Cheyne-stokes respiration and prognosis in congestive heart failure

doi:10.1016/S0002-9149(96)00608-X

The American Journal of Cardiology

Volume 78, Issue 11, 1 December 1996, Pages 1260-1264

https://doi.org/10.1016/S0002-9149(96)00608-X Get rights and content

Abstract

Patients with congestive heart failure (CHF) frequently demonstrate Cheyne-Stokes respiration (CSR) with repetitive arousals and oxygen desaturations during sleep. Although it was evident from early publications that CSR during the daytime is a poor prognostic indicator in patients with CHF, it was speculated recently that CSR occurring during sleep could impede left ventricular function and even survival. We therefore followed up 36 patients with CHF and a left ventricular ejection fraction ≤40% who underwent a sleep study at our institution. The patients showed a reduced ejection fraction (20 ± 8%) and CSR with a median of 19% of total sleep time (lower and upper quartiles 9% and 56%). In 12 ± 9% of their time in bed, the arterial oxygen saturation was < 90%. No patient was lost to follow-up, which lasted for 32 ± 15 months (range 11 to 53). One-year survival was 86 ± 6%, and 2-year survival was 66 ± 8%. Univariate comparisons for survival between groups stratified by the amount of CSR revealed no significant difference (log rank test, p = 0.84). However, the 20 patients with a left ventricular ejection fraction < 20% had a shorter mean survival time than patients with an ejection fraction ≥20% (9.5 vs 28.3 months; log rank test, p = 0.013). Two patients with CSR during the daytime died within 1 month. No other patient had CSR during the daytime, and only 1 patient without daytime CSR died within 1 month (chi-square test, p < 0.001). Higher age, reduced carbon dioxide end-tidal partial pressure, and increased transit time were found to be significantly related to the amount of nocturnal CSR. In conclusion, CSR occurring during sleep has no important prognostic impact in patients with CHF, but CSR present during the daytime suggests a high likelihood of dying within a few months.

References (33)

R Hoffman et al.
Cheyne-Stokes respiration in patients recovering from acute cardiogenic pulmonary edema
Chest
(1990)
GC Butler et al.
Continuous positive airway pressure increases heart rate variability in congestive heart failure
J Am Coll Cardiol
(1995)
S Andreas et al.
Improvement of exercise capacity with treatment of Cheyne-Stokes respiration in patients with congestive heart failure
J Am Coll Cardiol
(1996)
DM Kaye et al.
Adverse consequences of high sympathetic nervous activity in the failing heart
J Am Coll Cardiol
(1995)
TG DiSalvo et al.
Preserved right ventricular ejection fraction predicts exercise capacity and survival in advanced heart failure
J Am Coll Cardiol
(1995)
P Hanly et al.
Pathogenesis of Cheyne-Stokes respiration in patients with congestive heart failure
Chest
(1993)
H Feld et al.
A cyclic breathing pattern in patients with poor left ventricular function and compensated heart failure: a mild form of Cheyne-Stokes respiration?
J Am Coll Cardiol
(1993)
HR Figulla et al.
Myocardial enterovirus infection with left ventricular dysfunction: a benign disease compared with idiopathic dilated cardiomyopathy
J Am Coll Cardiol
(1995)
LJ Findley et al.
Cheyne-Stokes respiration during sleep in patients with left ventricular heart failure
South Med J
(1985)
PJ Hanly et al.
Respiration and abnormal sleep in patients with congestive heart failure
Chest
(1989)

S Javaheri et al.

Occult sleep-disordered breathing in stable congestive heart failure

Ann Intern Med

(1995)

J Cheyne

A case of apoplexy, in which the fleshy part of the heart was converted into fat

Dublin Hospital Report

(1818)

W Stokes

The Disease of the Heart and the Aorta

MH Kryger

Sleep and heart failure

Eur Respir J

(1990)

VK Somers et al.

