(Circulation. 1999;99:1435-1440.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Prognostic Value of Nocturnal Cheyne-Stokes Respiration in Chronic Heart Failure
From the Division of Cardiology (P.A.L., E.B., G.M., P.G.), Division of Pulmonary Disease (A.B., C.F.D.), and Department of Bioengineering (R.C.), Salvatore Maugeri Foundation, IRCCS, Veruno, Italy.
Correspondence to Paola A. Lanfranchi, Division of Cardiology, Centro Medico, 28010 Veruno (NO), Italy. E-mail planfranchi{at}fsm.it
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Abstract |
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Background—Nocturnal Cheyne-Stokes respiration (CSR) occurs frequently in patients with chronic heart failure (CHF), and it may be associated with sympathetic activation. The aim of the present study was to evaluate whether CSR could affect prognosis in patients with CHF.
Methods and Results—Sixty-two CHF patients with left
ventricular ejection fraction 
35%, in NYHA class II to
III, underwent clinical evaluation, Doppler
echocardiography, ergospirometry,
phenylephrine test, Holter recording, and a sleep
study to evaluate the occurrence of CSR, expressed as percentage of
periodic breathing, and apnea/hypopnea index (AHI) (ie, the number of
apneas and hypopneas per hour of recording). During a mean
follow-up of 28±13 months, 15 patients died of cardiac causes.
Nonsurvivors were in a higher NYHA functional class than survivors
(P<0.001) and had a more depressed left
ventricular ejection fraction (P<0.03), a
shorter deceleration time of early filling (P<0.05),
larger left and right atria (P<0.05 and
P<0.02, respectively) and a lower peak
O2 (P<0.05).
Nonsurvivors also spent a greater percentage of the night in periodic
breathing (P<0.01) with a greater AHI
(P<0.03) and showed lower values of diurnal baroreflex
sensitivity (P<0.05) and of heart rate variability
(sdNN: P<0.01). Multivariate
analysis revealed the AHI (
2, 10.4;
P<0.01), followed by left atrial area
(2, 5.7; P<0.01), as the only
independent and additional predictors of subsequent cardiac death.
Patients at very high risk for fatal outcome could be identified by an
AHI 
30/h and left atria 25 cm2.
Conclusions—The AHI is a powerful independent predictor of poor
prognosis in clinically stable patients with CHF. The presence of an
AHI 30/h adds prognostic information compared with other clinical,
echocardiographic, and autonomic data and identifies
patients at very high risk for subsequent cardiac death.
Key Words: heart failure • sleep • prognosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Cheyne-Stokes respiration (CSR) is a form of disordered breathing characterized by recurrent episodes of central apneas or hypopneas, alternating with hyperpneas, during which there is a crescendo-decrescendo pattern of tidal volume.1 2
Since its first description, this breathing disorder has been commonly observed both in awake conditions and during sleep, not only in acute heart failure but also in many clinically stable patients with chronic heart failure (CHF) and left ventricular systolic dysfunction.3 4 5 6 7 Although several experimental and clinical studies have described its potential detrimental effects on autonomic and cardiac function,3 8 sleep disordered breathing has been given modest attention in the heart failure literature, and it has not been systematically evaluated in any of the large studies that have examined the natural history of heart failure.9 Mortality appears to be increased in heart failure patients with nocturnal CSR compared with those without CSR, despite a similar degree of left ventricular dysfunction.6 7 10 However, contrasting results have been reported concerning the prognostic value of nocturnal CSR.6 7 10 11
Accordingly, the aim of the present study was to evaluate the impact of nocturnal CSR on survival in a population of patients with CHF.
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Methods |
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Consecutive patients with CHF due to either ischemic or idiopathic dilated cardiomyopathy were enrolled from the Heart Failure Unit of the Cardiology Department of our institution. The entry criteria were (1) at least 1 previous episode of clinical heart failure, (2) an echocardiographic left ventricular ejection fraction
35%, and (3) stable clinical conditions under oral therapy
for at least 1 month before evaluation. Patients were ineligible if
they had a body mass index >30 kg/m2 or if they
had any of the following: atrial fibrillation, primary valvular
heart disease, coronary artery bypass procedures during the
previous 6 months, obstructive lung disease as demonstrated by a forced
expiratory volume in 1 second/forced vital capacity <70%, clinical
signs of central or peripheral nervous system impairment or
a history of stroke, or cocaine or alcohol abuse. Sixty-six patients (8
women) 57±9 years old met the entry criteria and were enrolled in the
study. All patients gave written informed consent to perform the study
protocol and to participate in this prospective study, which had been
approved by the Science and Ethics Committee of our
institution.
Study Protocol
The study consisted of 2 parts: (1) functional evaluation at
entry and (2) follow-up. Entry evaluation included historic data
collection, functional classification, Doppler
echocardiography, ergospirometry, 24-hour Holter
recording, the phenylephrine test, and a sleep
study. The functional status of patients was determined according to
the classification of the New York Heart Association (NYHA).
Echocardiography
A complete 2-dimensional echocardiography
and a Doppler ultrasound examination were performed by standard
techniques with a Hewlett-Packard ultrasound system (model 77729-A or
77622-A). Left ventricular volumes were calculated from
orthogonal apical views by the area-length method. The ejection
fraction was derived from the standard equation. The maximal atrial
area and the right ventricular end-diastolic
diameter 1 cm below the tricuspid annulus were also measured. For the
mitral Doppler variables, traces of 5 to 8 consecutive cardiac
cycles were analyzed with a microcomputer-based digitizing
system, and deceleration time of early filling was measured. Mitral and
tricuspid regurgitation were semiquantitatively graded
by color flow Doppler as none, mild, moderate, or severe as
previously reported.12
Ergospirometry
Multistage symptom-limited bicycle exercise testing with
spirometry was used to evaluate the peak oxygen consumption.
