Nocturnal Cheyne-Stokes Respiration Research Articles

Implications of revised AASM rules on scoring apneic and hypopneic respiratory events in patients with heart failure with nocturnal Cheyne-Stokes respiration.

This study investigated the implications of the revised scoring rules of the American Academy of Sleep Medicine (AASM) in patients with heart failure (HF) with Cheyne-Stokes respiration (CSR). Ninety-one patients (NYHA ≥II, LVEF ≤45%; age 73.6 ± 11.3years old; 81 male subjects) with documented CSR underwent 8h of cardiorespiratory polygraphy recordings. Those were analyzed by a single scorer strictly applying the 2007 recommended, 2007 alternative, and the 2012 scoring rules. Compared with the AASM 2007 recommended rules, apnea-hypopnea index (AHI) and hypopnea index (HI) increased significantly when the 2007 alternative and 2012 rules were applied (AHI 34.1 ± 13.5/h vs 37.6 ± 13.2/h vs 38.3 ± 13.2/h, respectively; HI 10.2 ± 9.4/h vs 13.7 ± 10.7/h vs 14.4 ± 11.0/h, respectively; all p < 0.001). Duration of CSR increased significantly with the alternate versus recommended 2007 rules (182.2 ± 117.0 vs 170.1 ± 115.0min; p ≤ 0.001); there was a significant decrease in CSR duration for the 2012 versus 2007 alternative rules (182.2 ± 117.0 vs 166.7 ± 115.4min; p ≤ 0.001). AHI was higher using the AASM 2012 scoring rules due to a less strict definition of hypopnea. Data on the prognostic effects of CSR in patients with HF and the benefits of treatment are mostly based on the AASM 2007 recommended rules, so differences between these and the newer version need to be taken into account.

Validation of blood pressure monitoring using pulse transit time in heart failure patients with Cheyne–Stokes respiration undergoing adaptive servoventilation therapy

Using pulse transit time (PTT) and an ECG appears to be a promising alternative for invasive or noninvasive monitoring of blood pressure (BP). This study assessed the validity of PTT for BP monitoring in clinical practice. Twenty-nine patients with chronic heart failure (HF; 27 male, 70.5 ± 9.9 years) and nocturnal Cheyne-Stokes respiration were noninvasively ventilated for one hour using adaptive servoventilation (ASV) therapy (PaceWave, ResMed). BP was measured using two devices (oscillometrically via Task Force Monitor, CNSystems and PTT via SOMNOscreen, Somnomedics) at least every 7 min for 30 min before, during, and after ASV. Mean systolic BP was 118.1 ± 14.4 mmHg vs. 115.9 ± 14.1 mmHg for oscillometric method vs PTT, respectively. Corresponding values for diastolic BP were 72.3 ± 10.3 mmHg and 69.4 ± 11.1 mmHg. While clinically comparable, differences between the two methods were statistically significant (p < 0.05). The difference between the two methods showed an increasing trend over time. A total of 18.5 % of PTT-based measurements could not be analyzed. The direction of a change in BP was opposite for PTT vs oscillometry for 17.0 % and 32.8 % of systolic and diastolic BP measurements, respectively. When monitoring BP in HF patients, overall BP monitoring using PTT is comparable to oscillometry for a period of 2 h (including a 1-h ASV phase). However, PTT shows a tendency to underestimate BP over time and during ASV.

Correlations of physiological activities in nocturnal Cheyne-Stokes respiration.

