The effect of successful heart transplant treatment of heart failure on central sleep apnea

STUDY OBJECTIVE: Central sleep apnea (CSA) associated with Cheyne-Stokes respiration in patients with congestive heart failure (CHF) is thought to be an acquired pattern of respiratory control instability related, at least in part, to elevated sympathetic nervous system activity. The effect of restoring heart function to normal with heart transplantation in patients with CHF and CSA has only been reported within weeks of the transplant and with varying results. The purpose of the study was to evaluate the impact of successful heart transplant on sympathetic nervous system activity and CSA severity in patients with CHF. DESIGN: Controlled prospective trial. SETTING: University hospital. PATIENTS: Twenty-two patients with CHF (13 patients with CSA, and 9 patients with no sleep-disordered breathing [SDB]). INTERVENTIONS AND MEASUREMENTS: Polysomnography, left ventricular ejection fraction (LVEF), and overnight urinary norepinephrine excretion (UNE) were measured before and > 6 months after successful heart transplantation. RESULTS: In the CSA group, there was a fall in apnea-hypopnea index (AHI) [mean +/- SD, 28 +/- 15 to 7 +/- 6/h; p < 0.001] and UNE (48.1 +/- 30.9 to 6.1 +/- 4.8 nmol/mmol creatinine, p < 0.001) associated with normalization of LVEF (19.2 +/- 9.3% to 53.7 +/- 6.1%, p < 0.001) at 13.2 +/- 8.3 months following heart transplantation. Of the CSA group following transplantation, seven patients had no SDB (AHI < 5/h), three patients had persistent CSA (AHI, 12.3 +/- 0.9/h) and four patients acquired obstructive sleep apnea (OSA) [AHI, 11.2 +/- 7.4/h]. In comparison, none of the control group acquired CSA or OSA after transplantation. CONCLUSIONS: We conclude that CSA may persist despite normalization of heart function and sympathetic nerve activity.     

Overnight shift from obstructive to central apneas in patients with heart failure: role of PCO2 and circulatory delay

BACKGROUND: Obstructive (OSA) and central sleep apnea (CSA) can coexist in patients with congestive heart failure (CHF). However, the reason why OSA events occur at one time and CSA events at another has not been determined. We hypothesized that a change in PCO(2) would be associated with an alteration in apnea type: a decrease in PCO(2) should lead to CSA. METHODS AND RESULTS: To test this hypothesis, we evaluated minute ventilation (V(I)), transcutaneous PCO(2) (PtcCO(2)), circulation time, and periodic breathing cycle length during overnight polysomnography in 12 patients with CHF and coexisting OSA and CSA. V(I) was significantly greater (mean+/-SEM, 9.4+/-1.3 versus 8.0+/-0.9 L/min; P:<0.05) and PtcCO(2) was lower (39.4+/-1.0 versus 41.9+/-1.1 mm Hg, P:<0.01) during episodes of CSA than of OSA. These changes were associated with significant lengthening of circulation time (23.6+/-3.7 versus 21.1+/-3.6 seconds, P:<0.01) and periodic breathing cycle length (53.7+/-3.5 versus 49.6+/-2.9 seconds, P:<0.01). In addition, the proportion of obstructive events decreased (from 68.5+/-11.4% to 22.5+/-7.2%, P:<0.001) and of CSA events increased (from 31.5+/-11.4% to 77.5+/-7.2%, P:<0.001) from the first to the last quarter of the night in association with a significant decrease in PtcCO(2) (from 42.6+/-0.9 to 40.8+/-0.9 mm Hg, P:<0.01). CONCLUSIONS: In patients with CHF, the shift from OSA to CSA is associated with a reduction in PCO(2). This appears to be related to an overnight deterioration in cardiac function as suggested by the concurrent lengthening of circulation time. Therefore, in CHF patients, alterations in cardiac function may influence apnea type.     