Baroreflex Sensitivity Assessment
Arterial baroreceptor function was evaluated by
administration of phenylephrine (2 to 4 µg/kg), as
previously described.13 Baroreflex sensitivity (BRS) was
measured in ms/mm Hg as the slope of the regression line relating the
RR interval to systolic arterial pressure
increments.
24-Hour Ambulatory ECG Recording
Recordings were performed by means of a commercial
device (Marquette 8500), and measures of RR-interval variability were
derived. Heart rate variability was assessed both over the whole
24-hour period of the recording and separately during the night
(from 12 PM to 5 AM) and day (from 7
AM to 7 PM) periods. The mean normal-to-normal
(NN) intervals, the standard deviation of NN (sdNN), and the percentage
of >50-ms differences between adjacent NNs (pNN50) were
evaluated.14
Sleep Study
All patients underwent an overnight sleep study by means of an
unattended system (Night-Watch, Healthdyne Inc) recording body
position, eye and leg movements, cardiotachography, nasobuccal air
flow, chest and abdominal effort, and pulse oximetry. A central apnea
was defined as the absence of flow and thoracoabdominal movements
lasting at least 10 seconds. Central hypopnea was defined as a 50%
decrease in the sum of thoracoabdominal movements lasting 10 seconds or
more, followed by a reduction in SaO2
of 2%. Periodic breathing was measured and reported as a percentage
of total recording time and as a central apnea-hypopnea index
(AHI), which was defined as the number of apneas and hypopneas per hour
of recording. When obstructive events exceeded 5 episodes per
hour, the patient was excluded from further analysis.
Follow-Up
After entry evaluation, patients were seen in our outpatient
clinic at regular intervals of 6 months. The follow-up of patients who
did not attend the scheduled appointments was obtained by personal
communication with the patient's physician or by means of a telephone
interview with the patient. The outcome event considered was
cardiac mortality.
Statistical Analysis
All descriptive data are given as mean±SD. Differences between
patients were compared by Student's unpaired t test and
frequency of parameters and events by
2 test with Yates' correction. In the
comparison between survivors and nonsurvivors, patients who received
heart transplants and those with noncardiac death were excluded from
analysis. Those variables that showed a significant
association with the outcome (P<0.1) were included in a
multivariate logistic stepwise regression
analysis model. Survival was estimated by the product-limit
Kaplan-Meier method, in which heart transplantations and noncardiac
deaths were included as censored data. Differences between survival
curves were tested with the log-rank 2
statistic. A value of P<0.05 was considered significant.
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Results |
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Of the 66 patients initially enrolled, 4 were excluded because they presented periodic breathing with obstructive apneas, leaving 62 patients as the final study population. The cause of heart failure was ischemic dilated cardiomyopathy in 33 patients and nonischemic dilated cardiomyopathy in 29. Patients were taking a variety of medications, including digitalis (78%), ACE inhibitors (94%), nitrates (48%), and diuretics (91%). Mean ejection fraction was 23±6%. At the sleep study, 46 patients (74%) showed an AHI
10/h during the
night.
Follow-Up
Patients were followed up for 28±13 months. During that period,
21 patients had at least 1 new episode of CHF that required
hospitalization, 6 patients received heart transplants, 2 patients died
of noncardiac causes, and 15 patients died of cardiac causes: sudden
death (7 patients), refractory heart failure (7 patients), and
myocardial infarction (1 patient). The 1- and 2-year cumulative
mortality rates were 12% and 25%, respectively. Clinical,
echocardiographic, sleep, and autonomic data are
summarized in Table 1
. Nonsurvivors were
in a higher NYHA functional class than survivors (P<0.001).
They had a more depressed left ventricular ejection
fraction (P<0.03), a shorter deceleration time of early
filling (P<0.05), larger left and right atria
(P<0.05 and P<0.02, respectively), a larger
right ventricular diameter (P<0.03), and a
lower peak O2 at the
cardiopulmonary test (P<0.05). Nonsurvivors also
had a greater percentage of the night in periodic breathing
(P<0.01) with a higher value of AHI (P<0.03),
but no difference was found in the time spent at <90% and <85%
SaO2 levels. Finally,
nonsurvivors showed a more depressed diurnal BRS (P<0.05)
and lower 24-hour and nocturnal mean NN (P<0.01), sdNN
(P<0.01 and P<0.05, respectively), and pNN50
(P<0.01). No specific medications at baseline emerged as
significantly associated with prognosis.
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Multivariate regression analysis revealed AHI
(but not percent of periodic breathing) followed by left atrial (LA)
area as the only independent and additional predictors of subsequent
cardiac death (Table 2). Mortality was
significantly higher in patients with AHI 30/h than in those with AHI
<30/h (59% versus 14%, P<0.001) and in patients with LA
area 25 cm2 than in those with LA area <25
cm2 (43% versus 12%, P<0.01) and
considerably higher in patients with both higher AHI and enlarged LA
area than in those without (75% versus 5%, P<0.001).
Survival according to the value of AHI and LA area is shown in Figure 1. The cumulative 1- and 2-year cardiac
mortalities were, respectively, 21.4% and 50% in patients with AHI
30/h versus 5.4% and 26.2% in those with AHI <30/h
(P<0.01); 16% and 62.5% in patients with LA 25
cm2 versus 3.8% and 6.6% in those with LA <25
cm2 (P<0.01); and 33.3% and 85.8%
in patients with both AHI 30/h and LA 25 cm2
versus 4.8% and 20.8% in the other patients (P<0.0001).
The risk of cardiac death increased progressively with an increase in
the value of AHI and LA dimensions: patients at very high risk for
fatal outcome can be identified by an AHI 30/h and enlarged left
atria 25 cm2 (Table 3 and Figure 2).