We have conducted a power–spectrum–density (PSD) analysis of the distinct sleep stages of a previously diagnosed nocturnal Cheyne–Stokes respiration patient (NCSR) and studied the correlations of different physiological activities. This is the first study where the correlations were analyzed separately for different sleep stages and the influence of arousals was completely eliminated. Mathematical analysis of the polysomnographical records revealed clear indicators of the disorder in the form of large peaks in a very-low frequency range of f ≈ 0.02 Hz. We have shown existence of the significant entrainment of the cerebral and cardiac activities with respiration during different stages of sleep in the patient. The entrainment is highly pronounced in light (stage 2) and deep (stage 3) sleep, but is significantly less pronounced in rapid eye movement sleep. A correlation functions analysis revealed that the correlations between the central activities and respiration attain maximum at negative lag times. Lagging of respiration behind the central activities favors the central hypothesis of generation of NCSR. On the basis of comparison of PSD plots of a NCSR patient and a healthy patient we speculate that the vasomotor center of a NCSR patient assumes the control function in the respiratory control system. Clinical applications of the findings of the study may lead to the development of novel low-cost methods of diagnostic of NCSR based on easy-to-obtain electrocardiogram or electroencephalogram records of patients and emergence of some forms of “substitution therapy”.

Long-term assessment of nocturnal Cheyne-Stokes respiration in patients with heart failure

Cheyne-Stokes respiration (CSR) is a known controversial prognostic marker in patients with heart failure (HF). Little is known, moreover, about the development and progress of CSR in such patients. The CSR progress over time may be indicative for clinical deterioration in patients with HF disease Prospective cohort sleep studies, with algorithm-based analyses of continuously or periodically monitored changes over time using standard pulse oximeter. Home testing for 4 months of patients recruited from the cardiology department of a large community medical center in Haifa, Israel. A total of 36 patients, 31 men and five women, aged between 50 and 74 years, with symptomatic chronic HF. Out of the 36 patients, 15 (42%) patients were found to have CSR. The CSR cycle length was chosen as the characteristic parameter which determines the periodicity of the event and its length. Analyses of CSR cycle length and duration in the 15 patients showed changes over time in the length of the CSR event only in patient with New York Heart Association (NYHA) 4 classification. Nocturnal CSR in patients with HF show small variations over time in the prevalence or duration of the cycle length and could be a marker for entering stage 4 or deterioration in the NYHA class of HF patient. Moreover, it may take years for HF patients to develop CSR or to increase the length of the cycle length of existing CSR, if they develop it at all.

Adaptive servoventilation in diastolic heart failure and Cheyne-Stokes respiration

A high prevalence of nocturnal Cheyne-Stokes respiration (CSR) has been documented in patients with heart failure with normal left ventricular ejection fraction (HFNEF). The aim of the present study was to investigate the effects of adaptive servoventilation (ASV) for treatment of CSR in these patients. In 60 patients with HFNEF, defined according to current European Society of Cardiology guidelines, CSR was documented by polysomnography (apnoea/hypopnoea index (AHI) of >15 events x h(-1)). ASV treatment was offered to all patients; 21 initially rejected treatment, withdrew from treatment or presented noncompliant during follow-up (controls), whereas ongoing ASV therapy was initiated in 39 patients (ASV group). Echocardiography, cardiopulmonary exercise testing and measurement of N-terminal-pro-brain natriuretic peptide were performed at baseline and follow-up (11.6+/-3 months). ASV therapy led to a significant reduction in AHI, longest apnoea and hypopnoea length, maximum and mean oxygen desaturation by pulse oximetry, percentage of study time with an oxygen saturation of <90% and arousal index. In addition, significant positive effects could be confirmed on absolute and predicted peak oxygen consumption, oxygen consumption at the individual aerobic-anaerobic threshold, oxygen pulse, as well as left atrial size, and transmitral flow patterns (mean early diastolic lengthening velocity and the ratio of peak early Doppler mitral inflow velocity to this lengthening velocity). ASV effectively attenuates CSR in patients with HFNEF and improves heart failure symptoms and cardiac function. Whether or not this is accompanied by an improved prognosis remains to be determined.