Variation in severity and type of sleep-disordered breathing throughout 4 nights in patients with heart failure

BACKGROUND: Over 50% of patients with chronic heart failure (CHF) have sleep-disordered breathing (SDB). Any variation in the type of SDB in CHF will have implications for patient management. Currently there is good evidence for treatment of obstructive sleep apnea (OSA) in CHF with continuous positive airway pressure; however, for central sleep apnea (CSA) the treatment is less clear. AIMS: The aim of this study was to investigate the variation in the severity and type of SDB (OSA vs. CSA) throughout 4 consecutive nights in CHF patients with SDB. METHODS: Nineteen male CHF patients (mean+/-sd: age 61+/-9 years; left ventricular ejection fraction: 34+/-10% and percent predicted peak VO2: 67+/-19%) underwent cardiorespiratory monitoring in their own home throughout 4 consecutive nights. RESULTS: There was minimal variation in apnea-hypopnea index (AHI) throughout 4 nights in CHF patients with SDB [intraclass correlation coefficient (95% confidence interval (CI)): 0.97 (95% CI 0.76 and 0.97)]. Eight patients [42% (95% CI 20% and 64%)] demonstrated a shift in the type of their SDB, from CSA to OSA or vice versa; these patients had significantly smaller neck circumference (group mean+/-sd) 42+/-2 vs. 44+/-2 cm; p=0.04), and had significant variation in the central AHI [intraclass correlation coefficient: 0.51 (95% CI 0.16 and 0.85)]. CONCLUSIONS: A single night of cardiorespiratory monitoring is representative of moderate-to-severe SDB in patients with CHF. However, a high proportion of patients shift their type of SDB over 4 nights. These findings may have implications for the management of SDB in CHF.     

Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure

Obstructive sleep apnea (OSA) is highly prevalent among patients with congestive heart failure (CHF) and may contribute to progression of cardiac dysfunction via hypoxia, elevated sympathetic nervous system activity, and systemic hypertension. Our aim was to assess the long-term effect of OSA treatment with nocturnal continuous positive airway pressure (CPAP) on systolic heart function, sympathetic activity, blood pressure, and quality of life in patients with CHF. Fifty-five patients with CHF and OSA were randomized to 3 months of CPAP or control groups. End points were changes in left ventricular ejection fraction, overnight urinary norepinephrine excretion, blood pressure, and quality of life. Nineteen patients in the CPAP group and 21 control subjects completed the study. Compared with the control group, CPAP treatment was associated with significant improvements in left ventricular ejection fraction (delta 1.5 +/- 1.4% vs. 5.0 +/- 1.0%, respectively, p = 0.04), reductions in overnight urinary norepinephrine excretion (delta 1.6 +/- 3.7 vs. -9.9 +/- 3.6 nmol/mmol creatinine, p = 0.036), and improvements in quality of life. There were no significant changes in systemic blood pressure. In conclusion, treatment of OSA among patients with CHF leads to improvement in cardiac function, sympathetic activity, and quality of life.     

The significance and outcome of continuous positive airway pressure-related central sleep apnea during split-night sleep studies

OBJECTIVE: To determine whether central sleep apnea (CSA) occurring during continuous positive airway pressure (CPAP) titration in patients with obstructive sleep apnea (OSA) reflects subclinical congestive heart failure (CHF), and whether these events will improve with CPAP therapy. DESIGN: Cross-sectional analysis of patients with suspected sleep-related breathing disorders referred for split-night polysomnography PATIENTS AND METHODS: Forty-two OSA patients with and without CPAP-related CSA were analyzed. All CSA patients (n = 21) and control subjects (n = 21) underwent echocardiography, pulmonary function testing, and arterial blood gas (ABG) analysis. Repeat polysomnography with CPAP was performed 2 to 3 months after adequate CPAP therapy in CSA group patients. RESULTS: Demographic, Epworth sleepiness scale, pulmonary function test, ABG, and baseline diagnostic polysomnography findings were similar in both groups. There was no difference in the prevalence of subclinical left ventricular systolic dysfunction in the CSA group vs the control group. CSA patients had decreased sleep efficiency (SE), increased sleep stage 1 percentage, sleep stages shift, wake time after sleep onset (WASO), and total arousals compared to control subjects. Twelve of 14 patients (92%) in the CSA group demonstrated complete or near-complete resolution of CSA events on follow-up polysomnography and showed improvement in SE, WASO, and total arousals compared to their baseline study. CONCLUSIONS: CSA events occurring during CPAP titration are transient and self-limited. They may be precipitated by the sleep fragmentation associated with initial CPAP titration and are not associated with an increased prevalence of occult CHF compared to OSA patients without CPAP-related CSA.     