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Baseline Characteristics of Patients With Breathing
Disorders
Patients with AHI 30/h, compared with those with AHI <30/h,
showed a more impaired ejection fraction (P<0.05), a
shorter deceleration time of early filling (P<0.01), a
lower peak O2
(P=0.02), and a lower level of diurnal
PO2 (P=0.02) but the
same level of PCO2 (Table 4). However, AHI was poorly related to
ejection fraction (r=-0.22, P=NS), deceleration
time of early filling (r=-0.28, P<0.05), and
peak O2
(P=-0.26, P=NS). Patients with AHI >30/h showed
a depressed BRS and an impaired heart rate variability as expressed by
sdNN and pNN50 in both the 24-hour (sdNN, P<0.001; pNN50,
P<0.01) and night periods (nocturnal sdNN,
P<0.01; nocturnal pNN50, P<0.01). The value of
AHI was well correlated with sdNN (r=-64,
P<0.0001) and BRS (r=-40,
P<0.01).
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Multivariate logistic analysis, including in
the model ejection fraction, NYHA class, deceleration time of early
filling, and BRS, indicated BRS to be the only predictor of the
sleep-related breathing disorder (2, 15.5;
P<0.001).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study shows that nocturnal CSR has a negative effect on survival in patients with moderate to severe CHF due to ischemic or nonischemic dilated cardiomyopathy. Although many variables are associated with cardiac mortality, our data indicate that this nocturnal breathing disorder gives independent and additional prognostic information in clinically stable patients, particularly in those with a more enlarged LA.
Previous studies on the prognostic value of nocturnal CSR in patients with heart failure are limited and contradictory. Initially, the prognostic value of nocturnal periodic breathing was reported as a corollary result of studies on CHF patients.6 7 The first study that specifically aimed to test survival in patients with stable CHF was conducted by Hanly and Zuberi-Khokhar,10 who reported a 3-year mortality of 56% in 8 patients with nocturnal CSR compared with 11% in 8 patients without CSR, despite similar functional status and left ventricular ejection fraction. By contrast, Andreas et al11 did not find any difference in mortality at 1, 2, and 4 years in 36 patients with or without CSR as defined by >20% CSR of total sleep time. This discrepancy may be due to either the different characteristics of the patients, the time of the evaluation, or the definition of breathing disorder used in the analysis. Specifically, in the study by Andreas et al, patients were evaluated when they had no signs of clinical acute heart failure. However, the duration of clinical stability was unclear.
Furthermore, in the Andreas study, nocturnal breathing disorder was evaluated as a percentage of periodic breathing, and the number of events, ie, apneas and hypopneas, was not considered.
In the present study, AHI, but not percentage of periodic
breathing, emerged as the most powerful independent predictor of
cardiac mortality among demographic, clinical,
echocardiographic, and some autonomic and sleep data,
indicating the greater impact on survival of the number of respiratory
events rather than the total time spent in periodic breathing. LA area
was shown to be an additional and independent prognostic indicator, in
line with some data reported in the literature.15 The risk
of cardiac death increased progressively with the value of AHI as well
as with LA area: patients at very high risk for fatal outcome can be
identified by an AHI 30/h and enlarged LA 25
cm2. Nevertheless, in patients with isolated
enlarged LA without important breathing disorders and vice versa, in
patients with AHI 30/h and relatively small LA, the risk was low
(Table 3
and Figure 2).
Clinical Relevance of CSR in Heart Failure
Early observations indicated an association between CSR and heart
failure,1 2 although not all patients with heart failure
have CSR. One determinant of the variable occurrence of CSR in
heart failure may be the severity of ventricular
dysfunction; however, a clear and unequivocal correlation between the
degree of ventricular dysfunction and the severity of CSR
has not yet been demonstrated,5 indicating that other
factors may be responsible for the occurrence of CSR in patients with
CHF.
Theoretical modeling indicates that instability of respiratory control may play a major role in the pathogenesis of CSR.16 In the setting of heart failure, this instability may be related to several factors that might contribute to the occurrence of this respiratory pattern, including reduced body stores of CO2 and O2, hyperventilation arising from pulmonary vagal afferent stimulation from pulmonary venous congestion, prolonged circulation time, changes in resistance of the upper airways, instability of baroreflex control (which could affect respiratory control as well), and individual variability in the apneic threshold for CO2 and in the ventilatory response to hypercapnia (central controller gain).5 17 18 The pathophysiological key to CSR in CHF is a tendency to hyperventilate, causing PCO2 to fall below an apneic threshold, triggering recurrent central apneas.17 Once periodic breathing is initiated, PCO2 oscillates above and below the apnea threshold during hyperpnea and apnea, respectively. Wakeful hypocapnia, due to hyperventilation or to the use of diuretic agents, has been suggested to be a critical factor in predisposing patients to develop CSR.
In our study, we did not find any difference in wakeful
arterial PCO2 of patients
with AHI 30/h compared with those with AHI <30/h (Table 4).
On the contrary, our patients with AHI 30/h showed lower
arterial oxygen tension, suggesting an impaired
ventilation/perfusion relationship arising from pulmonary
hypertension and interstitial edema, thus the result of a
more pronounced congestion. Although we did not find linear
correlations between specific values of AHI and ejection fraction or
deceleration time, patients with AHI 30/h generally had a more
depressed ejection fraction and a shorter transmitral Doppler
deceleration time of early filling as an index of restrictive
diastolic filling, which has been demonstrated to be highly
correlated with elevated filling pressure.12 These
findings confirm that this nocturnal breathing disorder arises
secondary to heart failure and suggest that it is related to the
severity of the disease. Importantly, our results indicate that its
presence can have still further adverse consequences and an additional
negative impact on prognosis (Figure 2). LA area proved to be
the second independent predictor of mortality. It is possible to
speculate that LA area affects survival probably because, over time, it
reflects the hemodynamic evolution of the heart and is
more an expression of the progression of the failing heart than the
actual atrial pressure and the degree of congestion.
CSR and the Autonomic Nervous System
CSR can have detrimental effects on cardiac function by inducing
both hemodynamic changes and sympathetic overactivity.