Sympathetic neural mechanisms in obstructive sleep apnea

J Clin Invest

(1995)

BJ Morgan et al.

Combined hypoxia and hypercapnia evokes long lasting sympathetic activation in humans

J Appl Physiol

(1995)

Cited by (161)

Positive Airway Pressure Therapies in Central Sleep Apnea
2021, Encyclopedia of Respiratory Medicine, Second Edition
Central sleep apnea (CSA) is associated with increased mortality, especially in patients with underlying cardiac diseases. However, optimal treatment of CSA is still under debate. While there is consensus on optimal treatment of any underlying cardio- or cerebrovascular disease, internal or neurologic comorbidities, the impact of positive airway pressure therapy (PAP) is less clear. Continuous, automatic and bilevel PAP have been shown to reduce CSA by 50%. Adaptive servoventilation is the optimal algorithm to normalize central breathing disturbances including periodic breathing. For today, it should be reserved to symptomatic patients with a left ventricular ejection fraction ≥ 45% if CSA is predominant.
Exercise oscillatory ventilation in heart failure
2016, International Journal of Cardiology
Ventilation inefficiency has become a matter of interest for heart failure (HF) specialists, the most remarkable being exertional oscillatory ventilation (EOV). EOV is an abnormal ventilatory phenomenon, originally described as anecdotal, but now considered a marker of disease severity and worst prognosis in HF. EOV is a cyclic fluctuation of minute ventilation (VE) and expired gas kinetics occurring during exercise: it is a slow, prominent, consistent rather than random, fluctuation in VE that may be evanescent or transient and can follow several distinct patterns. In contrast to the periodic breathing observed in Cheyne–Stokes respiration and central sleep apnea, the gradual increase and decrease in minute ventilation (VE) are not spaced by periods of apnea. This review will discuss EOV in HF and the overlap with Cheyne–Stokes respiration.
A novel therapeutic approach for central sleep apnea: Phrenic nerve stimulation by the remedē® System
2016, International Journal of Cardiology
Citation Excerpt :
Notably CSA is more prevalent in HF than in any other pathological condition due to the pathogenesis of this type of SDB. Furthermore, in HF, CSA is associated with a higher degree of mortality than OSA [4,5]. Central sleep apnea is characterized by temporary lapses of central respiratory drive, resulting in cessation of diaphragmatic muscle activity and airflow.
Central sleep apnea is a devastating disease which occurs in approximately 40% of patients with heart failure as well as patients with a history of stroke, opioid use and neurological conditions. It is associated with increased morbidity and mortality in heart failure likely due to the recurrent episodes of hypoxia and nor-epinephrine release. There have historically been few therapeutic options; positive airway pressure therapies have been the most common treatment to date. However, the adoption of positive airway pressure therapies has been limited due to poor patient adherence and acceptance and recent evidence of increased cardiovascular mortality in low ejection fraction heart failure patients with CSA. The remedē® System, utilizing transvenous stimulation of the phrenic nerve, offers a novel physiologic approach to therapy that eliminates the need for positive airway pressure and patient adherence. Studies have shown that this therapy improves sleep, oxygenation, and quality of life and ongoing trials are expected to give additional randomized data to support the therapeutic benefit of the remedē® System.
Current treatment approaches and trials in central sleep apnea
2016, International Journal of Cardiology
Central sleep apnea (CSA) is one of the most common comorbidities in patients with heart failure with reduced ejection fraction and is associated with negative consequences. Despite several recent advances, there are currently no widely accepted therapies for CSA. In this review we will discuss available therapies for CSA and review the published trials addressing treatment of CSA in HFrEF patients.
Epidemiology of central sleep apnoea in heart failure
2016, International Journal of Cardiology
