiratory Care, Institute of Pneumology at the University of Cologne, Solingen,
Germany.
2
Sleep Disorders Unit, Dept of Respiratory Medicine, School of Medicine, University
of Crete, Greece.
3
Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
Germany.
4
Institute of Translational Pharmacology (IFT), Palermo branch, National Research
Council (CNR), Palermo, Italy.
5
Centre d'investigation et de recherche sur le sommeil, Centre hospitalier universitaire
vaudois, 1011 Lausanne.
6
Istituto Auxologico Italiano IRCCS, Milan, Italy.
7
Department of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy.
8
European Lung Foundation (ELF), Sheffield, United Kingdom.
9
Center of Sleep Medicine, University Hospital Charité Berlin, Berlin, Germany.
10
Univ. Grenoble Alpes, HP2 Laboratory, Inserm U1300, Grenoble.
11
Faculty of Medicine and Health Sciences, Ghent University, Department of
Pulmonary Medicine, Ghent University Hospital.
12
Department of Respiratory and Sleep Medicine, St Vincent's University Hospital and
School of Medicine, University College Dublin, Dublin, Ireland.
13
IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
14
Department of Pulmonology, University Hospital Zurich, Zurich, Switzerland. Centre
of Competence Sleep & Health Zurich, University of Zurich, Zurich, Switzerland.

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 Address correspondence to:

Winfried Randerath Clinic of Pneumology and Allergology, Center for Sleep Medicine

and Respiratory Care, Bethanien Hospital, Solingen, Germany. Tel.: 0049/212/63-

6000; fax: 0049/212/63-6005. E-Mail: [email protected].

Take-home message

ASV has no negative cardiovascular impact, but positive effects on patient-reported

outcomes in optimally treated heart failure (HF) with preserved and reduced (30-45%)

ejection fraction.

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 Abstract

Adaptive servo-ventilation (ASV) has been considered effective in controlling various

forms of central sleep apnoea (CSA) and also any additional obstructive sleep apnoea
(OSA) component. However, after the publication of the SERVE-HF study, its use was
restricted in patients with systolic heart failure and prevalent CSA and was withheld
from many patients with symptomatic CSA. In the meantime, the devices have been
further developed and the algorithms adapted, and there is new evidence from
randomised controlled trials and observational studies that makes it necessary to re-
evaluate some societies’ statements on the use of ASV, especially in patients with
heart failure and CSA and with the current ASV devices. This short statement is based
on a review of the effect of ASV on hard cardiovascular endpoints, echocardiographic
parameters and exercise capacity as well as on sleep architecture and sleep quality,
symptoms and quality of life (QoL) in patients with CHF. The expert group concludes
that ASV has positive effects on CSA and quality of life in various forms of CSA that
current ASV devices have no negative effect on hard cardiovascular endpoints and
that ASV has positive effects on patient-reported outcomes. Moreover, it is used by TF
members after optimal treatment of the underlying disease and after an unsuccessful
CPAP trial in patients with heart failure with preserved ejection fraction, but also in
patients with LVEF 30-45%. In the latter group, however, initiation is performed in
expert centres only. In severe systolic heart failure, ASV is sometimes evaluated in a
palliative therapy concept for severely symptomatic patients with CSA.

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 Introduction

The presence of heart failure (HF) poses a significant public health burden [1]. Up to
60% of patients with HF experience sleep-disordered breathing (SDB), including
obstructive and central sleep apnoea (OSA, CSA), co-existing OSA and CSA and
Cheyne-Stokes respiration (CSR) [2-6]. Adaptive servo-ventilation (ASV) has proven
to be the most effective treatment for suppressing CSA and CSR [7-9]. It is superior to
medical therapy of underlying diseases alone, specific pharmaceutical therapies (e.g.,
acetazolamide), non-invasive ventilation, neural stimulation therapy and nocturnal
oxygen therapy [7-11]. Nevertheless, ASV indications and usage in patients with
predominant CSA and left ventricular ejection fraction (LVEF) ≤45% have been
restricted since the publication of the SERVE-HF (Treatment of Sleep-Disordered
Breathing with Predominant Central Sleep Apnea by Adaptive Servo Ventilation in
Patients with Heart Failure) study in 2015 [12-16]. The restrictive statements or
information of manufacturers, scientific societies, and health administrations [13-15,
17] were valid only for this clearly defined group representing less than 10% of ASV
indications in sleep clinics [18-20]. ASV therapy has not only proven to be effective in
controlling CSA/CSR in heart failure, but is also an established and effective treatment
modality for other forms of CSA, particularly treatment-emergent CSA and opiate-/
opioid-induced CSA, as well as post-stroke CSA or idiopathic CSA [21, 22]. In these
patients, ASV could continue to be used in symptomatic patients without restriction
after SERVE-HF if CPAP is not working.

Numerous scientific publications have thoroughly examined the strengths and

weaknesses of the SERVE-HF study, regarding device algorithms and settings,
adherence, and the populations investigated [23-26]. Moreover, since the publication
of SERVE-HF further research priorities were defined [27, 28] and several prospective
cohorts, randomised controlled trials (RCTs), and real-life data in HF have been made
available in the field [22, 29-44]. Most recently, the ADVENT-HF (Adaptive servo-
ventilation for sleep-disordered breathing in patients with heart failure with reduced
ejection fraction) trial, another multinational, multi-centre, prospective RCT on ASV in
heart failure with reduced ejection fraction (HFrEF) was published [28].

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 Data from RCTs are the mainstay for therapeutical algorithms. However, conclusions
derived from long-term RCTs are limited due to strict patient selection and the
exclusion of highly symptomatic patients for ethical reasons. Therefore, data from well-
performed large cohorts and registries provide indispensable and complementary
contributions to the scientific evidence [45]. There are many new data from recent
studies - including ADVENT-HF - on cardiovascular outcomes, mortality and
hospitalisation rates in these patients [33, 35, 38, 44, 46, 47], which question the
concerns of harm. Specific phenotypes of good responders to ASV have been
consistently highlighted [4, 5, 33, 46, 47]. In addition, HF phenotypes with reduced
ejection fraction (HFrEF), mildly reduced ejection fraction (HFmrEF) and preserved
ejection fraction (HFpEF) differ in prevalence of CSA and outcomes under ASV
treatment [4, 5, 33, 46, 47].

This novel evidence requires re-consideration of the previous statements on ASV in

CSA. While it is obvious that any treatment may only be used if it does no harm (primum
non nocere), decisions on treatment should consider both major outcome parameters
and patient-reported outcome measures.

A re-consideration is also of crucial relevance because of major changes in

technologies. The early studies, including SERVE-HF, used devices that applied a
minimum pressure support of three mbar and a fixed expiratory pressure (EPAP).
These devices have not been used for almost a decade and subsequent studies in
patients with HF and sleep apnoea were performed using algorithms with variable
EPAP and without minimal pressure support. It is unclear whether these or other
differences are causative for any new findings.

Methods

ERS and ESRS established a group of European experts in the fields of respiratory
sleep medicine and cardiology focussing on the evaluation and interpretation of
available studies with a special focus on the currently available ASV algorithms. The
panel reviewed the evidence for benefits and potential harms of ASV with respect to
major non-cardiac and cardiac events, cardiac surrogate parameters, quality of life,

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 and patient-reported outcomes in patients with CSA with and without heart failure. It
agreed on the following PICO question:

Is there evidence of improvement or harm regarding major cardiovascular outcomes

and/ or breathing disturbances, sleep quality, patient-reported or functional outcomes
(outcome) in adult patients with CSA (including CSR) (population) under currently
available ASV devices (intervention) compared with optimal treatment of the underlying
disease or continuous positive airway pressure (CPAP) (comparison)?

Group members carried out a literature search in Medline using the following search
strategy:
(((central sleep[Title/Abstract] OR CSA[Title/Abstract] OR central breat*[Title/Abstract]
OR Cheyne[Title/Abstract])) OR (("Sleep Apnea, Central"[Mesh]) OR "Cheyne-Stokes
Respiration"[Mesh])) AND (("adaptive serv*"[Title/Abstract] OR ASV[Title/Abstract] OR
servo-vent*[Title/Abstract] OR servovent*[Title/Abstract])).

RCTs, meta-analyses, cohort and observational studies on patients older than 18

years published in English language between 1995 (invention of ASV) and October
2024 were considered for further evaluation. Case reports, reviews, studies with less
than ten patients and studies without description of ASV type were excluded. After an
abstract and full-text screening, the task force members additionally checked the
references of the included studies to identify if there were additional studies that should
be included. The results of the search are presented in the PRISMA flow diagram
(Figure 1).

Abstract and full-text screening to identify eligible articles on the effect of ASV on one
of the outcomes defined in the PICO was performed by the panel and two authors
focused on a specific group of outcomes to extract data and summarise key findings.
These key findings, methodologies and conclusions from the relevant studies were
extracted and a summary shared with the expert panel for discussion. The statements
were developed in a multi-stage process that included literature review, data synthesis
and expert discussion of the summarised evidence between the panel members. To
reach final agreement on the statements and a shared conclusion, the expert panel
convened for a final virtual meeting during which the final statements were drafted.

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 Panellists were asked to evaluate the draft and provide final feedback on the accuracy,
clarity and relevance of each statement to ensure that the final statements reflect the
collective evaluation and interpretation of the expert panel. A patient representative
who uses ASV was part of the process from the start and the assignment was agreed
with the European Lung Foundation (ELF).

Description of the evidence

Does ASV influence major adverse cardiac events (MACEs)?

Five RCTs and an important post-hoc analysis [12, 24, 33, 35, 48, 49], 13 observational
studies [37, 38, 44, 46, 50-58] and 4 meta-analyses [47, 59-61] on the effect of ASV in
HF on MACE were included (Table 1). One study included only HFpEF [57], the two
analyses of the FACE study [46, 58] included both HFrEF and HFpEF, all other studies
included only patients with reduced systolic function (HFrEF).

Based on the evidence from RCTs and prospective observational studies following the
publication of the SERVE-HF trial [12], ASV has no effect on the occurrence of MACE
in a heterogeneous unselected group of patients with HF and sleep-disordered
breathing (SDB) [33, 35, 37, 46]. After SERVE-HF, all studies were either neutral or
even showed a benefit with regard to mortality and MACE risk. There was no evidence
or signal of increased risk of mortality or MACEs in either observational studies or
RCTs, although the findings of ADVENT-HF were underpowered for final conclusions
to assess mortality [35]. A meta-analysis of eight studies (> 2,000 patients, 3 RCTs)
also including trials from before 2015, found no significant effect of ASV on mortality,
but a reduction in MACEs under ASV compared to usual care at LVEF >33% [47]. A
Cochrane review based on RCTs only including patients with HFrEF found no
significant effect of ASV on mortality [59]. Based on the RCT data, the panel concludes
that there is no effect of ASV on MACEs or mortality, not only on the basis of more
recent studies with current devices, but also considering all pooled evidence from
RCTs.