Periodicity of obstructive sleep apnea in patients with and without heart failure

STUDY OBJECTIVE: To determine whether the duration of the apnea-hyperpnea cycle is longer in patients with congestive heart failure (CHF) and obstructive sleep apnea (OSA) than in patients with OSA alone, and whether this is related to prolonged circulation time. DESIGN: Retrospective study. SETTING: Sleep laboratory of a university teaching hospital.Patients and intervention: Male patients with OSA and CHF (n = 22) or without CHF (n = 18) underwent overnight polysomnography. MEASUREMENTS AND RESULTS: Hyperpnea duration, time to peak tidal volume (Vt), and lung-to-ear circulation time (LECT) were measured in all patients. Compared to the non-CHF patients, those with CHF had significantly longer hyperpneas (25.7 +/- 7.8 s vs 17.6 +/- 5.6 s, p < 0.001) and LECT (14.9 +/- 3.4 s vs 9.0 +/- 1.8 s, p < 0.001) [mean +/- SD]. There was also a significant relationship between LECT and hyperpnea duration (r = 0.67, p < 0.001). CONCLUSION: In patients with CHF, prolonged lung-to-chemoreceptor circulation time influences the cycling characteristics of OSA such that it prolongs hyperpnea and sculpts a pattern resembling Cheyne-Stokes respiration. These findings further suggest that the increased tendency to periodic breathing in CHF may predispose to, or alter the physiologic manifestations of OSA.     

Sleep-disordered breathing in patients with symptomatic heart failure: a contemporary study of prevalence in and characteristics of 700 patients

AIM: Evaluation of the prevalence and nature of sleep-disordered breathing (SDB) in patients with symptomatic chronic heart failure (CHF) receiving therapy according to current guidelines. METHODS AND RESULTS: We prospectively screened 700 patients with CHF (NYHA class> or =II, LV-EF< or =40%) for SDB using cardiorespiratory polygraphy (Embletta). Furthermore, echocardiography, cardiopulmonary exercise and 6-min walk testing were performed. Medication included ACE-inhibitors and/or AT1-receptor blockers in at least 94%, diuretics in 87%, beta-blockers in 85%, digitalis in 61% and spironolactone in 62% of patients. SDB was present in 76% of patients (40% central (CSA), 36% obstructive sleep apnoea (OSA)). CSA patients were more symptomatic (NYHA class 2.9+/-0.5 vs. no SDB 2.57+/-0.5 or OSA 2.57+/-0.5; p<0.05) and had a lower LV-EF (27.4+/-6.6% vs. 29.3+/-2.6%, p<0.05) than OSA patients. Oxygen uptake (VO(2)) was lowest in CSA patients: predicted peak VO(2) 57+/-16% vs. 64+/-18% in OSA and 63+/-17% in no SDB, p<0.05. 6-min walking distances were 331+/-111 m in CSA, 373+/-108 m in OSA and 377+/-118 m in no SDB (p<0.05). CONCLUSIONS: This study confirms the high prevalence of SDB, particularly CSA in CHF patients. CSA seems to be a marker of heart failure severity.     

Sleep disorders in systolic heart failure: a prospective study of 100 male patients. The final report