Central sleep apnoea occurs in about a third of patients with reduced systolic heart failure and is a marker of increased mortality. Such patients usually are older males with advanced heart failure (i.e., high pulmonary wedge pressure), often in atrial fibrillation, with evidence of hyperventilation (i.e., low PaCO₂) in the absence of hypoxemia. Characteristically, ventilation waxes and wanes in a sinusoidal pattern, with mild hypoxemia, occurring in the lighter levels of sleep usually when supine. Snoring may also occur in central sleep apnoea, often at the peak of hyperventilation, sometimes contributing to the confusion or overlap with obstructive sleep apnoea. Central sleep apnoea is associated with orthopnoea, paroxysmal nocturnal dyspnoea and an oscillatory respiratory pattern with an incremental cardiopulmonary exercise study. Importantly, heart failure therapies (e.g., afterload reduction, diuresis, pacemakers, transplantation) attenuate central sleep apnoea. Night to night variability in severity of central sleep apnoea may occur with changes in patients' posture during sleep (less severe when sleeping on-side or upright).
Apnea-hypopnea and desaturations in heart failure with reduced ejection fraction: Are we aiming at the right target?
2016, International Journal of Cardiology
Citation Excerpt :
Indeed, SDB in HF is associated with myocardial ischemia, LV remodeling [6] and arrhythmias [7,8]. Central SDB appears to constitute an independent risk factor for mortality in patients with systolic HF [9–15] even if this association remains somewhat controversial [16,17]. The severity of SDB in HFrEF patients is commonly assessed by the number of apneas and hypopneas per hour of sleep (apnea–hypopnea index; AHI) and by the presence of Cheyne–Stokes respiration (CSR).
Sleep disordered breathing (SDB) is common in patients with heart failure with reduced ejection fraction (HFrEF). An increased apnea–hypopnea index (AHI) is associated with poor outcomes. We examined whether an analysis of nocturnal desaturations (NDs) can improve the risk stratification.
Three-hundred seventy-six consecutive patients with stable chronic HFrEF and LVEF ≤ 45% were prospectively screened using polygraphy. Sleep apnea (SA) was defined as an AHI ≥ 15. The mean age was 59 ± 13 years, the mean LVEF was 30 ± 6%, and the median AHI was 18 [IQR: 9.33). The composite end-point of death, heart transplantation or LV assistance occurred in 98 patients (26%) within 3 years. Minimal oxygen saturation (MOS) during sleep, the number of desaturations < 90%/h and the time spent with oxygen saturation < 90% were significantly associated with adverse events (adjusted HR 1.25 [1.03–1.52], 1.25 [1.03–1.53], and 1.28 [1.04–1.59]), whereas the AHI was not (1.10 [0.86–1.39]). The best MOS cut-off value for poor outcomes was ≤ 88%. The patients with an MOS ≤ 88% had a significantly higher event rate (31.9%) than those with an MOS > 88% (15.6%; p < 0.01). The risk assessment using an MOS of ≤ 88% in addition to established prognostic markers yielded a net reclassification index (NRI) of nearly 6% and was particularly useful in the subgroup of patients with events (NRI: 8.4%).
In HFrEF patients, ND ≤ 88% appears to be predictive of adverse events, independent of the presence of SA. This suggests that the risk assessment in HFrEF should also include ND in top of AHI.

View all citing articles on Scopus

View full text

Cheyne-stokes respiration and prognosis in congestive heart failure

Abstract

Chest

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Chest

J Am Coll Cardiol

J Am Coll Cardiol

Cheyne-Stokes respiration during sleep in patients with left ventricular heart failure

South Med J

Respiration and abnormal sleep in patients with congestive heart failure

Chest

Occult sleep-disordered breathing in stable congestive heart failure

Ann Intern Med

A case of apoplexy, in which the fleshy part of the heart was converted into fat

Dublin Hospital Report

The Disease of the Heart and the Aorta

Sleep and heart failure

Eur Respir J

Sympathetic neural mechanisms in obstructive sleep apnea

J Clin Invest

Combined hypoxia and hypercapnia evokes long lasting sympathetic activation in humans

J Appl Physiol