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 Observational studies indicate improved event-free survival (death, cardiovascular
death, hospitalisation for worsening heart failure) under ASV in the subgroups of
patients with more pronounced nocturnal hypoxaemia, with longer nightly ASV usage,
with HFpEF, and with pre-dominant OSA [38, 46]. However, despite efforts to correct
for MACE-relevant confounders, the observational studies may not have considered
all potential confounders. RCTs in the population with HFpEF are missing.

Based on pooled data from RCTs, there is no evidence that ASV increases mortality
or the risk of MACEs, neither in patients with HFrEF nor in HFpEF, and particularly not
with the current ASV settings

What are the effects of ASV treatment on other outcome measures, especially cardiac
surrogate parameters, or exercise tolerance?

Five RCTs including one secondary analysis [32, 34, 62-64], ten observational studies
[41, 56, 65-72] and two meta-analyses [32, 34, 62-64] on the effect of ASV on exercise,
echocardiographic parameters and N-terminal brain natriuretic peptide (NT-pro-BNP)
were evaluated (Table 2).

In addition to mortality and major cardiac events, effects on cardiac surrogate

parameters may influence therapeutical decisions. These include arrhythmias,
echocardiographic measures, as well as functional findings such as exercise tolerance.
Starting with short-term trials of 1h, ASV showed favourable haemodynamic effects of
ASV in HF patients with CSR as revealed by increased stroke volume indices
compared to healthy volunteers [72]. ASV was compared to other SDB treatment such
as oxygen therapy, bilevel positive airway pressure (BPAP) and CPAP. Compared to
oxygen therapy, in a single night RCT, ASV reduced cardiac overload, attenuated
sympathetic nervous activity and ongoing myocardial damage effectively in 42 HFrEF
patients with SDB [64]. ASV was superior to oxygen (O2) treatment in ameliorating
brain and atrial natriuretic peptide levels. An RCT including 37 HFrEF patients with
NYHA classes II and III compared BiPAP versus ASV over six weeks. Besides better
evidence of improvement in LVEF in BiPAP users, there were no differences in terms
of blood pressure and echocardiographic parameters, such as end-diastolic diameter
and shortening fraction between the ventilation modalities [62]. In contrast, ASV was

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 superior to CPAP after three months of follow up in terms of echocardiographic
parameters and six-minute walk test (6MWT). The ASV mode showed significant
reductions in plasma NT-pro-BNP and an increase 6MWT distance [63, 68]. Left
ventricular end-systolic diameter and LVEF increased, while mitral regurgitation area
decreased in the ASV mode group compared to the CPAP-mode group [63]. ASV
significantly reduced urinary norepinephrine excretion and increased six-minute
walking distance whereas CPAP did not [68].

As compared to cardiovascular standard care alone, ASV ameliorated LVEF and

NYHA class in prospective studies on CSR-CSA [56, 65, 70]. In cardiopulmonary
exercise testing, workload increased by 5.4 watts and peak oxygen uptake (VO2) peak
improved compared to patients without ASV [65, 70]. Moreover, in association with
suppression of CSA in HF patients, ASV also improved muscle sympathetic nerve
activity and LVEF after three months [67]. While ASV and standard care both reversed
LV remodelling, only ASV treatment was able to reduce left atrial volume [34]. Toyama
et al. also showed ameliorations in cardiac sympathetic nerve activity, cardiac function,
exercise capacity, and symptoms in HF patients with CSR after six months of therapy
[32]. A study by Oldenburg and colleagues demonstrated that ASV increased the
workload during cardiopulmonary exercise testing and the VO 2 at the anaerobic
threshold and predicted peak VO 2. LVEF and NT-proBNP levels also improved in
response to ASV treatment [71].

Regarding arrhythmias, Nagasaka et al. retrospectively analysed 141 consecutive

hospitalised patients with HF due to ischaemic heart disease. 75 patients started ASV
during the hospitalisation and were compared to 66 controls with a follow-up period of
one year after dismission. At the one-year follow up, the ASV group presented fewer
arrhythmia events, including paroxysmal atrial fibrillation or ventricular tachycardia,
compared to the non-ASV group and showed improvement in estimated glomerular
filtration rate (eGFR) after adjusting for demographic and cardiovascular disease risk
factors.[69]. Piccini et al. confirmed the role of ASV in reducing atrial fibrillation burden
in 35 HF patients compared to standard care [41].

A follow up of almost one year showed that ASV therapy versus no treatment of CSA
in HFpEF patients led to a significant increase in peak V’O2, predicted peak V’O2,

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 anaerobic threshold, oxygen pulse and V’E/V’CO2. ASV also improved
echocardiographic parameters of left ventricular function (e.g. E/A, A, e' and E/e'). [73].

Two meta-analyses studied the effects of ASV on cardiac function and exercise
parameters. Sharma et al. found that the weighted mean difference in AHI and LVEF
both significantly favoured ASV. In addition, ASV improved the 6MWT distance, but
had no influence on peak oxygen uptake, minute ventilation to carbon dioxide output
(VE/ VCO2 slope), or quality of life [9]. These results were confirmed by Wu et al. in
their meta-analysis on seven studies involving 301 patients. The weighted mean
difference in AHI, LVEF, urinary noradrenaline, and exercise capacity measured by
six-minute walk distance improved under ASV as compared to control. There were no
differences in LV end-diastolic diameter and ESS [74]. Overall, ASV was more effective
than control conditions in improving SDB, cardiac function and exercise capacity [75].

Does ASV influence sleep parameters?

Three RCT [39, 63, 76], two clinical trials [77, 78] , one comparative study [31] and one
research support study [79] were included.

Data on changes of sleep macro- (sleep stages) and microstructure (arousals) under
ASV are scarce and controversial. This may be due to substantial methodological
differences related to study design, heterogeneity of populations included (e.g. HFpEF,
HFrEF, treatment emergent CSA), different pathophysiologic mechanisms,
comorbidities, sleep pattern at baseline, or follow-up period.

A pre-planned sub-study of SERVE-HF showed that the respiratory arousal index (RAI)
was significantly lower and the periodic limb movements (PLMS) and PLMS-related
arousal index were significantly higher under ASV [39]. As compared to control, ASV
showed some improvement in sleep efficiency, sleep latency and respiratory arousal
index, mainly after twelve months of treatment, but differences were not considered
clinically relevant. Moreover, the PLMS index, a predictor of all-cause and cardiac
mortality in HF patients, increased markedly in the first three months after initiation of
ASV and was significantly higher in the ASV versus control group at twelve months

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 [39]. Similarly, Xie et al. and Bradley et al. observed an increased PLMS index and
PLMS-arousal index in HF patients under ASV [35, 79].

However, early studies showed that patients with chronic HF with CSA had a significant
improvement in sleep parameters after switching from CPAP treatment to ASV [63,
80]. The same results came from a study of Teschler et al. showing that sleep quality
improved significantly under ASV as compared to other treatment modalities in patients
with HF and CSA/CSR [76]. Roder et al. performed a retrospective PSG analysis of 30
ASV-treated patients with stable HFrEF and moderate-to-severe CSA. The results
showed a reduction in non-rapid eye movement (NREM) N1 and N3 sleep stages and
an increase of N2 and REM sleep. The authors discussed that the changes in sleep
structure could be explained by the autonomic imbalance with higher sympathetic tone
in REM sleep and reduced vagal predominance in N3 sleep under ASV. In addition,
ASV was associated with a significant reduction in respiratory related arousals without
differences in PLMS arousal index. However, the study was limited by its retrospective
design and the small sample size, and several comorbidities may have influenced the
results [78]. Most recently, the ADVENT-HF trial showed that ASV significantly
improved the total number of arousals and the number of respiratory arousals, N3 and
REM sleep duration [35].

The results of Heider et al. in a cohort of 114 HFpEF patients are in line with these
improvements in sleep micro- and macro-structure. They retrospectively showed an
increase in both, N3 and REM sleep during ASV treatment [81]. A marked increase in
N3 with an increased alertness level, as quantified by Maintenance of Wakefulness
Test, has also been reported in a recent paper by Karimi et al. [77].

All these results highlight the need for a better understanding of the origin of sleep
impairment in HF patients with CSA. The diagnosis of impaired sleep at baseline and
under treatment, including arousals, PLMS, and disturbed sleep, can play a pivotal role
in better defining treatment indication and selecting therapeutical options.

What are the effects of ASV treatment in patient-reported outcomes?

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 16 RCTs [8, 12, 32, 33, 35, 62, 63, 68, 75, 82-88] and ten observational studies (six
on HFrEF, 4 HFpEF) on the effect of ASV in HF on quality of life and symptoms were
identified [22, 25, 37, 46, 50, 77, 89-92].

The major long-term randomised controlled trials ASV had no or modest effects on
symptoms and quality of life [12, 35]. Short-term studies in patients with symptomatic
CSA ASV exhibited greater effects on sleepiness and/or measure of QoL [33, 86], while
RCTs of ASV in non-sleepy patients showed no significant effects on sleepiness and
QoL [82].

In SERVE-HF, ASV did not improve general (assessed by the EuroQol Group 5-
Dimension Self-Report Questionnaire, EQ-5D), or HF-specific measures of QoL
(Minnesota Living with Heart Failure questionnaire, MLHFQ), or NYHA classification
[12]. However, ASV showed a modest improvement in ESS scores as compared to
control.

The ADVENT-HF study demonstrated improved sleepiness and HF-specific quality of

life (MLHFQ) under ASV [35]. While the improvements were modest, these persisted
over the course of the 5-year trial and were associated with improvements in NYHA
class and objective sleep structure [35, 93].

In a small cross-over study including sleepy HFrEF patients with CSA, ASV
significantly improved objective daytime sleepiness (Osler maintenance of
wakefulness test [86].

Following SERVE-HF study, the randomised controlled CAT-HF Trial [33] enrolled
hospitalised patients with HFrEF, HFmrEF and HFpEF and used an ASV device for
treatment of CSA and OSA. It revealed no significant benefits of ASV on functional
capacity, as indicated by 6-minute walk distance, NYHA functional class, ESS, and
general QoL measures (Duke Activity Status Index; EQ-5D, Patient Health
Questionnaire-9, Pittsburgh Sleep Quality Index). However, patients treated with the
ASV device had numerical improvements in HF-specific QoL (Kansas City
Cardiomyopathy Questionnaire score) compared to the control group.

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 Smaller RCTs investigating the effect of ASV on cardiac symptoms, such as angina
pectoris [75], dyspnoea and heart failure related QoL did not always show consistent
results (table 4) [8, 32, 33, 62, 68, 82, 83, 85-88].

RCTs are complemented by observational studies [22, 25, 37, 46, 50, 77, 89-92] with
more representative study populations. Two of those were large multicentre
observational studies [22, 46]. Recent findings from the READ-ASV Registry
(Treatment of Central and Complex Sleep-Disordered Breathing with Adaptive Servo-
Ventilation) [5, 22], including consecutive ASV-users (sleep clinic population, 23% with
heart failure) indicated that a twelve-months treatment with ASV for CSA, with or
without coexisting OSA, led to significant improvements in disease-specific QoL
(FOSQ) and reduced daytime sleepiness (ESS). These improvements were
particularly notable in individuals who had symptoms of SDB prior to the initiation of
therapy (62% of the population) [5, 22], whereas the results of the observational FACE
study, which included non-sleepy HF patients, indicated that two years of ASV therapy
did not result in any clinical improvement in MLHFQ and ESS scores in patients with
chronic HFrEF, HFmrEF or HFpEF and SDB [46].