The sympathetic nerve traffic increases progressively throughout the
period of central apnea, because combined hypoxia and
hypercapnia have a synergistic effect on both the respiratory
chemoreceptors and central sympathetic neurons.19 During
the hyperpneic phase, the inspiratory effort, combined with
hypoxia, is a factor that provokes arousals from sleep at the
peak of hyperventilation20 and hinders the transition to
deep sleep and the restoration of nocturnal vagal tone.21
Thus, hypercapnic hypoxia and arousals from sleep result in
sympathetic overactivity with surges of catecholamine
release: overnight urinary norepinephrine and daytime
plasma norepinephrine concentrations are markedly higher in
patients with CHF and CSR than in similar CHF patients without CSR and
are directly related to the frequency of arousals from sleep and degree
of hypoxia but not to left ventricular ejection
fraction.3 In other words, CSR can trigger sympathetic
activation in some patients with CHF, so that the increased sympathetic
drive is not simply a compensatory response to low cardiac output but
may be related at least in part to the sleep disorder.
Although we did not directly assess neurohumoral activation, patients
with AHI 30/h had evident autonomic abnormalities, as demonstrated by
the phenylephrine test and heart rate variability
analysis. They had, indeed, an impaired arterial
baroreflex gain, expression of impaired vagal efferent nerve traffic
response to baroreceptor stimulation.22 Moreover, both in
the 24-hour period and during the night, they also showed a reduction
of both sdNN (which reflects all the cyclic components responsible for
variability) and pNN50 (which reflects the high-frequency component of
variability, ie, those vagally mediated) as expressions of a lack of
responsiveness of the sinus node to neural inputs and of a withdrawal
of parasympathetic tone in conditions of marked
sympathoexcitation.23 Although it is possible to argue
that the majority of these alterations may be related to the condition
of heart failure per se, BRS was the best predictor of the AHI.
Furthermore, preliminary data from our laboratory suggest that the
improvement in BRS parallels AHI improvement over time, independently
of ejection fraction.24
Because sympathetic overactivity aggravates myocardial injury and affects prognosis, the available data suggest that CSR is part of a vicious circle whereby CHF leads to CSR, which provokes greater activation of the sympathetic nervous system, which, in turn, aggravates cardiac failure. Thus, the sympathetic nervous system may be the link between CSR and prognosis.
Limitations of the Study
We investigated the prognostic value of nocturnal breathing
disorder in a group of clinically stable patients with CHF due to
ischemic or primary cardiomyopathy while in
sinus rhythm. Thus, our results are not necessarily applicable to all
patients with heart failure. Further investigations should be performed
to assess the impact of nocturnal periodic breathing on survival in
patients with other forms of cardiomyopathies
and/or in atrial fibrillation.
We did not conduct a formal polysomnographic study, because the sleep study was performed by means of an unattended system that only provided information about the respiratory pattern and oxygen saturation. Thus, no information was available about sleep architecture and arousals. However, the characteristics of sleep were not the aim of the study, and a high correlation between the apneic events and arousals has already been documented.3 We used the unattended system because of its easy applicability, and the results of our study indicate that this form of sleep study should be performed in all CHF patients (particularly among those with an enlarged LA) to identify which of them have nocturnal breathing disorders.
The use of a single sleep study to assess prognosis has some
limitations because the breathing pattern may change during the
follow-up period, mainly because of the long-term effect of medical
therapy for heart failure. Despite the dynamic nature of periodic
breathing, our data indicate that patients with AHI 30/h should be
considered at higher risk for adverse outcome whenever this breathing
disorder is documented. Serial follow-up sleep examinations are needed
to provide further insights into the complex breathing dynamics during
sleep and to investigate whether a reversible respiratory disorder with
long-term medical therapy for heart failure or with specific treatment
for CSR (continuous positive airway pressure or oxygen supplements) may
predict (or be associated with) a more favorable prognosis.
Conclusions
The AHI is a powerful independent predictor of poor prognosis in
clinically stable patients with moderate to severe CHF. The presence of
a high AHI (30/h) as an expression of severe breathing disorder adds
prognostic information compared with other clinical,
echocardiographic, and autonomic data, and it
identifies patients at very high risk for subsequent cardiac death.
Because breathing disorders are generally underdiagnosed in the CHF population, our results indicate that more attention should be devoted to their diagnosis in this setting.
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Acknowledgments |
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This study was supported by grant Ricerca Corrente 1995/1996 from the Ministero della Sanità, Rome, Italy, and the Salvatore Maugeri Foundation, Pavia, Italy. We are grateful to Rosemary Allpress for English-language assistance in preparation of the manuscript and to Andrea De Gaetano for statistical consultation.
Received September 1, 1998; revision received November 18, 1998; accepted December 17, 1998.