BACKGROUND: Heart failure is a highly prevalent disorder. The main aims of this study were to determine the prevalence, consequences and markers of sleep apnea and the periodic limb movements (PLMS) in heart failure. METHODS AND RESULTS: This is a prospective study of 100 of 114 consecutive eligible patients with heart failure and LVEF <45%. Forty-nine percent of patients had sleep apnea with an average index of 49 per hour. Thirty-seven percent of patients had CSA and 12% had OSA. Comparing patients with CSA to those without sleep apnea, the markers associated with CSA were poorer functional classification, atrial fibrillation, PaCO2 <36 mm Hg, LVEF <20%, and nocturnal ventricular arrhythmias including >30 PVC's, >1 couplets and >1 episodes of ventricular tachycardia/hour. In contrast, comparing heart failure patients with CSA to OSA, OSA patients were significantly obese (mean body weight 109+/-27 vs 78+/-18 kg) and had habitual snoring (83% vs 38%). Twenty percent of patient with heart failure had PLMS with an average index of 35 per hour. PLMS resulted in a mildly increased number of arousals (3.4+/-2 per hour). CONCLUSIONS: 49% of male patients with systolic heart failure suffer from sleep apnea and 20% have PLMS. CSA occurs in about 37%, and OSA in 12% of patients. Habitual snoring and obesity are the hallmarks of OSA. In contrast, heart failure patients with CSA are commonly thin and mostly do not snore. Hallmarks of CSA are Class III New York Heart, artrial fibrillation, frequent nocturnal ventricular arrhythmias, low arterial PCO2 and LVEF <20%.     

Washout Rate of Cardiac Iodine-123 Metaiodobenzylguanidine is High in Chronic Heart Failure Patients With Central Sleep Apnea

BackgroundThe association between sleep-disordered breathing (SDB) assessed by polysomnography and cardiac sympathetic nerve activity (SNA) assessed by cardiac iodine-123 metaiodobenzylguanidine (123I-MIBG) imaging has not been investigated in patients with chronic heart failure (CHF).Methods and ResultsWe performed cardiac 123I-MIBG scintigraphy and overnight polysomnography in 59 patients with stable CHF. The patients were classified into the 3 groups: 19 with no or mild SDB (NM-SDB, apnea-hypopnea index <15); 21 with central sleep apnea (CSA), and 19 with obstructive sleep apnea (OSA). The cardiac washout rate (WR) of 123I-MIBG was obtained from initial and delayed planar 123I-MIBG images. The WR was higher in patients with CSA (54.2 ± 11.6%) than in those with OSA (37.9 ± 8.6%, P < .05) or NM-SDB (40.8 ± 8.8%, P < .05). The WR correlated positively with central apnea index (ρ = 0.40, P = .002). A stepwise multiple regression analysis selected CSA and plasma brain natriuretic peptide levels as independent variables associated with the WR.ConclusionsThe WR was higher in CHF patients with CSA than in those with OSA or NM-SDB, and CSA was independently associated with the WR, suggesting a link of CSA to increased cardiac SNA in CHF.     

Possibility of close relationship between sleep disorder breathing and acute coronary syndrome

OBJECTIVES: Sleep apnea syndrome and acute coronary syndrome (ACS) are related, but any further association with congestive heart failure (CHF) remains unclear. METHODS: Sixty-five patients with ACS (ACS group) and 48 patients with CHF (CHF group)underwent Holter electrocardiography and respiratory monitoring to identify sleep apnea. RESULTS: There were significant differences in age, sex, frequency of smoking, and ejection fraction between the two groups. The apnea hypopnea index showed similar high values in both ACS group (21.7 +/- 17.0/hr) and CHF group (19.4 +/- 17.9/hr). In the ACS group, 24 patients (37%) had central sleep apnea syndrome and 29 patients (45%) had obstructive sleep apnea syndrome. There were no significant differences in the incidences of central and obstructive sleep apnea syndromes between the two groups. Sympathetic nerve activity was significantly higher in ACS group than in CHF group (low/high frequency power ratio in overall study, 2.64 +/- 2.43 vs 1.24 +/- 1.05, p = 0.0003; in asleep study, 2.64 +/- 2.35 vs 1.23 +/- 1.04, p = 0.0002; in awake study, 2.73 +/- 2.36 vs 1.50 +/- 1.46, p = 0.002). CONCLUSIONS: Sleep apnea was observed at the same frequency in the ACS group and the CHF group including higher sympathetic nerve activity, and there was no significant difference in frequency of desaturation. This study suggested that sleep disorder breathing is frequently and similarly associated with both CHF and ACS.     