Most recently published data (after the current paper was finalised) from the French
registry confirm these findings in a huge variety of CSA entities [94]. Based on the
results of literature search and a discussion and consensus process, the panel agreed
on the following statements. These statements reflect the re-assessed practice of the
experts and are not intended as a general recommendation (Figure 2).

Statements

1. ASV has clear positive effects in improving breathing disturbances and QoL in CSA/
periodic breathing in HF, treatment-emergent CSA, drug-induced CSA, CSA in
neurological or other medical disorder, and idiopathic CSA. Improvements in sleep
parameters, exercise performance, and cardiac surrogate parameters are less
consistent. Recent data on the use of ASV devices with the currently available
technique do not report any increase in mortality or MACEs.

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 2. In patients with CSA/ periodic breathing due to a cause other than HF, there is no
evidence for a negative impact of ASV on major outcome parameters. The members
of the panel treat symptomatic patients with ASV if treatment of any underlying disease
and a CPAP trial have failed. This includes patients with idiopathic CSA, drug-induced
CSA, treatment-emergent CSA, and CSA in neurological diseases or non-cardiac
medical disorders.
3. There is growing evidence of positive effects of ASV not only on polysomnographic
and functional parameters, but also on PROMs. There is evidence from observational
studies that ASV has a positive effect on MACEs in subgroups or specific phenotypes
(longer nightly ASV usage; HFpEF; pre-dominant OSA) of HF patients. In their clinical
practice, the members of the panel decide on treatment based on a comprehensive
patient evaluation including functional parameters (sleep quality; exercise tolerance)
and patient-reported outcomes after optimisation of any underlying disorder or
condition. As an initial step, they give preference to CPAP due to availability, feasibility
and cost-effectiveness.
4. In HF patients with predominant OSA, there is no evidence of a negative impact of
ASV on major outcome parameters. The members of the panel treat symptomatic
patients with ASV if treatment of any underlying disease and a CPAP trial have failed.
In HF patients with LVEF ≤45% and predominant OSA, treatment is initiated in expert
centres.
5. In HF patients with predominant CSA and an LVEF between 30 and 45%, there is
no evidence for a negative impact of ASV with current devices and settings on major
outcome parameters. The members of the panel treat symptomatic patients with ASV
if treatment of any underlying disease and a CPAP trial have failed and initiate
treatment in expert centres.
6. HF patients with predominant CSA with an LVEF <30% have a very high mortality
in general (comparable to advanced lung cancer). In a palliative care setting, despite
lacking scientific evidence, the members of the panel sometimes use ASV as a
palliative care option in highly symptomatic patients if there is no other option to reduce
symptom burden, and initiate treatment in expert centres.

Discussion

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 The panel reviewed the available literature and reassessed its current practice in the
use of ASV. The resulting approach is described in the differentiated statements on
various entities of CSA. The main focus is on CSA in HF patients, while there are no
changes in our current practice for other entities. This statement considers data on
efficacy in controlling CSA and improving its symptoms and markers of cardiac
function, as well as safety and hard cardiovascular endpoints. Data from prospective
observational studies are discussed in addition to evidence from RCTs. RCTs focus
on selected populations in RCTs and do not adequately represent different subgroups
of patients with heart failure and sleep apnoea, which per se have different prognoses
and require separate assessment (see specific statements), as well as groups that are
underrepresented in RCTs, such as HFpEF and sleepy patients.

In summary, the current evidence from RCTs and prospective observational studies
suggests that ASV is effective in controlling various forms of CSA and is superior to
CPAP in stabilizing breathing and suppressing central events, particularly in CSA/CSR,
TECSA and opiate-induced CSA. Although ASV generally improves sleep quality and
other patient reported outcomes and although today's common ASV algorithms and
settings are ideally adapted to the pathophysiology of CSA with periodic breathing and
can optimally control CSA, its use has been limited in the last ten years, at least in
HFrEF, due to safety concerns. This is now being reconsidered on the basis of new
evidence. The previous practice was mainly driven by the SERVE-HF study published
a decade ago, which has been challenged by more recent evidence, including the
ADVENT-HF. Both were prospective, multinational, parallel group RCTs in patients
with symptomatic HFrEF (LVEF ≤ 45%, AHI >15/h). SERVE-HF [12] randomised 1,325
patients with predominant central apnoeas. 1,161 patients completed the study and
were treated with optimal cardiac therapy alone or additional ASV. According to the
current technical standard at the time of the study initiation, the ASV device applied a
minimal pressure support of three mbar and a fixed expiratory pressure (EPAP). The
study documented 232 MACEs in 666 ASV group and 193 in 659 controls. While there
was no difference in the primary combined end-point (neutral results), all-cause
mortality and cardiovascular mortality were significantly higher under ASV. A multistate
modelling analysis showed that the mortality risk was increased in patients with LVEF
≤ 30% and in those without previous hospital admission [24].

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 ADVENT-HF included not only HF patients with predominant CSA, but also non-sleepy
HF patients with predominant OSA. The ADVENT-HF population included less patients
in NYHA stages III and IV, but the mean LVEF was similarly and severely reduced in
both studies. All sleep studies of the ADVENT-HF were evaluated in a core laboratory
to avoid misdiagnoses and heterogeneity of scoring. As the study was discontinued
prematurely due to the Philips device recall and the SARS-CoV-2 pandemic with 731
subjects been randomised, it was statistically underpowered, in particular to definitely
address safety issues. There was no significant difference in the pre-defined end-
points, although the Hazard Ratio (HR) for mortality was in favour of ASV, at the level
as pre-calculated (HR 0.78). In contrast to SERVE-HF, ADVENT-HF did not provide
any evidence that ASV may cause harm, but the early termination did not allow a robust
safety analysis. ASV improved the Epworth Sleepiness Scale (ESS) score and sleep
parameters [35] in comparison to standard care. The reason for the increased mortality
in SERVE-HF is not clear. It is possible that differences in the study populations
between SERVE-HF and ADVENT-HF have influenced the different findings. As
mentioned above, the ASV algorithm and settings used in SERVE-HF differed from the
more recent studies, including ADVENT-HF. While the historical algorithms applied
unavoidable pressure support and invariable EPAP, the current technology allows for
zero pressure support during hyperventilation and varies the EPAP allowing for
minimal pressure application. However, the relevance of this technical difference is
unclear.

In addition, we have learned from prospective observational studies with a broader,

less selected patient population that phenotyping is crucial for long-term outcome
independent of sleep apnoea therapy and that there are indeed phenotypes of HF
patients with sleep apnoea that may even benefit in terms of MACE [46]. However,
these subgroups have not been included in the large RCTs and there are no RCTs
specifically in HFpEF. Adherence to ASV, which is different in different subgroups,
must also be taken into account for the treatment effect and is often higher in
observational studies than in RCTs. Thus, a differentiated view of different groups with
CSA is indicated as reflected in the statements.

Recognising the potential risks of any intervention in certain subgroups, particularly

those with severe systolic heart failure and poor autonomic regulation, the panel uses

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 ASV, like any other treatment for sleep-disordered breathing in potentially vulnerable
subgroups only in experienced centres with good monitoring (e.g. attended in-
laboratory sleep study). This includes the need to consider both long-term outcome
measures and PROMs when making treatment decisions, as they contribute
significantly to the assessment of treatment efficacy.

Previous studies on ASV were not designed to study the effects or true effect size on
PROMs, since the vast majority of patients are asymptomatic or oligosymptomatic [12,
35]. Sleepiness and impaired sleep-apnoea related QoL have been identified as
important predictors for clinically relevant effects of ASV on sleepiness and disease
specific QoL [22]. Although the available studies did not consistently show
improvements in PROMs, the potential positive effects on symptoms and quality of life
are promising and symptoms and treatment goals should be considered in relation to
PROMs. It is therefore important for the future that cardiologists treating patients with
heart failure refer patients with symptomatic sleep apnoea to experienced sleep
centres for an assessment of the type of sleep apnoea and phenotyping, and for a
treatment recommendation that considers all the listed outcomes.

Conclusions

The available evidence suggests that ASV improves breathing disturbances and QoL
in the various entities of CSA without any increase in mortality or MACEs. It may have
positive effect on MACEs in subgroups or specific phenotypes of HF patients.
Therefore, if treatment of any underlying disease and a CPAP trial have failed, the
members of the panel use ASV for the treatment of symptomatic patients with
idiopathic CSA, drug-induced CSA, treatment-emergent CSA, CSA in neurological
diseases, CSA in non-cardiac medical disorders, and in HF patients with predominant
OSA. In HF with predominant CSA with LVEF ≥ 30 % the panel initiates ASV treatment
in expert centres. Close cooperation between the cardiologists treating patients with
heart failure and the respiratory sleep specialists as ASV experts is of crucial
importance. The literature appraisal done for this statement suggests the need and
feasibility of formal evidence syntheses to support a clinical practice guideline on the
topic.

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 Figure 1: PRISMA diagram

Identification of studies via databases and registries

Identification

Records identified from PubMed

(n = 338)

Records identified from

references (n = 25)

Records excluded (n = 232)

Not in English (n = 25)
Records screened (n= 363) Age <19 (n = 173)
Review (n = 8)
Case report / series (n = 26)

Reports sought for retrieval

(n = 131) Reports not retrieved (n = 0)
Screening

Reports assessed for eligibility Reports excluded (n = 69):

(n = 131) Review/Statements (n = 5)
Protocol (n = 4)
Case report / series (n = 12)
Sub-study in same population (n = 2)
Various entities/ OSA/ no HF (n = 28)
Diagnostics (n = 4)
Not ASV (n = 4)
Not English (n = 4)
Others (n = 6)
Included

Studies included in review

(n = 62)

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 Figure 2
The figure describes the current practice of how the members of the Task Force treat
patients with central sleep apnoea and is not intended as a general recommendation.