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A. Giannoni, M. Emdin, F. Bramanti, G. Iudice, D. P. Francis, A. Barsotti, M. Piepoli, and C. Passino Combined increased chemosensitivity to hypoxia and hypercapnia as a prognosticator in heart failure. J. Am. Coll. Cardiol., May 26, 2009; 53(21): 1975 - 1980. [Abstract] [Full Text] [PDF]
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D Yumino, H Wang, J S Floras, G E Newton, S Mak, P Ruttanaumpawan, J D Parker, and T D Bradley Relationship between sleep apnoea and mortality in patients with ischaemic heart failure Heart, May 1, 2009; 95(10): 819 - 824. [Abstract] [Full Text] [PDF]
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 L. Luthje, B. Renner, R. Kessels, D. Vollmann, T. Raupach, B. Gerritse, S. Tasci, J. O. Schwab, M. Zabel, D. Zenker, et al. Cardiac resynchronization therapy and atrial overdrive pacing for the treatment of central sleep apnoea Eur J Heart Fail, March 1, 2009; 11(3): 273 - 280. [Abstract] [Full Text] [PDF]
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G. D. Pinna, R. Maestri, A. Mortara, P. Johnson, D. Andrews, P. Ponikowski, T. Witkowski, E. Robbi, M. T. La Rovere, and P. Sleight Pathophysiological and clinical relevance of simplified monitoring of nocturnal breathing disorders in heart failure patients Eur J Heart Fail, March 1, 2009; 11(3): 264 - 272. [Abstract] [Full Text] [PDF]
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 V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al. Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) Circulation, September 2, 2008; 118(10): 1080 - 1111. [Full Text] [PDF]
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V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al. Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) J. Am. Coll. Cardiol., August 19, 2008; 52(8): 686 - 717. [Full Text] [PDF]
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M. Arzt, R. Wensel, S. Montalvan, T. Schichtl, S. Schroll, S. Budweiser, F. C. Blumberg, G. A. J. Riegger, and M. Pfeifer Effects of Dynamic Bilevel Positive Airway Pressure Support on Central Sleep Apnea in Men With Heart Failure Chest, July 1, 2008; 134(1): 61 - 66. [Abstract] [Full Text] [PDF]
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T. Kara, M. Novak, J. Nykodym, K. A. Bybee, J. Meluzin, M. Orban, Z. Novakova, J. Lipoldova, D. L. Hayes, M. Soucek, et al. Short-term Effects of Cardiac Resynchronization Therapy on Sleep-Disordered Breathing in Patients With Systolic Heart Failure Chest, July 1, 2008; 134(1): 87 - 93. [Abstract] [Full Text] [PDF]
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 C. H. Manisty, K. Willson, J. E. R. Davies, Z. I. Whinnett, R. Baruah, Y. Mebrate, P. Kanagaratnam, N. S. Peters, A. D. Hughes, J. Mayet, et al. Induction of oscillatory ventilation pattern using dynamic modulation of heart rate through a pacemaker Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R219 - R227. [Abstract] [Full Text] [PDF]
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A. Garcia-Touchard, V. K. Somers, L. J. Olson, and S. M. Caples Central Sleep Apnea: Implications for Congestive Heart Failure Chest, June 1, 2008; 133(6): 1495 - 1504. [Abstract] [Full Text] [PDF]
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 D. Yumino and T. D. Bradley Central Sleep Apnea and Cheyne-Stokes Respiration Proceedings of the ATS, February 15, 2008; 5(2): 226 - 236. [Abstract] [Full Text] [PDF]
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L. J. Olson, A. M. Arruda-Olson, V. K. Somers, C. G. Scott, and B. D. Johnson Exercise Oscillatory Ventilation*: Instability of Breathing Control Associated With Advanced Heart Failure Chest, February 1, 2008; 133(2): 474 - 481. [Abstract] [Full Text] [PDF]
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 K. A. Franklin From the author Eur. Respir. J., November 1, 2007; 30(5): 1023 - 1024. [Full Text] [PDF]
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T. Brack, I. Thuer, C. F. Clarenbach, O. Senn, G. Noll, E. W. Russi, and K. E. Bloch Daytime Cheyne-Stokes Respiration in Ambulatory Patients With Severe Congestive Heart Failure Is Associated With Increased Mortality Chest, November 1, 2007; 132(5): 1463 - 1471. [Abstract] [Full Text] [PDF]
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A. Rossi, M. Cicoira, S. Bonapace, G. Golia, L. Zanolla, L. Franceschini, and C. Vassanelli Left atrial volume provides independent and incremental information compared with exercise tolerance parameters in patients with heart failure and left ventricular systolic dysfunction Heart, November 1, 2007; 93(11): 1420 - 1425. [Abstract] [Full Text] [PDF]
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M. T. La Rovere, G. D. Pinna, R. Maestri, E. Robbi, A. Mortara, F. Fanfulla, O. Febo, and P. Sleight Clinical relevance of short-term day-time breathing disorders in chronic heart failure patients Eur J Heart Fail, September 1, 2007; 9(9): 949 - 954. [Abstract] [Full Text] [PDF]
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O. Oldenburg, L. Faber, J. Vogt, A. Dorszewski, F. Szabados, D. Horstkotte, and B. Lamp Influence of cardiac resynchronisation therapy on different types of sleep disordered breathing Eur J Heart Fail, August 1, 2007; 9(8): 820 - 826. [Abstract] [Full Text] [PDF]
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L. J. Olson and V. K. Somers Treating Central Sleep Apnea in Heart Failure: Outcomes Revisited Circulation, June 26, 2007; 115(25): 3140 - 3142. [Full Text] [PDF]
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M. Arzt, J. S. Floras, A. G. Logan, R. J. Kimoff, F. Series, D. Morrison, K. Ferguson, I. Belenkie, M. Pfeifer, J. Fleetham, et al. 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, June 26, 2007; 115(25): 3173 - 3180. [Abstract] [Full Text] [PDF]
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R. Schulz, A. Blau, J. Borgel, H. W. Duchna, I. Fietze, I. Koper, R. Prenzel, S. Schadlich, J. Schmitt, S. Tasci, et al. Sleep apnoea in heart failure Eur. Respir. J., June 1, 2007; 29(6): 1201 - 1205. [Abstract] [Full Text] [PDF]