Altered blood rheology in obstructive sleep apnea as a mediator of cardiovascular risk

BACKGROUND: Cardiovascular complications are common in patients with obstructive sleep apnea (OSA). Blood rheology is a major determent of coagulation and an established risk factor for cardiovascular events. Since nocturnal hypoxemia could influence parameters of blood rheology, we hypothesized that OSA alters blood rheology independent of other cardiovascular risk factors. METHODS: One hundred and ten consecutive patients admitted to the sleep laboratory were included. The association of plasma fibrinogen and viscosity (as parameters of blood rheology) with OSA was evaluated. RESULTS: One hundred and ten patients aged 61.4+/-10.1 years (body mass index 28.4+/-4.1 kg/m2) were included. OSA was confirmed in 63 patients (57.2%) with an apnea-hypopnea index (AHI) of 28.7+/-14.9 events/hour. Patients with OSA showed higher levels of plasma viscosity (1.36+/-0.09 vs. 1.31+/-0.08 mPas, p=0.005). Nevertheless, hypertensive apneics have even higher levels of plasma viscosity than nonapneics (1.38+/-0.091 vs. 1.32+/-0.028 mPas, p=0.018). Similar results were found in patients with coronary artery disease, where OSA was associated with elevated plasma viscosity (1.36+/-0.076 vs. 1.31+/-0.081 mPas, p=0.007). Plasma fibrinogen was correlated with nocturnal minimal oxygen saturation (r=-0275, p=0.0036) and AHI (r=0.297, p=0.001). OSA was associated with higher plasma fibrinogen (353+/-83 vs. 317+/-62 mg/dl, p=0.015). These differences persist with control for cardiovascular risk factors. CONCLUSIONS: Patients with OSA have elevated morning fibrinogen levels and a higher plasma viscosity, which correlate positively with indices of sleep apnea severity. These changes in blood rheology are independent of cardiovascular risk factors, and therefore, might be specific mechanisms of OSA. This supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor.     

Sleep-disordered breathing and inappropriate defibrillator shocks in chronic heart failure

Purpose

Supraventricular tachyarrhythmias are a major cause of inappropriate defibrillator shocks. Sleep-disordered breathing (SDB) is a known risk factor for atrial fibrillation (AF). We hypothesized that Cheyne–Stokes respiration (CSA) and obstructive sleep apnea (OSA) have an impact on inappropriate defibrillator discharges in patients witch chronic heart failure (CHF) and cardiac resynchronization therapy with defibrillator (CRT-D).

Methods

In this study, 172 patients with CHF (LVEF ≤?45?%, NYHA-class ≥?2) and CRT-D underwent overnight polygraphy; 54 had no SDB (apnea–hypopnea index Results In all, 17 patients had inappropriate defibrillator shocks (9.9?%; eight oversensing due to lead fractures, five caused by atrial fibrillation, four because of sinus tachycardia). Mean event-free survival time was 33.5?±?1.2 months in the CSA group, 35.2?±?0.7 months in the OSA group, and 32.1?±?1.5 months in the no SDB group, respectively (CSA vs. no SDB p?=?0.63; OSA vs. no SDB p?=?0.31; CSA vs. OSA p?=?0.45). Stepwise Cox proportional hazard regression analysis revealed an independent association for age (per year: hazard ratio 0.90, 95?% confidence interval 0.85–0.96, p?Conclusions SDB was not associated with inappropriate defibrillator shocks. We assume this is due to the low incidenceand low proportion of inappropriate therapies in response to AF.     

Cardiorespiratory effects of added dead space in patients with heart failure and central sleep apnea