CSA

OSA ≥50%, CSA ≥50%,

CSA <50% OSA <50%

Idiopathic CSA
CSA with LVEF CSA with LVEF CSA with Drug-induced CSA,
CPAP
>45% 30-45% LVEF< 30% Treatment-emergent CSA
CSA in medical/ neurological
disorders
Optimal Optimal Optimal
ASV cardiac cardiac cardiac Optimal
treatment treatment treatment treatment of
underlying
disease
Palliative care,
CPAP CPAP including CPAP,
oxygen, ASV, initiate CPAP
in experienced centres

ASV, initiate in
ASV experienced
centres ASV

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 European Respiratory Society and European Sleep Research Society Statement
on the treatment of central sleep apnoea with adaptive servo-ventilation:
Supplemental Tables

Winfried J. Randerath1, Sophia E. Schiza2, Michael Arzt 3, Maria Rosaria Bonsignore4 ,

Raphael Heinzer5, Carolina Lombardi6,7, Robert Lyssens8, Gianfranco Parati6,7,
Thomas Penzel9, Jean Louis Pepin10, Dirk Pevernagie11, Silke Ryan12, Luca
Vignatelli13, Esther I. Schwarz14

1
Bethanien Hospital, Clinic of Pneumology and Allergology, Center for Sleep
Medicine and Respiratory Care, Institute of Pneumology at the University of Cologne,
Solingen, Germany.
2
Sleep Disorders Unit, Dept of Respiratory Medicine, School of Medicine, University
of Crete, Greece.
3
Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
Germany.
4
Institute of Translational Pharmacology (IFT), Palermo branch, National Research
Council (CNR), Palermo, Italy
5
Centre d'investigation et de recherche sur le sommeil, Centre hospitalier
universitaire vaudois, 1011 Lausanne.
6
Istituto Auxologico Italiano IRCCS, Milan, Italy;
7
Department of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy.
8
European Lung Foundation (ELF), Sheffield, United Kingdom
9
Center of Sleep Medicine, University Hospital Charité Berlin, Berlin, Germany.
10
Univ. Grenoble Alpes, HP2 Laboratory, Inserm U1300, Grenoble
11
Faculty of Medicine and Health Sciences, Ghent University, Department of
Pulmonary Medicine, Ghent University Hospital.
12
Department of Respiratory and Sleep Medicine, St Vincent's University Hospital
and School of Medicine, University College Dublin, Dublin, Ireland.
13
IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
14
Department of Pulmonology, University Hospital Zurich, Zurich, Switzerland.
Centre of Competence Sleep & Health Zurich, University of Zurich, Zurich,
Switzerland.

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 Table 1: MACEs

Year Year, Author Study type, population Intervention Follow-up Summary of outcome ASV type and Interpretation
and size group(s) time setting range

2011 Yoshihisa • Prospective • ASV 6 months • Event free rate higher • ASVpf Positive
[1] comparison • non-ASV in ASV group • EPAP titration, • cardiovascular
• HF, NYHA ≥ II - CSR set minimum and outcome
• n = 60 maximum IPAP
2012 Takama [2] • Prospective • ASV ≥ 12 months • Higher survival rate • ASVmv Positive
observation 4h/night and fewer • EPAP 4-cmH2O, • Mortality
• CHF NYHA II-IV - • ASV < cardiovascular events IPAP 3–8 cmH2O • Cardiovascular
SDB 4h/night in good adherence outcome
• n = 85 group (>4h)
2012 Miyata [3] • RCT • ASV 12 months • Event-free rate higher • ASVpf Positive
• HF with cardiac • Standard in ASV (driven by • cardiac function
resynchronisation care hospitalisations) • cardiac events
therapy,
predominant CSA
• n = 22

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 2013 Yoshihisa • Observational • ASV 18 months • Event-free rate • ASVmv Positive
[4] • LVEF > 50% • Standard significantly higher in • EPAP 5-8 • cardiac diastolic
• n = 36 care the ASV group cmH2O, pressure function
support 3-10 • event-free rate
cmH2O Neutral
• LVEF
2013 Owada [5] • Observational • ASV 6 months • Event-free rate • ASVmv Positive
• HF, SDB • non-ASV significantly higher in • EPAP 4-8 • cardiac function
• n = 80 the ASV group cmH2O, pressure • event-free rate
support 3-10
cmH2O
2014 Takama [6] • Prospective • ASV in LVEF 6 months • Improvement in LVEF • ASVmv Positive
comparison < 30%; n = • Reduction in BNP • EPAP 4 cmH2O, • cardiac function
• CHF - OSA/CSA 42 • No difference in PS 3–8 cmH2O Neutral
• n = 76 • LVEF ≥ 30%; survival/hospitalization • cardiovascular
n = 34 outcome
2014 Suzuki [7] • Prospective • ASV 6 months • Cardiac event-free • ASVpf Positive
observational • non-ASV rate significantly • cardiac event-
• HF, SDB higher in ASV in free rate
• n = 139 anaemia, no
difference in ASV vs
no ASV without
anaemia

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 2015 Cowie • RCT • ASV Median • No significant • ASVmv Negative
SERVE-HF • HFrEF, NYHA class • OMT follow-up difference in time to • EPAP 5 mbar, • Mortality
[8] III or IV - CSA 31 months hospitalisation/ life- IPS 3 -10 cmH2O • Exercise
• n = 1325 saving cardiovascular capacity (6MWD)
intervention, Neutral
worsening CHF or • cardiovascular
time to death, change outcome
in NYHA class, 6MWD • dyspnoea
(NYHA and
6MWD)
• QoL (EQ5D,
MLHF)
Positive
• sleep
parameters
• sleepiness (ESS)
2015 Momomura • RCT • ASV 6 months • No significant • ASVmv Neutral
[9] • CHF - SDB (AHI • OMT difference in • Settings not • cardiac function
≥15/h) improvement in LVF disclosed
• n = 213 and BNP
2016 Imamura • Retrospective • ASV 24 months • All-cause mortality Positive
[10] • Advanced HF • Non-ASV and cardiac death rate • mortality
• n = 85 significantly lower in • cardiac death
ASV • cardiac function

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 2016 Hetzenecker • Comparative study • ASV • Not • Changes on AHI, • ASV Positive
A et al. [11] • CHF patients with defined. arousal index and • Setting not Reduction of AHI ,
• CPAP
last night sleep stages specified stage N1 and
central sleep
of PAP Arousal index
apnoea (CSA) Increase of REM
therapy
CPAP-non- sleep
(CPAP or
responders
ASV)
before the
patient
was
discharged
2017 O’Connor • RCT • ASV 6 months • Significantly greater • ASVmv Positive
CAT-HF [12] • Hospitalised • OMT reduction in AHI under • Setting not • Sleep
unselected CHF - ASV specified parameters
SDB • No improvement in 6- Neutral
• n = 126 month, disease • cardiovascular
specific QOL, outcome
sleepiness and • disease specific
cardiovascular QOL (PSQI) and
outcomes sleepiness (ESS)

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 2017 Hetland [13] • Retrospective • ASV 18 months • No difference in • ASVmv Neutral
• HFrEF, CSA > 25% • Non-ASV exercise capacity, cv • EPAP 5 cmH2O, • Death
• n = 75 death; trend toward pressure support • dyspnoea
better outcome 3-10 cmH2O (NYHA functional
regarding class)
cardiovascular event- Positive
free survival in ASV • QoL (MLHF)
• Improvement of heart
failure related QoL
2018 Oldenburg • Prospective • ASV 79 months • ASV had no • ASVmv Positive
[14] • HFrEF, predominant • OMT statistically significant • Pressure support • Symptoms
CSA effect on survival 3-10 cmH2O (NYHA
• n = 550 functional
class)
Neutral
• Survival
• LVEF
• Exercise
capacity

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 2022 Tamisier • Prospective • ASV 3 months • 3-month rate of • ASVmv
[15] • HFrEF and HFpEF primary outcome
• AHI > 15/h events was
significantly higher in
cluster 1 (men with
low LVEF and CSA
and low ASV
adherence)
2023 Sun [16] • Retrospective cohort • ASV pf n =77 Median 64 • No increase in • ASVmv and Neutral
• HFrEF-CSA • ASV mv n months mortality ASVpf • mortality
• n = 90 =13 • Trend towards • EPAP 4-14
negative correlation cmH2O, IPS 0.5–
between ASV mv with 12
fixed EPAP and
survival
2023 Kida [17] • Retrospective follow- • ASV 12 months • Significant reduction • Details Positive
up of hospitalisation for unavailable • morbidity
• HFpEF - SDB HF in 12 months after
• n = 36 ASV initiation
compared to before
initiation

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 2023 Tamisier • Prospective, • ASV 2 years • More than half of all • ASVmf Positive
[18] observational cohort • OMT patients benefitted • Min EPAP 4-5 • mortality
FACE study with ASV cmH2O, min IPS • cardiovascular
• CHF with CSA or • Benefit was 3 cmH2O outcome
TECSA dependent on LCA Neutral
• n = 324 cluster • quality of life and
• Sleepiness (ESS) and symptoms
quality of life (MLHFQ) (FOSQ and ESS)
were comparable
between the ASV and
non-ASV groups
among follow-up in
the subset of patients
in those these data
were reported

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 2024 Bradley • RCT • ASV pf 5 years • No significant • ASVpf Neutral
ADVENT- • HFrEF - CSA/OSA • OMT difference in time to • EPAP min 4 • Mortality
HF [19] • n = 731 death or cmH2O, min IPS • cardiovascular
hospitalisation for 0 cmH2O outcome
cardiovascular events, Positive
new onset AF/AFL or • Sleep
ICD shock fragmentation
• Significant and sleep
improvements in sleep structure
structure and • Quality of life and
reduction of sleep symptoms
fragmentation (MLHF, NYHA
• Significant functional class
improvement of heart and ESS)
failure related QoL,
exercise capacity
(NYHA functional
class) and sleepiness
(ESS)

18 original studies investigating the effect of adaptive servo-ventilation and major adverse cardiovascular events. The four meta-analyses
on the topic are not listed here. 6MWD: 6-minute walk distance, AHI: apnoea-hypopnoea-index, ASV: adaptive servo-ventilation, CHF:
chronic heart failure, CSA: central sleep apnoea, EPAP: expiratory positive airway pressure, EQ5D: European Quality of Life 5
Dimensions 5 Level Version, ESS: Epworth Sleepiness Scale, FOSQ: function outcomes sleep questionnaire, HF: heart failure, HFpEF:
heart failure with preserved ejection fraction, HFrEF: heart failure with reduced ejection fraction, ICD: implanted cardioverter defibrillator,

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 IPS: inspiratory pressure support, LVEF: left ventricular ejection fraction, MLHF: Minnesota Living with Heart Failure Questionnaire,
NYHA: New York Heart Association, OMT: optimal medical treatment, OSA: obstructive sleep apnoea, PS: pressure support, PSQI:
Pittsburgh Sleep Quality Index, QoL: quality of life, RCT: randomised controlled trial, SDB: sleep-disordered breathing, TECSA:
treatment-emergent central sleep apnoea

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 Table 2: Other cardiac parameters

Year Author Study type, population Intervention Follow-up Summary of outcome ASV type and setting Interpretation
and size group(s) time

2008 Oldenburg [20] • Prospective • ASV versus 5.7 months • Workload during AutoSet™ CS2 Positive
• HFrEF with CSR no ASV CPX testing EPAP 4–5 cmH2O, ASV improve
• N=29 increased oxygen inspiratory positive SDB, CPX test
uptake (VO2) at the airway pressure results, LV-EF and
anaerobic threshold (IPAP): minimum 3 NT-proBNP
and predicted peak cm H2O, maximum 8– concentrations.
VO2 . LV-EF 10 cm H2O.
increased and NT-
proBNP levels
decreased.
2008 Fietze [21] • RCT • ASV 6 weeks • Significant reduction AutoSetCS Neutral
• HFrEF (NYHA II-III) • BPAP in AHI in ASV and EPAP 4 - 10 cm H2O, • sleep
• n = 37 BPAP delta EPAP/IPAP 7 - parameters
9 cm H2O • symptoms