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A. Noda, H. Izawa, H. Asano, S. Nakata, A. Hirashiki, Y. Murase, S. Iino, K. Nagata, T. Murohara, Y. Koike, et al. Beneficial Effect of Bilevel Positive Airway Pressure on Left Ventricular Function in Ambulatory Patients With Idiopathic Dilated Cardiomyopathy and Central Sleep Apnea-Hypopnea: A Preliminary Study Chest, June 1, 2007; 131(6): 1694 - 1701. [Abstract] [Full Text] [PDF]
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S. Javaheri, R. Shukla, H. Zeigler, and L. Wexler Central Sleep Apnea, Right Ventricular Dysfunction, and Low Diastolic Blood Pressure Are Predictors of Mortality in Systolic Heart Failure J. Am. Coll. Cardiol., May 22, 2007; 49(20): 2028 - 2034. [Abstract] [Full Text] [PDF]
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H. Wang, J. D. Parker, G. E. Newton, J. S. Floras, S. Mak, K.-L. Chiu, P. Ruttanaumpawan, G. Tomlinson, and T. D. Bradley Influence of Obstructive Sleep Apnea on Mortality in Patients With Heart Failure J. Am. Coll. Cardiol., April 17, 2007; 49(15): 1625 - 1631. [Abstract] [Full Text] [PDF]
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A. Vazir, P.C. Hastings, M. Dayer, H.F. McIntyre, M.Y. Henein, P.A. Poole-Wilson, M.R. Cowie, M.J. Morrell, and A.K. Simonds 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, March 1, 2007; 9(3): 243 - 250. [Abstract] [Full Text] [PDF]
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O. Oldenburg, B. Lamp, L. Faber, H. Teschler, D. Horstkotte, and V. Topfer Sleep-disordered breathing in patients with symptomatic heart failure A contemporary study of prevalence in and characteristics of 700 patients Eur J Heart Fail, March 1, 2007; 9(3): 251 - 257. [Abstract] [Full Text] [PDF]
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 C. H. Manisty, K. Willson, R. Wensel, Z. I. Whinnett, J. E. Davies, W. L. G. Oldfield, J. Mayet, and D. P. Francis Development of respiratory control instability in heart failure: a novel approach to dissect the pathophysiological mechanisms J. Physiol., November 15, 2006; 577(1): 387 - 401. [Abstract] [Full Text] [PDF]
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O. Oldenburg, B. Lamp, and D. Horstkotte Cardiorespiratory screening for sleep-disordered breathing. Eur. Respir. J., November 1, 2006; 28(5): 1065 - 1067. [Full Text] [PDF]
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S. Ferreira, J. Winck, P. Bettencourt, and F. Rocha-Goncalves Heart failure and sleep apnoea: To sleep perchance to dream Eur J Heart Fail, May 1, 2006; 8(3): 227 - 236. [Abstract] [Full Text] [PDF]
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P. C. Hastings, A. Vazir, D. M. O'Driscoll, M. J. Morrell, and A. K. Simonds Symptom burden of sleep-disordered breathing in mild-to-moderate congestive heart failure patients. Eur. Respir. J., April 1, 2006; 27(4): 748 - 755. [Abstract] [Full Text] [PDF]
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C Philippe, M Stoica-Herman, X Drouot, B Raffestin, P Escourrou, L Hittinger, P-L Michel, S Rouault, and M-P d'Ortho Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period Heart, March 1, 2006; 92(3): 337 - 342. [Abstract] [Full Text] [PDF]
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J. P. Ribeiro Periodic Breathing in Heart Failure: Bridging the Gap Between the Sleep Laboratory and the Exercise Laboratory Circulation, January 3, 2006; 113(1): 9 - 10. [Full Text] [PDF]
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S. M. Caples, R. Wolk, and V. K. Somers Influence of cardiac function and failure on sleep-disordered breathing: evidence for a causative role J Appl Physiol, December 1, 2005; 99(6): 2433 - 2439. [Abstract] [Full Text] [PDF]
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 T. D. Bradley, A. G. Logan, R. J. Kimoff, F. Series, D. Morrison, K. Ferguson, I. Belenkie, M. Pfeifer, J. Fleetham, P. Hanly, et al. Continuous Positive Airway Pressure for Central Sleep Apnea and Heart Failure. N. Engl. J. Med., November 10, 2005; 353(19): 2025 - 2033. [Abstract] [Full Text] [PDF]
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V. K. Somers Sleep -- A New Cardiovascular Frontier N. Engl. J. Med., November 10, 2005; 353(19): 2070 - 2073. [Full Text] [PDF]
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A D Staniforth, S C Sporton, M J Early, J A Wedzicha, A W Nathan, and R J Schilling Ventricular arrhythmia, Cheyne-Stokes respiration, and death: observations from patients with defibrillators Heart, November 1, 2005; 91(11): 1418 - 1422. [Abstract] [Full Text] [PDF]
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L J Cormican and A Williams Sleep disordered breathing and its treatment in congestive heart failure Heart, October 1, 2005; 91(10): 1265 - 1270. [Abstract] [Full Text] [PDF]
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J. M. Legramante and A. Galante Sleep and Hypertension: A Challenge for the Autonomic Regulation of the Cardiovascular System Circulation, August 9, 2005; 112(6): 786 - 788. [Full Text] [PDF]
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T. Brack, A. Jubran, F. Laghi, and M. J. Tobin Fluctuations in End-Expiratory Lung Volume during Cheyne-Stokes Respiration Am. J. Respir. Crit. Care Med., June 15, 2005; 171(12): 1408 - 1413. [Abstract] [Full Text] [PDF]
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E. Skobel, C. Norra, A. Sinha, C. Breuer, P. Hanrath, and C. Stellbrink Impact of sleep-related breathing disorders on health-related quality of life in patients with chronic heart failure Eur J Heart Fail, June 1, 2005; 7(4): 505 - 511. [Abstract] [Full Text] [PDF]
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F. Series, R. J. Kimoff, D. Morrison, M. H. Leblanc, M. Smilovitch, J. Howlett, A. G. Logan, J. S. Floras, and T. D. Bradley Prospective Evaluation of Nocturnal Oximetry for Detection of Sleep-Related Breathing Disturbances in Patients With Chronic Heart Failure Chest, May 1, 2005; 127(5): 1507 - 1514. [Abstract] [Full Text] [PDF]