BACKGROUND: Inhaled CO(2) has been shown to stabilize the breathing pattern of patients with central sleep apnea (CSA) with and without congestive heart failure (CHF). Added dead space (DS) as a form of supplemental CO(2) was effective in eliminating idiopathic CSA. The efficacy and safety of DS has not yet been evaluated in patients with CHF and CSA. METHODS: We examined the respiratory and cardiovascular effects of added DS in eight patients with CHF and CSA. The DS consisted of a facemask attached to a cylinder of adjustable volume. During wakefulness, the cardiorespiratory response to 200 to 600 mL of DS was tested. Cardiac output and stroke volume were measured using echocardiography with and without DS. During the nocturnal study, patients slept with and without DS, alternating at approximately 1-h intervals. RESULTS: Values are expressed as the mean +/- SE. The wakefulness study revealed a plateau in the partial pressure of end-tidal CO(2) (PETCO(2)) and the partial pressure of end-tidal O(2) between DS amounts of 400 and 600 mL. The mean stroke volume index (33 +/- 7 vs 34 +/- 7 mL/m(2), respectively) and the mean cardiac index (1.9 +/- 0.3 vs 1.9 +/- 0.4 L/min/m(2), respectively) were not affected by DS. Neither heart rate nor BP showed a significant change in response to DS of < or = 600 mL. During sleep, DS increased the PETCO(2) (40.7 +/- 2.7 vs 38.9 +/- 2.6 mm Hg, respectively; p < 0.05), reduced apnea (1 +/- 1 vs 29 +/- 7 episodes per hour, respectively; p < 0.01) and arousal (21 +/- 8 vs 30 +/- 8 arousals per hour, respectively; p < 0.05), increased the mean arterial oxygen saturation (SaO(2)) [94.4 +/- 1.0% vs 93.5 +/- 1.1%, respectively; p < 0.01), and reduced SaO(2) oscillations (DeltaSaO(2) from maximum to minimum, 1.8 +/- 0.4% vs 5.5 +/- 0.9%, respectively; p < 0.01). CONCLUSION: DS stabilized CSA and improved sleep quality in patients with CHF without significant acute adverse effects on the cardiovascular function.     

Continuous positive airway pressure improves nocturnal baroreflex sensitivity of patients with heart failure and obstructive sleep apnea

OBJECTIVES: To determine the acute effects of continuous positive airway pressure (CPAP) on baroreceptor reflex sensitivity (BRS) for heart rate during sleep in congestive heart failure (CHF) patients with obstructive sleep apnea (OSA). DESIGN AND METHODS: In eight CHF patients with OSA not previously treated with CPAP, spontaneous BRS was assessed during overnight polysomnography prior to the onset of sleep, and during stage 2 non-rapid eye movement sleep (NREM) before, during and after application of CPAP. RESULTS: CPAP alleviated OSA and acutely increased the slope of BRS (median, 25%,75%) [from 3.9 (3.5, 4.8) to 6.2 (4.6, 26.2) ms/mmHg, P<0.05]. Increases in the slope of BRS persisted following withdrawal of CPAP [4.9 (4.3, 6.9) ms/mmHg, P<0.05]. CPAP also lowered heart rate (from 81.3 +/- 4.9 to 76.0 +/- 5.7 bpm, P< 0.05), an effect which persisted after its withdrawal (76.7 +/- 5.7 bpm, P < 0.05). Systolic blood pressure at the midpoint of the pressure range of BRS sequences fell while on CPAP (from 139 +/- 8 to 120 +/- 7 mmHg, P < 0.05), and remained lower following CPAP withdrawal (124 +/- 9 mmHg, P < 0.05). CONCLUSIONS: In CHF patients with OSA, CPAP increases acutely BRS during sleep, lowers heart rate and resets the operating point for BRS to a lower blood pressure. These effects of CPAP persist after its withdrawal, suggesting that nocturnal CPAP therapy may cause sustained improvement in the neural control of heart rate.     