Treating Central Sleep Apnea in Heart Failure

A recent enhanced appreciation of sleep–cardiovascular interactions, particularly in patients with congestive heart failure (CHF), has prompted careful consideration of the relevance of sleep-disordered breathing to CHF pathophysiology, progression, and treatment.1 Sleep-disordered breathing may be broadly classified as either obstructive sleep apnea (OSA) or central sleep apnea (CSA).1 The former is characterized by repetitive collapse of the upper airway, whereas in patients with CHF, the latter is most often due to periodic alternation of diminished ventilatory drive and compensatory hyperventilation typical of Cheyne-Stokes respiration (Figure 1). CSA is likely a consequence rather than a cause of CHF. Although the mechanisms that underlie CSA/Cheyne-Stokes respiration in patients with CHF are not well understood, pulmonary congestion with increased lung J-receptor stimulation and greater chemosensitivity may play a role in the genesis of the periodic breathing that characterizes this disorder.1,2 Figure 1. Ventilation during sleep from a patient with CHF and CSA. The ventilatory pattern is characteristic of Cheyne-Stokes respiration: apnea followed by crescendo-decrescendo breathing followed by apnea. The cycle may be repeated throughout sleep. Article p 3173 Of 5 million North Americans with CHF, an estimated 50% may have coexistent sleep apnea. Although the prevalence of OSA is much higher than CSA in the general population,3 it appears that this relationship may be reversed among patients with systolic heart failure. Case series have reported frequencies of CSA exceeding 40% for stable, ambulatory patients with CHF in a ratio >2:1 relative to the frequency of OSA. Indeed, the frequency of OSA in these same series was similar to that observed in the general population, whereas the frequency of CSA was strikingly higher.4,5 Furthermore, in patients with CHF, CSA has been associated with increased morbidity and mortality,5–7 increased neurohormonal activation,1 increased ventricular arrhythmia,8 decreased exercise capacity, …

Syndrome d'apnées du sommeil et insuffisance cardiaque

More than half of all patients with stable heart failure are affected by sleep apnea syndrome. The mechanism of apnea may be either obstructive, by collapse of the upper airways, or central with nocturnal Cheyne-Stokes respiration. Changes in intrathoracic pressure, awakening and hypoxemia all lead to an increase in left ventricular afterload and to sympathetic activation, which can aggravate heart failure and prognosis. Treatment with positive pressure ventilation improves symptoms as well as cardiac function and prognosis. Sleep respiratory disorders are underdiagnosed and undertreated in patients with stable heart failure. To improve management of sleep apnea, patients with stable heart failure should be screened with small outpatient oximeters.

Sleep and Hypertension

Even though sleep is widely considered to be a restorative and refreshing process, it is characterized by complex activity of the cardiovascular autonomic mechanisms and by relevant changes of arterial pressure and heart rate. It has been widely reported that fluctuations and variability of cortical and visceral activities involve a differential autonomic regulation of the cardiovascular system in relationship to different sleep cycles. During non–rapid eye movement (REM) sleep, arterial pressure and heart rate tend to decrease, whereas periods of relative hypertension and tachycardia characterize REM periods. With regard to the cardiovascular autonomic modulation, non-REM sleep is characterized by a vagal predominance, whereas during REM sleep, a relative increase in sympathetic activity is demonstrated by an increased sympathetic outflow to muscle blood vessels.1–3 See p 849 Therefore, this continuous cycling of non-REM and REM phases, with the consequent cardiovascular autonomic changes, makes sleep a period of considerable physiological turbulence characterized by sudden and abrupt blood pressure and heart rate changes. This cardiovascular instability has stimulated the investigation of the neural mechanisms involved in maintaining the cardiovascular homeostasis during the different sleep phases. The first pivotal study conducted with the Oxford technique in normotensive and hypertensive subjects4 clearly showed that changes in baroreflex function investigated by quantifying the reflex RR interval lengthening in response to a pharmacologically induced increase in systolic blood pressure (obtained through intravenous injection of phenylephrine), occurred ongoing from wakefulness to sleep. These changes consisted of an increase in the reflex sensitivity and of a resetting, moving the operating point of the reflex toward lower blood pressure values.4 In the past few years, this issue has been further investigated because it is now possible to investigate the arterial baroreflex function by analyzing the correlated blood pressure and spontaneous heart rate …