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 2010 Bitter [22] • Prospective • ASV versus 11 +- 3 positive effects on AutoSet™ CS2 Positive
• HFpEF with CSR-CSA no therapy months absolute and EPAP 4–5 cm H2O, ASV effectively
• N=60 predicted peak inspiratory positive attenuates CSR
oxygen airway pressure and improves
consumption, (IPAP): minimum 3 heart failure
oxygen consumption cm H2O, maximum 8– symptoms and
at the individual 10 cm H2O. cardiac function
aerobic–anaerobic
threshold, oxygen
pulse, and left atrial
size, and transmitral
flow patterns
2010 Kasai [23] • RCT ASV versus 3 months • The improvements in Flow triggered ASV Positive
• HFrEF with CSR-CSA CPAP quality-of-life and left with HEART PAP ASV more
and OSA ventricular ejection Philips Repironics efficacious than
• N=31 fraction were greater Manual titration CPAP
in the ASV group EPAP 4-10 cm H2O)
to eliminate
OSA, IPAP min =
EPAP IPAP max 1=
EPAP min +10 cm
H2O

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 2011 Yoshihisa [1] • Prospective • ASV 6 months • Event free rate ASV with HEART Positive
comparison • non-ASV higher in ASV group PAP Philips • cardiovascular
• HF, NYHA ≥ II Repironics outcome
• n = 60 Manual titration
EPAP) to eliminate
OSA, and then set
minimum and
maximum inspiratory
positive
airway pressures
(IPAP)

2011 Oldenburg [24] • Prospective • ASV 3-6 months • SDB, NYHA class, AutoSetTM CS2 Positive
comparison • Control LVEF, 6MWD, NT- (REsMED) • respiratory and
• CHF, NYHA ≥ II proBNP and EPAP) 4–5 cm H2O, functional
• n = 115 exercise test (IPAP), minimum 3 indices
improved cm H2O, maximum 8–
significantly under 10 cm H2O.
ASV

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 2012 Joho [25] • Prospective • ASV versus 3 months • Ejection fraction and ASV (AutoSet-CS; Positive
comparative study no ASV MSNA ResMed, EPAP 4 cm ASV decreases
• Hf and CSA • Changes in AHI and H2O, IPAP of 3–8 cm MSNA and
• N = 32 the average use of H2O. improves cardiac
ASV were function in
independent association with
predictors of suppression of
changes in ejection CSA in patients
fraction (both P < with HF.
.01).
2012 Yoshihisa [26] • RCT • ASV versus 1 night • Both O2 and ASV ASV (VPAP Adapt Positive
• HFrEF and SDB (CSa O2 reduced the AHI, SV/Auto Set CS, ASV reduces
and OSA) CAI, arousal index, ResMed, Sydney, cardiac overload,
• N = 42 mean heart rate NSW, Australia). attenuates
during sleep, and the Manually titrated: sympathetic
levels of EPAP 4-9 cm H2O, nervous activity
noradrenalin urinary PSmin 3-5, PS max and ongoing
catecholamines, and 6-12 cm H2O. myocardial
high-sensitivity damage
troponin T.
• Only ASV, not O2,
decreased the levels
of ANP and BNP.

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 2013 Kasai [27] • RCT • ASV versus 3 months • ASV ameliorate AHI, ASV device (HEART Positive
• HF with CSA CPAP LVEF PAP, Respironics,
• N = 23 Murrysville, ASV superior than
Pennsylvania). EPAP CPAP in HF
manually titrated PS patients with CSA
0-2 cm H2O, max that do not
IPAP 10 cm H2O, respond to CPAP
backup rate automatic
or >10bpm
2013 Bitter [28] • Prospective • ASV versus 21 +- 15 • Event-free survival AutoSet™ CS2 Positive
observational refused months from (a) appropriate EPAP 4–5 cm H2O, decrease of
• HF with ICD and CSR- therapy cardioverter- inspiratory positive appropriate
CSA defibrillator therapies airway pressure defibrillator
• N = 195 and (b) appropriately (IPAP): minimum 3 therapies by ASV
monitored ventricular cm H2O maximum 8– treated CSR in
arrhythmias was 10 cm H2O. patients with CHF
shorter in the and ICD.
untreated group
2015 Spiesshofer [29] • Prospective study • ASV in HF 1h • Stroke volume index ASV (Pace-wave; Positive
• HF CSR-CSA versus increased. ResMed maximum favourable
• N=27 volunteers EPAP and IPAP of 15 haemodynamic
cm H2O and 30 cm effects of ASV
H2O.

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 2017 Toyama [30] • RCT • ASV versus 6 months • Nuclear imaginings, ASV device (HEART Positive
• HFrEF and CSR-CSA non ASV exercise capacity, PAP, Respironics, ASV ameliorated
• N=31 delayed Murrysville, AHI, TDS, H/M on
heart/mediastinum Pennsylvania). EPAP 123I-MIBG
activity ratio (H/M), manually titrated 4-10 imaging, changes
delayed total defect PS 0-2 cm H2O, max of LVEF and
score (TDS), and IPAP 10 cm H2O, NYHA class
washout rate (WR). backup rate automatic
or >10 bpm
2018 Piccini [31] • CHF with • ASV vs. 6 months • 39% absolute • ASVmv Positive
pacemaker/defibrillator standard reduction in AF • Setting not Cardiovascular
- SDB care burden specified parameter
• n = 35
2018 Daubert [32] • RCT • ASV 6 months • Reverse LV • ASVmv Positive
• HF versus remodeling in both • Setting not cardiac function
• n = 126 standard care groups specified
• Reduced LA volume
under ASV
2021 Nagasaka [33] • Prospective • ASV versus 12 months • Incidence of ASV (AutoSet-CS; Positive
• Ischemic HF no ASV arrhythmias, ResMed, EPAP 4 cm Reduced
• N=141 including paroxysmal H2O, IPAP of 3–8 cm arrhythmia and
atrial fibrillation H2O. increased eGFR
(PAF) and
ventricular
tachycardia (VT),

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 The table presents the results of randomised controlled or observational trials with a number of participants ≥ 20 and a follow-up period > 6 weeks.

RCT = randomised-controlled trial, HFrEF = heart failure with reduced ejection fraction, ASV = adaptive servoventilation, BPAP = bilevel positive
airway pressure, HF = heart failure, eGFR = estimated glomerular filtration rate, LVEF = left ventricular ejection fraction, LVF = left ventricular
function, SDB = sleep-disordered breathing, OSA = obstructive sleep apnoea, OMT = optimal medical therapy, T90 = time spent under 90% oxygen
saturation, CAI = central apnoea index, OAI = obstructive apnoea index, 6MWD = 6 minute walk distance, AF/AFL = atrial fibrillation/atrial flutter,
ICD = implanted cardioverter-defibrillator, T90 = time spent at <90% oxygen saturation, FOSQ = functional outcome of sleep questionnaire, ESS =
Epworth sleepiness scale

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 Table 3: Sleep parameters

Year Author Study type, population Intervention Follow-up time Summary of outcome ASV type and setting Interpretation
and size group(s)

2001 Teschler [34] • Clinical Trial • ASV vs Baseline vs one • Changes of on sleep The adaptive servo- Large increases
• HF patients other night of and breathing after ventilator (AutoSet CS; in slow-wave and
• N: 40 treatment CSA treatments treatment ResMed, Sydney, rapid eye
(CPAP, Australia) movement (REM)
nasal provides a baseline sleep with ASV
oxygen) degree of ventilatory but
support (pressure not with oxygen
swing or CPAP.
4 mbar) superimposed
on 5 mbar CPAP. End-
inspiratory pressure
is 9 mbar and mean
pressure is
approximately 7 mbar.

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 2010 Kasai [23] • RCT ASV versus 3 months • The improvements in Flow triggered ASV Positive
• HFrEF with CSR-CSA CPAP quality-of-life and left with HEART PAP ASV more
and OSA ventricular ejection Philips Repironics efficaious than
• N=31 fraction were greater Manual titration CPAP
in the ASV group EPAP 4-10 mbar to
eliminate
OSA, IPAP min =
EPAP IPAP max 1=
EPAP min +10 mbar.
2016 Hetzenecker • Comparative study • ASV 12 weeks • ASV significantly (ASV, BiPAP-ASV, Positive
[35] • CHF – CSA/OSA • OMT reduced sleep Philips Respironics) • sleep
• n = 63 fragmentation EPAP 4-10 mbar parameter
IPS 1-10 mbar

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 2019 Roder [36] • Clinical Study • ASV in Follow-up was • Changes in sleep ASV ResMed AutoSet • Disturbances
• 30 pts with stable HF 109 ± 32 days architecture during CS/2 in 27 patients, of sympatho-
HFrEF and CSA ASV treatment in and ResMed AutoSet vagal balance
HFrEF patients CS PaceWave in 3 during ASV
patients. Average might help
minimal EPAP was 6 explain
mbar, minimal increased
inspiratory pressure mortality during
support was 3 mbar ASV.
and maximal pressure
support was 12 mbar.

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 2019 Xie [37] • Research report • ASV Baseline and ASV • PLMS in CSA ASV titration, minimum Although
• N: 314 titration patients without EPAP was 4 or 5 treatment with
comorbid HF mbar; PS started at 3 ASV reduces
• PLMS changes mbar was increased to breathing events,
during treatment of achieve optimal a paradoxical
CSA by ASV. ventilation increase in PLMS
is observed in HF
patients,
more pronounced
among elderly
subjects and
subjects with low
LVEF.
2022 Tamisier [38] • Retrospective sub- • ASV Baseline, 3- and • Better sleep efficiency Auto Set CS, ResMed, Neutral
analysis of SERVE-HF • OMT 12-months and lower respiratory Setting as COWIE • sleep
• CHF arousal index in ASV 2015 parameters
• n = 312 group • cardiac
• Increased PLMS function
arousal index in ASV
• No change in LVEF

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 2023 Karimi [39] • Clinical trial • ASV Baseline, 1 and 6 • Changes of sleep The device pressure ASV treatment in
• HF with PB months of follow- quality, range was 5 - 30 CHF patients
• N: 8 up neurocognition and mbar. The expiratory with CSR may
daytime performance pressure automatically improve sleep
after ASV treatment adjusts up and quality,
in HF patients. down within the neurocognition
available range (5 and daytime
mbar to 15 mbar). The performance
maximum inspiratory
support level is up to
30 mbar minus the
expiratory pressure.

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 Table 4: Patient-reported outcome measure (PROMs)

Year Author Study type, population and Intervention Follow-up time Summary of outcome ASV type and setting Interpretation
size group(s) range

2002 Pepperell • RCT • ASV 1 month Active ASV reduced • ASVmv Positive
[40] • HFrEF CSA-CSR • Subthera excessive daytime • EPAP 5 cmH2O • Sleep
• 30 peutic sleepiness (Osler test). • IPS 3-10 cmH2O parameters
ASV On active ASV, • Sleepiness
(Control) significant falls occurred (OSLER test)
in plasma brain • Cardiac
natriuretic peptide and function (BNP)
urinary metadrenaline
excretion.