Apnea-hypopnea threshold for CO2 in patients with congestive heart failure

To understand the pathogenesis of central sleep apnea (CSA) in patients with congestive heart failure (CHF), we measured the end-tidal carbon dioxide pressure (PET(CO2)) during spontaneous breathing, the apnea-hypopnea threshold for CO2, and then calculated the difference between these two measurements in 19 stable patients with CHF with (12 patients) or without (7 patients) CSA during non-rapid eye movement sleep. Pressure support ventilation was used to reduce the PET(CO2) and thereby determine the thresholds. In patients with CSA, 1.5-3% CO2 was supplied temporarily to stabilize breathing before determining the thresholds. Unlike patients without CSA whose eupneic PET(CO2) increased during sleep (37.7 +/- 1.4 mm Hg versus 40.2 +/- 1.5 mm Hg, p < 0.01), patients with CSA showed no rise in PET(CO2) from wakefulness to sleep (37.5 +/- 0.9 mm Hg versus 38.2 +/- 1.0 mm Hg, p = 0.2). Patients with CHF and CSA had their eupneic PET(CO2) closer to the threshold PET(CO2) than patients without CSA (DeltaPET(CO2) [eupneic PET(CO2) - threshold PET(CO2)] was 2.8 +/- 0.3 mm Hg versus 5.1 +/- 0.7 mm Hg for apnea, p < 0.01; 1.7 +/- 0.7 versus 4.1 +/- 0.5 mm Hg for hypopnea, p < 0.05). In summary, patients with CHF and CSA neither increase their eupneic PET(CO2) during sleep nor proportionally decrease their apnea-hypopnea threshold. The resultant narrowed DeltaPET(CO2) predisposes the patient to the development of apnea and subsequent breathing instability.     

Sleepiness and sleep in patients with both systolic heart failure and obstructive sleep apnea

BACKGROUND: Adverse effects of obstructive sleep apnea (OSA), including sleep deprivation, can contribute to the progression of heart failure. The usual indication to diagnose and treat sleep apnea is subjective sleepiness. Previous studies suggest that patients with both heart failure and obstructive sleep apnea often do not complain of sleepiness, albeit their sleep time may be reduced. Therefore, we tested the hypothesis that patients with heart failure have less sleepiness and sleep less compared with subjects without heart failure for a given severity of OSA. METHODS: Sleepiness assessed with the Epworth Sleepiness Scale and sleep structure measured with polysomnography were compared among 155 consecutive patients with heart failure and from a random community sample (n = 1139) according to categories of the apnea-hypopnea index (<5, no OSA; 5-14, mild OSA; and > or =15, moderate to severe OSA). RESULTS: Compared with the community sample, for any given severity of OSA, patients with heart failure had lower mean +/- SE Epworth Sleepiness Scale scores (7.1 +/- 0.4 vs 8.3 +/- 0.2 [P = .005]; 6.7 +/- 0.7 vs 9.2 +/- 0.3 [P < .001]; and 7.8 +/- 0.7 vs 9.8 +/- 0.4 [P = .01]), indicating less sleepiness despite sleeping less (total sleep time mean +/- SE [in minutes]: 306 +/- 7 vs 384 +/- 2, 295 +/- 19 vs 384 +/- 5, and 285 +/- 13 vs 359 +/- 7 for no, mild, and moderate to severe OSA, respectively; P < .001 for all comparisons). CONCLUSIONS: Patients with heart failure have less subjective daytime sleepiness compared with individuals from a community sample, despite significantly reduced sleep time, whether or not they have OSA. In patients with heart failure, the absence of subjective sleepiness is not a reliable means of ruling out OSA.     

Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.

In previous analyses of the occurrence of central (CSA) and obstructive sleep apnea (OSA) in patients with congestive heart failure (CHF), only men were studied and risk factors for these disorders were not well characterized. We therefore analyzed risk factors for CSA and OSA in 450 consecutive patients with CHF (382 male, 68 female) referred to our sleep laboratory. Risk factors for CSA were male gender (odds ratio [OR] 3.50; 95% confidence interval [CI], 1.39 to 8.84), atrial fibrillation (OR 4.13; 95% CI 1.53 to 11. 14), age > 60 yr (OR 2.37; 95% CI 1.35 to 4.15), and hypocapnia (PCO(2 )< 38 mm Hg during wakefulness) (OR 4.33; 95% CI 2.50 to 7. 52). Risk factors for OSA differed by gender: in men, only body mass index (BMI) was significantly associated with OSA (OR for a BMI > 35 kg/m(2), 6.10; 95% CI 2.86 to 13.00); whereas, in women, age was the only important risk factor (OR for age > 60 yr, 6.04; 95% CI 1.75 to 20.0). We conclude that historical information, supplemented by a few simple laboratory tests may enable physicians to risk stratify CHF patients for the presence of CSA or OSA, and the need for diagnostic polysomnography for such patients. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.     

Temporal worsening of sleep-disordered breathing in the acute phase of myocardial infarction.