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C. Carmona-Bernal, E. Quintana-Gallego, M. Villa-Gil, A. Sanchez-Armengol, A. Martinez-Martinez, and F. Capote Brain Natriuretic Peptide in Patients With Congestive Heart Failure and Central Sleep Apnea Chest, May 1, 2005; 127(5): 1667 - 1673. [Abstract] [Full Text] [PDF]
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M. Arzt, M. Schulz, R. Wensel, S. Montalvan, F. C. Blumberg, G. A. J. Riegger, and M. Pfeifer Nocturnal Continuous Positive Airway Pressure Improves Ventilatory Efficiency During Exercise in Patients With Chronic Heart Failure Chest, March 1, 2005; 127(3): 794 - 802. [Abstract] [Full Text] [PDF]
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C. Stellbrink, E. Skobel, and A.-M. Sinha Cardiac resynchronization therapy, central sleep apnea, and Cheyne-Stokes respiration in chronic heart failure patients: Reply J. Am. Coll. Cardiol., February 15, 2005; 45(4): 633 - 634. [Full Text] [PDF]
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S. Andreas, H. Reiter, L. Luthje, A. Delekat, R. W. Grunewald, G. Hasenfuss, and V. K. Somers Differential Effects of Theophylline on Sympathetic Excitation, Hemodynamics, and Breathing in Congestive Heart Failure Circulation, October 12, 2004; 110(15): 2157 - 2162. [Abstract] [Full Text] [PDF]
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E. Quintana-Gallego, M. Villa-Gil, C. Carmona-Bernal, G. Botebol-Benhamou, A. Martinez-Martinez, A. Sanchez-Armengol, J. Polo-Padillo, and F. Capote Home respiratory polygraphy for diagnosis of sleep-disordered breathing in heart failure Eur. Respir. J., September 1, 2004; 24(3): 443 - 448. [Abstract] [Full Text] [PDF]
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A.-M. Sinha, E. C. Skobel, O.-A. Breithardt, C. Norra, K. U. Markus, C. Breuer, P. Hanrath, and C. Stellbrink Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure J. Am. Coll. Cardiol., July 7, 2004; 44(1): 68 - 71. [Abstract] [Full Text] [PDF]
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H.F. Becker Bigger numbers needed! Eur. Respir. J., May 1, 2004; 23(5): 659 - 660. [Full Text] [PDF]
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T. Roebuck, P. Solin, D.M. Kaye, P. Bergin, M. Bailey, and M.T. Naughton Increased long-term mortality in heart failure due to sleep apnoea is not yet proven Eur. Respir. J., May 1, 2004; 23(5): 735 - 740. [Abstract] [Full Text] [PDF]
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B. K. Gehlbach and E. Geppert The Pulmonary Manifestations of Left Heart Failure Chest, February 1, 2004; 125(2): 669 - 682. [Abstract] [Full Text] [PDF]
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D. D. Sin and G. C. W. Man Cheyne-Stokes Respiration: A Consequence of a Broken Heart? Chest, November 1, 2003; 124(5): 1627 - 1628. [Full Text] [PDF]
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J. C. T. Pepperell, N. A. Maskell, D. R. Jones, B. A. Langford-Wiley, N. Crosthwaite, J. R. Stradling, and R. J. O. Davies A Randomized Controlled Trial of Adaptive Ventilation for Cheyne-Stokes Breathing in Heart Failure Am. J. Respir. Crit. Care Med., November 1, 2003; 168(9): 1109 - 1114. [Abstract] [Full Text] [PDF]
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S. Ancoli-Israel, E. R. DuHamel, C. Stepnowsky, R. Engler, M. Cohen-Zion, and M. Marler The Relationship Between Congestive Heart Failure, Sleep Apnea, and Mortality in Older Men Chest, October 1, 2003; 124(4): 1400 - 1405. [Abstract] [Full Text] [PDF]
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M. Hayashi, K. Fujimoto, K. Urushibata, S.-i. Uchikawa, H. Imamura, and K. Kubo Nocturnal Oxygen Desaturation Correlates With the Severity of Coronary Atherosclerosis in Coronary Artery Disease Chest, September 1, 2003; 124(3): 936 - 941. [Abstract] [Full Text] [PDF]
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 S. Velez-Roa, B. Kojonazarov, A. Ciarka, P. Godart, R. Naeije, V. K. Somers, and P. van de Borne Dobutamine potentiates arterial chemoreflex sensitivity in healthy normal humans Am J Physiol Heart Circ Physiol, August 7, 2003; 285(3): H1356 - H1361. [Abstract] [Full Text] [PDF]
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R. Wolk, T. Kara, and V. K. Somers Sleep-Disordered Breathing and Cardiovascular Disease Circulation, July 8, 2003; 108(1): 9 - 12. [Full Text] [PDF]
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J. J. Leite, A. J. Mansur, H. F. G. de Freitas, P. R. Chizola, E. A. Bocchi, M. Terra-Filho, J. A. Neder, and G. Lorenzi-Filho Periodic breathing during incremental exercise predicts mortality in patients with chronic heart failure evaluated for cardiac transplantation J. Am. Coll. Cardiol., June 18, 2003; 41(12): 2175 - 2181. [Abstract] [Full Text] [PDF]
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T. D. Bradley The ups and downs of periodic breathing: Implications for mortality in heart failure J. Am. Coll. Cardiol., June 18, 2003; 41(12): 2182 - 2184. [Full Text] [PDF]
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R. S. T. Leung, J. S. Floras, G. Lorenzi-Filho, F. Rankin, P. Picton, and T. D. Bradley Influence of Cheyne-Stokes Respiration on Cardiovascular Oscillations in Heart Failure Am. J. Respir. Crit. Care Med., June 1, 2003; 167(11): 1534 - 1539. [Abstract] [Full Text] [PDF]
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J. o-D. L. Lattimore, D. S. Celermajer, and I. Wilcox Obstructive sleep apnea and cardiovascular disease J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1429 - 1437. [Abstract] [Full Text] [PDF]
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M. Arzt, M. Harth, A. Luchner, F. Muders, S. R. Holmer, F. C. Blumberg, G. A.J. Riegger, and M. Pfeifer Enhanced Ventilatory Response to Exercise in Patients With Chronic Heart Failure and Central Sleep Apnea Circulation, April 22, 2003; 107(15): 1998 - 2003. [Abstract] [Full Text] [PDF]