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 2006 Philippe • RCT • ASV 6 months ASV and CPAP • ASVmv Positive
[41] • HFrEF CSA-CSR • CPAP decreased the AHI, only • EPAP 5 cmH2O • Sleep
• n = 25 ASV completely • IPS 3-10 cmH2O parameters
corrected CSA-CSR. At • Disease
six months compliance specific QoL
with CPAP was (MLHF)
significantly less than • Cardiac
with ASV. At six months, function (LVEF)
the improvement in QoL
was higher with ASV and Neutral
only ASV induced a • Sleepiness
significant increase in (ESS, MWT)
LVEF.
2007 Fietze [21] • RCT • ASV 1.5 months • Significant reduction in • ASVmv Neutral
• HFrEF (NYHA II-III) - • BPAP AHI in ASV and BPAP • EPAP 4 cmH2O • sleep
CSR • IPS 4-10 cmH2O parameters
• n = 37 • sleepiness
(ESS)

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 2008 Hastings • Prospective • ASV 6 months ASV significantly • ASVmv Positive
[42] observational • OMT reduced AHI and LVEF • EPAP 5 cmH2O, • Sleep
• HFrEF with SDB was increased • IPS 3 - 10 cmH2O parameters
• N=19 but not BNP. The • Sleepiness
energy/vitality score of (ESS)
the SF-36 QoL • General QoL
questionnaire was also (SF-36)
improved at 6 months. • Exercise
capacity
(6MWD)
• Cardiac
function (LVEF)

Neutral
• Disease
specific QoL
(MLHF)
• Cardiac
function (BNP)
• Exercise
capacity
(VO2max)

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 2009 Kasai [23] • RCT • ASv 3 months ASV more effectively • ASVpf Positive
• HFrEF/HFmrEF with • CPAP suppressed respiratory • EPAP 4-10 cmH2O, • Sleep
coexisiting OSA-CSA events.Compliance was • IPS 2-10 cmH2O parameters
• N=31 significantly greater with • General QoL
ASV than with CPAP. (SF-36)
The improvements in • Exercise
QoL and LVEF were capacity
greater in the ASV. (6MWD)
There was a similar • Cardiac
reduction of sleepiness function (BNP,
in the ASV and CPAP LVEF)
groups.

Neutral
• Sleepiness
(ESS)

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 2011 Su [43] • Prospective • ASV 0.25 months • ASV improved AHI, • Positive
observational • APAP central AI and • Sleep
• Severe OSA, residual sleepiness (ESS) parameters
sleepiness on APAP, • Sleepiness
residual sleepiness, no (ESS)
heart disese
• N=42
2011 Carnevale • Retrospective • ASV 36 months • ASV users had a • ASVmv Positive
[44] observational users significant reduction in • Mean EPAP 6 ± 1 • Sleep
• CSA due to heart • ASV non AHI, sleepiness and mbar parameters
failure, neurologic users dyspnoea • IPS 3 -10 cmH2O • Sleepiness
disease or idiopathic (ESS)
CSA • Dyspnoea
• N=74 (NYHA)

2012 Campbell • Cross-over RCT • ASV 8 weeks on each • No change of LVEF, • ASVmv Neutral: LVEF,
[84] • CSA due to HFrEF • Oxygen treatment, NT-BNP, urinary • IPS 3 -10 cmH2O NT-pro-BNP,
• N=10 2l/min 3 weeks wash-out catecholamines, urinary
shuttle walk distance catecholamines,
and symptoms by shuttle walk
either therapy distance and
symptoms

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 2013 Arzt [45] • RCT • ASV 3 months • More significant • ASVpf Positive
• HF - SDB • OMT reduction in AHI and • EPAP titration, • Sleep
• n = 72 NT-proBNP with ASV IPAP max 10 parameters
• Similar change in cmH2O above Neutral
LVEF EPAP • Cardiac
• Similar change in function
symptoms and QoL • Sleepiness
(ESS)
• Fatigue (FSS)
• General and
disease
specific QoL
(SF-36, MLHF)
2013 Hetland • RCT • ASV 3 months • ASV treatment • ASVmv Positive
[85] • HFrEF • OMT improved LVEF and • expiratory pressure • LVEF and
• CSA physical capacity (6- 5 cm H2O, • physical
• N = 51 MWT and NYHA- • inspiratory pressure capacity (6-
class) support between 3 MWT and
and 10 cm H2O NYHA class)
• backup respiratory
rate of 15 breaths
per minutes)

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 2014 Morgenth • RCT • ASV 3 months • AHI < 10 at 90 days in • ASVmv Positive vs.
aler [46] • TE-CSA • CPAP 89.7% versus 64.5% • ASV titrated CPAP
• n = 66 of participants treated according to a • PSG
with ASV and CPAP standardised parameters
• changes in ESS and protocol
Sleep Apnea Quality of Neutral vs. CPAP
Life Index were not • Sleepiness
significantly different (ESS)
between ASV and • Disease
CPAP groups specific QoL
(SAQLI)

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 2014 Galetke • RCT – cross-over • ASV 1 months • LVEF • ASV (Anticyclic Positive
[47] • N=39 • CPAP was increased modulated • sleep
• Cardiac disease and • No significantly only with ventilation, parameters
coexisting OSA-CSA treatment ASVC. Weinmann • cardiac function
Subjective sleepiness Hamburg)
significantly improved • EPAP 6.2 cmH20 Neutral
only with CPAP • EEPAP 8.9 cmH20 • sleepiness
whereas objective • EPAP 10.1 cmH20 (ESS)
sleep quality and
treatment adherence
were not
different between both
treatment modalities.
2014 Brill [48] • Observational • ASV 6 months • Significant • ASVmv Positive
• Stroke, LVEF>50% improvement in AHI • EPAP 5 cmH2O, • Sleepiness
• CSA and sleepiness IPS 3 - 10 cmH2O (ESS)
• N=15 (ESS)with ASV

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 2015 Cowie [8] • RCT • ASV Median follow-up • No significant • ASVmv Negative
• HFrEF, NYHA class III • OMT 31 months difference in time to • EPAP 5 mbar, IPS • Mortality
or IV - CSA hospitalisation/ life- 3 -10 cmH2O • Exersice
• n = 1325 saving cardiovascular capacity
intervention, (6MWD)
worsening CHF or time Neutral
to death, change in • cardiovascular
NYHA class, 6MWD outcome
• dyspnoea
(NYHA and
6MWD)
• QoL (EQ5D,
MLHF)
Positive
• sleep
parameters
• sleepiness
(ESS)
2015 Javaheri • Prospective • ASV 3 months • ASV significantly • ASVpf Positive
[49] • Observational improved sleepiness • Sleepiness
• CSA (ESS)
• N=26

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 2017 Olseng • RCT • ASV 3 months • ASV improved QoL • NA Positive
[50] • HFrEF -CSA • Non-ASV both in a per protocol • QoL (MLHF)
• N=30 analysis and in an
intention to treat
analysis.
2017 Toyama • RCT • ASV 6 months • Significant reduction in • ASVmv Positive
[30] • HFrEF - CSA • OMT AHI, changes of LVEF • EPAP 4-mbar, IPS • sleep
• n = 31 and NYHA class 3–8 cmH2O parameters
• cardiac function
• dyspnoea
(NYHA)
2017 O’Connor • RCT • ASV 6 months • Significantly greater • ASVmv Positive
[12] • Hospitalised unselected • OMT reduction in AHI under • Setting not • Sleep
CHF - SDB ASV specified parameters
• n = 126 • No improvement in 6- Neutral
month, disease • cardiovascular
specific QOL, outcome
sleepiness and • disease
cardiovascular specific QOL
outcomes (PSQI) and
sleepiness
(ESS)

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 2017 Hetland • retrospective • ASV 18 months • No difference in • ASVmv Neutral
[13] • HFrEF, CSA > 25% • Non-ASV exersice capacity, cv • EPAP 5 cmH2O, • death
• n = 75 death; trend toward pressure support 3- • dypnoea
10 cmH2O (NYHA
better outcome
functional
regarding
class)
cardiovascular
Positive
event-free survival in
• QoL (MLHF)
ASV
• Improvement of
heart failure related
QoL
2018 Oldenburg • prospective • ASV 79 months • ASV had no • ASVmv Positive
[14] • HFrEF, predominant • OMT statistically significant • Pressure support 3- • Symptoms
CSA effect on survival 10 cmH2O (NYHA
• n = 550 functional
class)
Neutral
• Survival
• LVEF
• Exercise
capacity

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 2023 Tamisier • Prospective, • ASV 2 years • More than half of all • ASVmf Positive
[18] observational cohort • OMT patients benefitted with • Min EPAP 4-5 • mortality
FACE study ASV cmH2O, min IPS 3 • cardiovascula
• CHF with CSA or • Benefit was dependent cmH2O r outcome
TECSA on LCA cluster Neutral
• n = 324 • Sleepiness (ESS) and • quality of life
quality of life and symptoms
(MLHFQ) were (FOSQ and ESS)

comparable between
the ASV and non-
ASV groups among
follow-up in the
subset of patients in
those these data
were reported
2023 Karimi [39] Prospective observational • ASV 1 and 6 months ASV significantly • ASVpf Positive
study improved neurocognition • EPAP min 5 Neurocognitive
HFrEF - CSA (less lapses) and cmH2O, function
N=8 objectively assessed • EPAP max 15 cm (Attention
daytime sleepiness cmH2O Network Test)
(MWT) • min IPS 0 cmH2O and sleepiness

• Max IPAP 30 (MWT)

cmH2O

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 2024 Bradley • RCT • ASV pf 5 years • No significant • ASVpf Neutral
[19] • HFrEF - CSA/OSA • OMT difference in time to • EPAP min 4 • mortality
• n = 731 death or cmH2O, min IPS 0 • cardiovascular
hospitalisation for cmH2O outcome
cardiovascular events, Positive
new onset AF/AFL or • Sleep
ICD shock fragmenta
• Significant tion and
improvements in sleep sleep
structure and reduction structure
of sleep fragmentation • quality of life
• Significant and symptoms
improvement of heart (MLHF, NYHA
failure related QoL, functional class
exercise capacity and ESS)
(NYHA functional
class) and sleepiness
(ESS)

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 2024 Arzt • Prospective cohort • ASV 12 months • Increased disease • ASVmf Positive
(READ) analysis specific QOL • Median applied • quality of life
[51] • CSA±OSA measured by FOSQ in EPAP (cmH20) 6.9 and symptoms
• n = 801 symptomatic patients [6.0; 8.0] and (FOSQ and
and improvement in IPAP (mbar) 10.1 ESS)
ESS [8.8; 11.8]
2024 Arzt • Multicenter RCT • ASV 3 months • Early treatment of • ASVmv Positive
(TEAM- • Early after acute • OMT SDB with ASV • Automatic EPAP 5- • Cardiac
ASV) [52] myocardial infarction salvaged myocardium 15 cmH2O healing
with SDB and decreased the • IPS 0-15 cmH2O (Myocardial
• N=39 infarct size. ASV had • Applied pressures: salvage index

no effect on angina • Median EPAP and infarct size

6.2±1.4 cmH2O assessed with

pectoris (Seattle
• Median IPAP cardiac
Angina
8.4±1.4 cmH2O magnetic
Questionnaire)
resonance)
Neutral
Angina pectoris
(Seattle Angina
Questionnaire)