Relation Between Oscillatory Ventilation at Rest Before Cardiopulmonary Exercise Testing and Prognosis in Patients With Left Ventricular Dysfunction

Although nocturnal Cheyne-Stokes respiration alternating between hyperpnea and hypopnea has been considered a sign of severe heart failure, the clinical status of cardiac patients who exhibit oscillatory ventilation during wakefulness has not been clarified. This study was carried out to determine the relation between oscillatory ventilation during wakefulness and exercise capacity in patients with chronic heart disease. We also evaluated retrospectively whether the presence of oscillatory ventilation influences the long-term prognosis in these patients. A total of 164 patients with left ventricular dysfunction performed a symptom-limited incremental exercise test. Respiratory gas exchange was measured on a breath-by-breath basis throughout the test. Oscillatory ventilation was defined when clear ventilatory oscillation of at least two consecutive cycles was identified at rest before exercise testing and the difference between the peak and nadir of oscillating ventilation was > 30% of the mean value of ventilation. Oscillatory ventilation was noted in 45 of 164 cardiac patients (27%), and the magnitude (mean +/- SD) of oscillation in these patients was 45.5 +/- 16.9%. Patients with oscillatory ventilation had significantly lower left ventricular ejection fraction than those without it (40.7 +/- 12.7% vs 44.9 +/- 11.6%, p < 0.05). However, parameters of exercise capacity such as the peak oxygen uptake (O(2)), the slope of the increase in O(2) relative to the increase in work rate (DeltaO(2)/DeltaWR), and the ratio of the increase in ventilation to the increase in carbon dioxide output (DeltaE/DeltaCO(2)) were not significantly different between the two groups. The mortality rate during 1,797 +/- 599 days of follow-up did not differ between the groups (p = 0.65). Oscillatory ventilation present at rest before cardiopulmonary exercise testing is not significantly related to the peak O(2), DeltaO(2)/DeltaWR, DeltaE/DeltaCO(2), or prognosis in patients with left ventricular dysfunction.

Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure.

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. 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 V(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 (chi2, 10.4; P<0.01), followed by left atrial area (chi2, 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. 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.

Nasal Continuous Positive Airway Pressure in Chronic Heart Failure with Sleep-disordered Breathing

Nasal continuous positive airway pressure (NCPAP) has been reported to improve daytime symptoms in patients with sleep disordered breathing due to heart failure. To examine this in a controlled manner, eight men with stable chronic heart failure (mean left ventricular ejection fraction 18% and mean frusemide dose 160 mg) were entered into a controlled trial of domiciliary nocturnal NCPAP. At polysomnography (with sleep apnea quantified as the number of > 4% dips in arterial saturation per hour), seven had nocturnal Cheyne-Stokes respiration (SaO2 dip rate 3 to 27/hr), and one both central and obstructive apneas (SaO2 dip rate 8/hr). After 2 wk nocturnal domiciliary NCPAP at < 1.5 cm H2O (placebo) and 7.5 cm H2O (active) in random order, bicycle exercise tolerance and heart failure symptoms (modified Likert questionnaire) were assessed by an observer unaware of the patients' NCPAP status. Pulse oximetry (all subjects) and radionuclide estimated left ventricular ejection fraction (three subjects) were also measured at the end of each period. Two subjects withdrew from the study because of worsening heart failure during active NCPAP (7.5 cm H2O), and one of these subjects died. In the remaining six subjects exercise tolerance, symptom scores, and the severity of sleep apnea were similar on active NCPAP compared with placebo. When it was measured, resting left ventricular ejection fraction was lower on active therapy than on placebo. These data exclude a 25% improvement in exercise tolerance with 95% confidence and suggest that a study of 160 subjects would be needed to exclude a 10% change in symptom score.(ABSTRACT TRUNCATED AT 250 WORDS)