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T. D. Bradley and J. S. Floras Sleep Apnea and Heart Failure: Part II: Central Sleep Apnea Circulation, April 8, 2003; 107(13): 1822 - 1826. [Full Text] [PDF]
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T. D. Bradley and J. S. Floras Sleep Apnea and Heart Failure: Part I: Obstructive Sleep Apnea Circulation, April 1, 2003; 107(12): 1671 - 1678. [Full Text] [PDF]
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D. Mansfield, D. M. Kaye, H. Brunner La Rocca, P. Solin, M. D. Esler, and M. T. Naughton Raised Sympathetic Nerve Activity in Heart Failure and Central Sleep Apnea Is Due to Heart Failure Severity Circulation, March 18, 2003; 107(10): 1396 - 1400. [Abstract] [Full Text] [PDF]
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P. A. Lanfranchi, V. K. Somers, A. Braghiroli, U. Corra, E. Eleuteri, and P. Giannuzzi Central Sleep Apnea in Left Ventricular Dysfunction: Prevalence and Implications for Arrhythmic Risk Circulation, February 11, 2003; 107(5): 727 - 732. [Abstract] [Full Text] [PDF]
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S. Andreas, C. Bingeli, P. Mohacsi, T. F. Luscher, and G. Noll Nasal Oxygen and Muscle Sympathetic Nerve Activity in Heart Failure Chest, February 1, 2003; 123(2): 366 - 371. [Abstract] [Full Text] [PDF]
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A. Koike, N. Shimizu, A. Tajima, T. Aizawa, L. T. Fu, H. Watanabe, and H. Itoh Relation Between Oscillatory Ventilation at Rest Before Cardiopulmonary Exercise Testing and Prognosis in Patients With Left Ventricular Dysfunction Chest, February 1, 2003; 123(2): 372 - 379. [Abstract] [Full Text] [PDF]
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T. Kohnlein, T. Welte, L.B. Tan, and M.W. Elliott Assisted ventilation for heart failure patients with Cheyne-Stokes respiration Eur. Respir. J., October 1, 2002; 20(4): 934 - 941. [Abstract] [Full Text] [PDF]
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A. A. El-Solh, E. Bozkanat, J. Mador, and B. J. B. Grant Association Between Plasma Endothelin-1 Levels and Cheyne-Stokes Respiration in Patients With Congestive Heart Failure* Chest, June 1, 2002; 121(6): 1928 - 1934. [Abstract] [Full Text] [PDF]
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R. Schulz, G. Baseler, H.A. Ghofrani, F. Grimminger, H. Olschewski, and W. Seeger Nocturnal periodic breathing in primary pulmonary hypertension Eur. Respir. J., April 1, 2002; 19(4): 658 - 663. [Abstract] [Full Text] [PDF]
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G. Lorenzi-Filho, E.R. Azevedo, J.D. Parker, and T.D. Bradley Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure Eur. Respir. J., January 1, 2002; 19(1): 37 - 40. [Abstract] [Full Text] [PDF]
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 R. Shabetai Depression and Heart Failure Psychosom Med, January 1, 2002; 64(1): 13 - 14. [Full Text] [PDF]
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R. S. T. LEUNG and T. DOUGLAS BRADLEY Sleep Apnea and Cardiovascular Disease Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2147 - 2165. [Full Text] [PDF]
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A. T. Yan, T. D. Bradley, and P. P. Liu The Role of Continuous Positive Airway Pressure in the Treatment of Congestive Heart Failure Chest, November 1, 2001; 120(5): 1675 - 1685. [Abstract] [Full Text] [PDF]
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H. TESCHLER, J. DOHRING, Y.-M. WANG, and M. BERTHON-JONES Adaptive Pressure Support Servo-Ventilation . A Novel Treatment for Cheyne-Stokes Respiration in Heart Failure Am. J. Respir. Crit. Care Med., August 15, 2001; 164(4): 614 - 619. [Abstract] [Full Text] [PDF]
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G.N. Willson, I. Wilcox, A.J. Piper, W.E. Flynn, M. Norman, R.R. Grunstein, and C.E. Sullivan Noninvasive pressure preset ventilation for the treatment of Cheyne-Stokes respiration during sleep Eur. Respir. J., June 1, 2001; 17(6): 1250 - 1257. [Abstract] [Full Text] [PDF]
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S Heindl, C Dodt, M Krahwinkel, G Hasenfuss, and S Andreas Short term effect of continuous positive airway pressure on muscle sympathetic nerve activity in patients with chronic heart failure Heart, February 1, 2001; 85(2): 185 - 190. [Abstract] [Full Text]
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P. SOLIN, T. ROEBUCK, D. P. JOHNS, E. HAYDN WALTERS, and M. T. NAUGHTON Peripheral and Central Ventilatory Responses in Central Sleep Apnea with and without Congestive Heart Failure Am. J. Respir. Crit. Care Med., December 1, 2000; 162(6): 2194 - 2200. [Abstract] [Full Text]
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 L. L. Clark Perioperative Treatment of Congestive Heart Failure Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2000; 4(4): 223 - 235. [Abstract] [PDF]
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D. P. Francis, K. Willson, L. C. Davies, A. J.S. Coats, and M. Piepoli Quantitative General Theory for Periodic Breathing in Chronic Heart Failure and its Clinical Implications Circulation, October 31, 2000; 102(18): 2214 - 2221. [Abstract] [Full Text] [PDF]
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D. D. Sin, A. G. Logan, F. S. Fitzgerald, P. P. Liu, and T. D. Bradley Effects of Continuous Positive Airway Pressure on Cardiovascular Outcomes in Heart Failure Patients With and Without Cheyne-Stokes Respiration Circulation, July 4, 2000; 102(1): 61 - 66. [Abstract] [Full Text] [PDF]
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 T. D. Bradley Continuous positive airway pressure for congestive heart failure Can. Med. Assoc. J., February 1, 2000; 162(4): 535 - 536. [Full Text] [PDF]
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D. D. SIN, F. FITZGERALD, J. D. PARKER, G. NEWTON, J. S. FLORAS, and T. D. BRADLEY Risk Factors for Central and Obstructive Sleep Apnea in 450 Men And Women with Congestive Heart Failure Am. J. Respir. Crit. Care Med., October 1, 1999; 160(4): 1101 - 1106. [Abstract] [Full Text]
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