RCT = randomised-controlled trial, HFrEF = heart failure with reduced ejection fraction, NYHA = New York Heart Association, CSR =
Cheyne-Stokes respiration, ASV = adaptive servoventilation (ASVmv = ASV minute-ventilation, ASVpf = ASV peak flow), BPAP = bilevel

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 positive airway pressure, AHI = apnoea-hypopnoea index, EPAP = expiratory positive airway pressure, IPAP = inspiratory positive airway
pressure, HF = heart failure, SDB = sleep-disordered breathing, OMT = optimal medical therapy, eGFR = estimated glomerular filtration
rate, LVEF = left ventricular ejection fraction, LVF = left ventricular function, CSA = central sleep apnoea, NT-proBNP = N-terminal
prohormone of brain natriuretic peptide, 6MWD = 6 minute walk distance, OSA = obstructive sleep apnoea, CAI = central apnoea index,
OAI = obstructive apnoea index, ACMV = anti-cyclic minute ventilation, PSG = polysomnography, IPS = inspiratory pressure support,
PLMS = periodic limb movements in sleep, TECSA = treatment-emergent central sleep apnoea, LCA = latent class analysis, T90 = time
spent under 90% oxygen saturation, AF/AFL = atrial fibrillation/atrial flutter, ICD = implanted cardioverter-defibrillator, T90 = time spent
at <90% oxygen saturation,QOL = quality of life, FOSQ = functional outcome of sleep questionnaire, ESS = Epworth sleepiness scale,
MLHF = Minesota Living with Heart Failure questionnaire, MWT = Maintenance of wakefulness test, SAQLI = Sleep Apnea Quality of
Life Index

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 Table combined

Year, Author Study type, population Intervention Follow-up Summary of outcome ASV type and setting Interpretation
and size group(s) time range

2002, • RCT • ASV 1 month Active ASV reduced • ASVmv Positive

Pepperell • HFrEF CSA-CSR • Subtherapeutic excessive daytime • EPAP 5 cmH2O • Sleep parameters
[40] • 30 ASV (Control) sleepiness (Osler test). • IPS 3-10 cmH2O • Sleepiness
On active ASV, (OSLER test)
significant falls occurred • Cardiac function
in plasma brain (BNP)
natriuretic peptide and
urinary metadrenaline
excretion.

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 2006, • RCT • ASV 6 months ASV and CPAP • ASVmv Positive
Philippe [41] • HFrEF CSA-CSR • CPAP decreased the AHI, only • EPAP 5 cmH2O • Sleep parameters
• n = 25 ASV completely • IPS 3-10 cmH2O • Disease specific
corrected CSA-CSR. At QoL (MLHF)
six months compliance • Cardiac function
with CPAP was (LVEF)
significantly less than
with ASV. At six months, Neutral
the improvement in QoL • Sleepiness (ESS,
was higher with ASV MWT)
and only ASV induced a
significant increase in
LVEF.
2007, Fietze • RCT • ASV 1.5 months • Significant reduction • ASVmv Neutral
[21] • HFrEF (NYHA II-III) - • BPAP in AHI in ASV and • EPAP 4 cmH2O • sleep parameters
CSR BPAP • IPS 4-10 cmH2O • sleepiness (ESS)
• n = 37

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 2008, • Prospective • ASV 6 months ASV significantly • ASVmv Positive
Hastings [42] observational • OMT reduced AHI and LVEF • EPAP 5 cmH2O, • Sleep parameters
• HFrEF with SDB was increased • IPS 3 - 10 cmH2O • Sleepiness (ESS)
• N=19 but not BNP. The • General QoL (SF-
energy/vitality score of 36)
the SF-36 QoL • Exercise capacity
questionnaire was also (6MWD)
improved at 6 months. • Cardiac function
(LVEF)

Neutral
• Disease specific
QoL (MLHF)
• Cardiac function
(BNP)
• Exercise capacity
(VO2max)

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 2009, • RCT • ASV 3 months ASV more effectively • ASVpf Positive
Kasai [23] • HFrEF/HFmrEF with • CPAP suppressed respiratory • EPAP 4-10 • Sleep parameters
coexisiting OSA-CSA events.Compliance was cmH2O, • General QoL (SF-
• N=31 significantly greater with • IPS 2-10 cmH2O 36)
ASV than with CPAP. • Exercise capacity
The improvements in (6MWD)
QoL and LVEF were • Cardiac function
greater in the ASV. (BNP, LVEF)
There was a similar
reduction of sleepiness Neutral
in the ASV and CPAP • Sleepiness (ESS)
groups.

2011, • Prospective • ASV 12 months • Increases in eGFR • ASVmv Positive

Koyama [2] • HF - SDB • OMT and LVEF with ASV • EPAP 5 cmH2O, • Renal and cardiac
[53] • n = 59 • IPS 3 -10 cmH2O function

2011, • Prospective • ASV 6 months • Event free rate higher • ASVpf Positive
Yoshihisa [1] comparison • non-ASV in ASV group • EPAP titration, set • Cardiovascular
• HF, NYHA ≥ II - CSR minimum and outcome
• n = 60 maximum IPAP

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 2011, • Prospective • ASV 0.25 • ASV improved AHI, • Positive
Su [43] observational • APAP months central AI and • Sleep parameters
• Severe OSA, residual sleepiness (ESS) • Sleepiness (ESS)
sleepiness on APAP,
residual sleepiness,
no heart disese
• N=42
2011, • Retrospective • ASV users 36 months • ASV users had a • ASVmv Positive
Carnevale observational • ASV non users significant reduction in • Mean EPAP 6 ± 1 • Sleep parameters
[44] • CSA due to heart AHI, sleepiness and mbar • Sleepiness (ESS)
failure, neurologic dyspnoea • IPS 3 -10 cmH2O • Dyspnoea (NYHA)
disease or idiopathic
CSA
• N=74
2011, • Prospective • ASV 3-6 months • SDB, NYHA class, • ASVmv Positive
Oldenburg comparison • OMT LVEF, 6MWD, NT- • EPAP 4–5 cmH2, • Respiratory and
[24] • HF, NYHA ≥ II - CSA proBNP and exercise IPAP 3–10 cmH2O functional indices
• n = 115 test improved
significantly under
ASV

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 2012, • RCT • ASV 12 months • CAI and BNP • ASVpf Positive
Randerath • HF – CSA/OSA • CPAP significantly more • EPAP titration, • Sleep parameters
[54] • n = 63 reduced with ASV IPAP 4-30 cmH2O • Cardiac function

2012, • Prospective • ASV ≥ 4h/night 12 months • Higher survival rate • ASVmv Positive
Takama [2] observation • ASV < 4h/night and fewer • EPAP 4-cmH2O, • Mortality
• CHF NYHA II-IV - cardiovascular events IPAP 3–8 cmH2O • Cardiovascular
SDB in good adherence outcome
• n = 85 group
2012, • RCT • ASV 12 months • Event-free rate higher • ASVpf Positive
Miyata [3] • HF with cardiac • standard care in ASV (driven by • cardiac function
resynchronisation hospitalisations) • cardiac events
therapy, predominant
CSA
• n = 22

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 2013, Arzt • RCT • ASV 3 months • More significant • ASVpf Positive
[45] • HF - SDB • OMT reduction in AHI and • EPAP titration, • Sleep parameters
• n = 72 NT-proBNP with ASV IPAP max 10 Neutral
• Similar change in cmH2O above • Cardiac function
LVEF EPAP • Sleepiness (ESS)
• Similar change in • Fatigue (FSS)
symptoms and QoL • General and
disease specific
QoL (SF-36,
MLHF)
2013, • Prospective • ASV alone Median 3.6 • Reduction in AHI • ACMV Positive
Oldenburg observation ± 1.2 • Improved sleep quality • Individual titration, • PSG parameters
[14] • CHF – CSA/mixed months • Improved NYHA settings not • cardiac function
• n = 45 functional class disclosed • symptoms
2013, • observational • ASV 18 months • event-free rate • ASVmv Positive
Yoshihisa • LVEF > 50% • standard care significantly higher in • EPAP 5-8 cmH2O, • cardiac diastolic
[26] • n = 36 the ASV group pressure support function
3-10 cmH2O • event-free rate
Neutral
• LVEF

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 2013, Owada • Observational • ASV 6 months • event-free rate • ASVmv Positive
[5] • HF, SDB • non-ASV significantly higher in • EPAP 4-8 cmH2O, • cardiac function
• n = 80 the ASV group pressure support • event-free rate
3-10 cmH2O
2014, • Prospective • ASV in LVEF < 6 months • Improvement in LVEF • ASVmv Positive
Takama [6] comparison 30% • Reduction in BNP • EPAP 4 cmH2O, • cardiac function
• CHF - OSA/CSA • LVEF ≥ 30%; n • No difference in IPS 3–8 cmH2O Neutral
• n = 76 = 34 survival/hospitalisation • cardiovascular
outcome
2014, • RCT • ASV 3 months • AHI < 10 at 90 days in • ASVmv Positive vs. CPAP
Morgenthaler • TE-CSA • CPAP 89.7% versus 64.5% • ASV titrated • PSG parameters
[46] • n = 66 of participants treated according to a
with ASV and CPAP standardised Neutral vs. CPAP
• changes in ESS and protocol • Sleepiness (ESS)
Sleep Apnea Quality • Disease specific
of Life Index were not QoL (SAQLI)
significantly different
between ASV and
CPAP groups

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 2014, • Prospective • ASV 9 months, • Significantly greater • ASVmv n =19, Positive
Javaheri [55] comparison • CPAP to 6 years reduction in AHI with ASVpf n=1 • sleep parameters
• Chronic opioid use ASV • EPAP titration, IPS
• n = 20 3 - 8 cmH2O

2014, Birner • RCT • ASV 3 months • Significant • ASVpf Positive

[56] • HF - CSA/OSA • OMT improvement in AHI • EPAP titration 4 • sleep parameters
• n = 32 with ASV cm – 10 cmH2O, • cardiac function
• Improvement in IPS 1-10 cmH2O
diastolic dysfunction
2014, • RCT – cross-over • ASV 1 months • LVEF • ASV (Anticyclic Positive
Galetke [47] • N=39 • CPAP was significantly modulated • sleep parameters
• Cardiac disease and • No treatment increased only with ventilation, • cardiac function
coexisting OSA-CSA ASV. Weinmann
Subjective sleepiness Hamburg) Neutral
significantly improved • EPAP 6.2 cmH20 • sleepiness (ESS)
only with CPAP • EEPAP 8.9 cmH20
whereas objective • EPAP 10.1 cmH20
sleep quality and
treatment adherence
were not
different between both
treatment modalities.

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 2014, • Observational • ASV 6 months • Significant • ASVmv Positive
Brill [48] • Stroke, LVEF>50% improvement in AHI • EPAP 5 cmH2O, • Sleepiness (ESS)
• CSA and sleepiness (ESS) IPS 3 - 10 cmH2O
• N=15 with ASV •

2014, Suzuki • Prospective • ASV 6 months • Cardiac event-free • ASVpf Positive

[7] observational • non-ASV rate significantly • cardiac event-free
• HF, SDB higher in ASV in rate
• n = 139 anaemia, no
difference in ASV vs
no ASV without
anaemia

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 2015, Cowie • RCT • ASV Median • No significant • ASVmv Negative
[8] • HFrEF, NYHA class III • OMT follow-up difference in time to • EPAP 5 mbar, IPS • Mortality
SERVE-HF or IV - CSA 31 months hospitalisation/ life- 3 -10 cmH2O • Exercise capacity
• n = 1325 saving cardiovascular (6MWD)
intervention, Neutral
worsening CHF or • cardiovascular
time to death, change outcome
in NYHA class, 6MWD • dyspnoea (NYHA
and 6MWD)
• QoL (EQ5D,
MLHF)
Positive
• sleep parameters
• sleepiness (ESS)
2015, • Prospective • ASV 3 months • AHI, CAI and OAI • ASVpf Positive
Shapiro [57] interventional (with/without significantly reduced • EPAP 4-15cmH2O • sleep parameters
• Chronic pain (≥ 100mg mandatory under ASV • IPS 0-21 Vs 6-21
morphine) - SDB pressure cmH2O
• n = 100 support)
2015, • RCT • ASV 6 months • No significant • ASVmv Neutral
Momomura • CHF - SDB (AHI • OMT difference in • Settings not • cardiac function
[9] ≥15/h) improvement in LVF disclosed
• n = 213 and BNP

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 2015, • Prospective • ASV 3 months • ASV significantly • NA Positive
Javaheri [49] • Observational improved sleepiness • Sleepiness (ESS)
• CSA
• N=26
2016, • Multicentre, RCT • ASV 12 weeks • ASV significantly • ASVpf Positive
Hetzenecker • CHF – CSA/OSA • OMT reduced sleep • EPAP 4-10 • sleep parameter
[35] • n = 63 fragmentation cmH2O, IPS 1-
10cmH20
2016, • Retrospective • ASV 24 months • All-cause mortality • NA Positive
Imamura [10] • Advanced HF • Non-ASV and cardiac death rate • mortality
• n = 85 significantly lower in • cardiac death
ASV • cardiac function
2017, • RCT • ASV 3 months • ASV improved QoL • NA Positive
Olseng [50] • HFrEF -CSA • Non-ASV both in a per protocol • QoL (MLHF)
• N=30 analysis and in an
intention to treat
analysis.
2017, • RCT • ASV 6 months • Significant reduction • ASVmv Positive
Toyama [30] • HFrEF - CSA • OMT in AHI, changes of • EPAP 4-mbar, IPS • sleep parameters
• n = 31 LVEF and NYHA 3–8 cmH2O • cardiac function
class • dypnoea
(NYHA)

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 2017, • RCT • ASV 6 months • Significantly greater • ASVmv Positive
O’Connor • Hospitalised • OMT reduction in AHI under • Setting not • Sleep parameters
[12] unselected CHF - ASV specified Neutral
CAT-HF SDB • No improvement in 6- • cardiovascular
• n = 126 month, disease outcome
specific QOL, • disease specific
sleepiness and QOL (PSQI) and
cardiovascular sleepiness (ESS)
outcomes
2017, • Retrospective • ASV 18 months • no difference in • ASVmv Neutral
Hetland [13] • HFrEF, CSA > 25% • Non-ASV exercise capacity, • EPAP 5 cmH2O, • death
• n = 75 cv death; trend pressure support • dypnoea (NYHA
3-10 cmH2O functional class)
toward better
Positive
outcome regarding
• QoL (MLHF)
cardiovascular
event-free survival
in ASV
• Improvement of
heart failure related
QoL

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 2018, Piccini • CHF with • ASV 6 months • 39% absolute • ASVmv Positive
[31] pacemaker/defibrillator • OMT reduction in AF • Setting not • Cardiovascular
CAT-HF - SDB specified parameter
burden
• n = 35

2018, • RCT • ASV 6 months • Reverse LV • ASVmv Positive

Daubert [32] • HF • OMT remodeling in both • Setting not • cardiac function
• n = 126 groups specified
CAT-HF • Reduced LA volume
under ASV
2018, Cowie • Sub-study of RCT • ASV 12 months • Addition of ASV had • ASVmv Neutral
[58] SERVE-HF • OMT no effect on cardiac • EPAP titration, IPS • cardiac and renal
SERVE-HF • Heart failure - CSA structure and function, 3-10cmH2O function
• n = 312 or on cardiac
biomarkers, renal
function and systemic
inflammation

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 2018, • prospective • ASV 79 months • ASV had no • ASVmv Positive
Oldenburg • HFrEF, predominant • OMT statistically significant • Pressure support • Symptoms
[14] CSA effect on survival 3-10 cmH2O (NYHA functional
• n = 550 class)
Neutral
• Survival
• LVEF
• Exercise
capacity
2020, • Multicentric, • ASV (various > 3 months • AHI normalised in • ASVmv n =409, Positive
Cantero [59] observational devices and 94% ASVpf n =39, ACMV • sleep parameters
• Unselected CSA with settings) n=10
ASV use > 3 months • Fixed and variable
• n = 458 EPAP, min IPS 0-
3cmH2O

2022, • Retrospective sub- • ASV Baseline, • Better sleep efficiency • ASVmv Neutral
Tamisier [38] analysis of SERVE-HF • OMT 3- and 12- and lower respiratory • EPAP 5 cmH2O, • sleep parameters
SERVE-HF • CHF - CSA months arousal index in ASV IPS 3 -10 cmH2O • cardiac function
• n = 312 • Increased PLMS
arousal index in ASV
• No change in LVEF

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 2023, Sun • Retrospective cohort • ASV pf n =77 Median 64 • No increase in • ASVmv and ASVpf Neutral
[16] • HFrEF-CSA • ASV mv n =13 months mortality • EPAP 4-14 • mortality
• n = 90 • Trend towards cmH2O, IPS 0.5–
negative correlation 12
between ASVmv with
fixed EPAP and
survival
2023, Kida • Retrospective follow- • ASV 12 months • Significant reduction • Details unavailable Positive
[17] up of hospitalisation for • morbidity
• HFpEF - SDB HF in 12 months after
• n = 36 ASV initiation
compared to before
initiation

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 2023, • Prospective, • ASV 2 years • More than half of all • ASVmf Positive
Tamisier [18] observational cohort • OMT patients benefitted • Min EPAP 4-5 • mortality
FACE study FACE study with ASV cmH2O, min IPS 3 • cardiovascular
• CHF with CSA or • Benefit was mmH2O outcome
TECSA dependent on LCA Neutral
• n = 324 cluster • quality of life and
• Sleepiness (ESS) symptoms
and quality of life (FOSQ and ESS)
(MLHFQ) were
comparable between
the ASV and non-
ASV groups among
follow-up in the
subset of patients in
those these data
were reported
2023, • RCT • ASV 12 weeks • ASV significantly • ASVpf Positive
Baumert [60] • HFrEF – OSA/CSA • OMT reduced T90 • EPAP titration 4- • respiratory
• n = 56 10cmH2O, IPS 1- parameters
10cmH2O

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 2023, Prospective • ASV 1 and 6 ASV significantly • ASVpf Positive
Karimi [39] observational study months improved neurocognition • EPAP min 5 neurocognitive
HFrEF - CSA (less lapses) and cmH2O, function (Attention
N=8 objectively assessed • EPAP max 15 cm Network Test) and
daytime sleepiness cmH2O sleepiness (MWT)
(MWT) • min IPS 0 cmH2O
• Max IPAP 30
cmH2O

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 2024, • RCT • ASV pf 5 years • No significant • ASVpf Neutral
Bradley [19] • HFrEF - CSA/OSA • OMT difference in time to • EPAP min • mortality
ADVENT-HF • n = 731 death or 4cmH2O, min IPS • cardiovascular
hospitalisation for 0 cmH2O outcome
cardiovascular events, Positive
new onset AF/AFL or • Sleep
ICD shock fragmentation
• Significant and sleep
improvements in sleep structure
structure and • quality of life and
reduction of sleep symptoms
fragmentation (MLHF, NYHA
• Significant functional class and
improvement of heart ESS)
failure related QoL,
exercise capacity
(NYHA functional
class) and sleepiness
(ESS)

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 2024, Arzt • Prospective cohort • ASV 12 months • Increased disease • ASVmf Positive
[51] analysis specific QOL • Median applied • quality of life and
READ-ASV • CSA±OSA measured by FOSQ in EPAP (cmH20) 6.9 symptoms
• n = 801 symptomatic patients [6.0; 8.0] and (FOSQ and ESS)
and improvement in IPAP (mbar) 10.1
ESS [8.8; 11.8]
2024, Arzt • Multicentre RCT • ASV 3 months • Early treatment of • ASVmv Positive
[52] • Early after acute • OMT SDB with ASV • Automatic EPAP • Cardiac healing
TEAM-ASV I myocardial infarction salvaged 5-15 cmH2O (Myocardial
with SDB myocardium and • IPS 0-15 cmH2O salvage index and
• N=39 decreased the infarct • Applied pressures: infarct size

size. ASV had no • Median EPAP assessed with

6.2±1.4 cmH2O cardiac magnetic

effect on angina
• Median IPAP resonance)
pectoris (Seattle
8.4±1.4 cmH2O Neutral
Angina
Angina pectoris
Questionnaire)
(Seattle Angina
Questionnaire)

The table presents the results of randomised controlled or observational trials with a number of participants ≥ 20 and a follow-up period > 6 weeks.

RCT = randomised-controlled trial, HFrEF = heart failure with reduced ejection fraction, NYHA = New York Heart Association, CSR = Cheyne-Stokes
respiration, ASV = adaptive servoventilation (ASVmv = ASV minute-ventilation, ASVpf = ASV peak flow), BPAP = bilevel positive airway pressure,
AHI = apnoea-hypopnoea index, EPAP = expiratory positive airway pressure, IPAP = inspiratory positive airway pressure, HF = heart failure, SDB =

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 sleep-disordered breathing, OMT = optimal medical therapy, eGFR = estimated glomerular filtration rate, LVEF = left ventricular ejection fraction,
LVF = left ventricular function, CSA = central sleep apnoea, NT-proBNP = N-terminal prohormone of brain natriuretic peptide, 6MWD = 6 minute
walk distance, OSA = obstructive sleep apnoea, CAI = central apnoea index, OAI = obstructive apnoea index, ACMV = anti-cyclic minute ventilation,
PSG = polysomnography, IPS = inspiratory pressure support, PLMS = periodic limb movements in sleep, TECSA = treatment-emergent central sleep
apnoea, LCA = latent class analysis, T90 = time spent under 90% oxygen saturation, AF/AFL = atrial fibrillation/atrial flutter, ICD = implanted
cardioverter-defibrillator, T90 = time spent at <90% oxygen saturation,QOL = quality of life, FOSQ = functional outcome of sleep questionnaire, ESS
= Epworth sleepiness scale, MLHF = Minesota Living with Heart Failure questionnaire, MWT = Maintenance of wakefulness test, SAQLI = Sleep
Apnea Quality of Life Index

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