BACKGROUND: Sleep apnea is an important risk factor for cardiovascular diseases, but whether the severity of sleep-disordered breathing (SDB) changes in the acute phase of myocardial infarction (MI) has not been well determined, nor has it been determined what type of SDB, central or obstructive, (CSA or OSA) is exacerbated. METHODS AND RESULTS: Polysomnography was performed in patients with acute phase of MI during the acute (days 3-5) and chronic (day 14) phases. On the same day, the ventilatory equivalent (VE)/carbon dioxide production (VCO(2)) slope, urinary catecholamines secretion and arterial carbon dioxide tension were assessed before sleep. The apnea/hypopnea index was significantly decreased in the chronic phase (13.26+/-11.30 vs 6.97+/-5.67, p<0.05). The distribution of the types of SDB was unchanged, indicating both CSA and OSA can be exacerbated in the acute phase of MI. The VE/VCO(2) slope and arterial carbon dioxide tension before sleep were also unchanged. Urinary norepinephrine secretion was slightly decreased, although the difference was not significant. CONCLUSIONS: SDB is temporarily worsened in the acute phase of AMI and both CSA and OSA are worsened in AMI.     

Sleep apnea, delirium, depressed mood, cognition, and ADL ability after stroke

OBJECTIVES: The incidence of sleep apnea and stroke increases with age. The aim of this study was to investigate the presence of sleep apnea after stroke and its relationship to delirium, depressed mood, cognitive functioning, ability to perform activities of daily living (ADLs), and psychiatric and behavior symptoms. DESIGN: Cross-sectional study. SETTING: Geriatric stroke rehabilitation unit. PARTICIPANTS: 133 patients (78 women and 55 men, mean age 77.1 +/- 7.7 years) consecutively admitted to a geriatric stroke rehabilitation unit. MEASUREMENTS: All patients underwent overnight respiratory sleep recordings at 23 +/- 7 days (range 11 to 41 days) after suffering a stroke. The patients were assessed using the Organic Brain Syndrome Scale, Montgomery-Asberg-Depression-Rating Scale, Mini-Mental State Examination (MMSE), and Barthel-ADL Index. Sleep apnea was defined as an apnea-hypopnea index (AHI) of 10 or more. RESULTS: The median of the AHI for the studied sample (N = 133) was 13 (range 0-79; interquartile range 6-28). Fifty-nine percent fulfilled the criteria for sleep apnea; 52% with first-ever stroke had sleep apnea. More patients with sleep apnea than without were delirious, depressed, or more ADL-dependent. Sleep apnea patients also had a higher frequency of ischemic heart disease and had more often suffered from an earlier cerebral infarction. Multivariate analysis showed that obesity, low ADL scores, ischemic heart disease, and depressed mood were independently associated with sleep apnea. Low ADL scores, apnea-related hypoxemia, body mass index < or = 27, and impaired vision were independently associated with delirium. The presence of sleep apnea was not associated with any specific type of stroke or location of the brain lesion. CONCLUSIONS: Sleep apnea is common in stroke patients and is associated with delirium, depressed mood, latency in reaction and in response to verbal stimuli, and impaired ADL ability. We suggest a trial investigating whether delirium, depressed mood, and ADL ability improve with nasal continuous positive airway pressure treatment of sleep apnea in stroke patients.     

Respiratory sleep disorders in patients with congestive heart failure

Respiratory sleep disorders (RSD) occur in about 40-50% of patients with symptomatic congestive heart failure (CHF). Obstructive sleep apnea (OSA) is considered a cause of CHF, whereas central sleep apnea (CSA) is considered a response to heart failure, perhaps even compensatory. In the setting of heart failure, continuous positive airway pressure (CPAP) has a definite role in treating OSA with improvements in cardiac parameters expected. However in CSA, CPAP is an adjunctive therapy to other standard therapies directed towards the heart failure (pharmacological, device and surgical options). Whether adaptive servo controlled ventilatory support, a variant of CPAP, is beneficial is yet to be proven. Supplemental oxygen therapy should be used with caution in heart failure, in particular, by avoiding hyperoxia as indicated by SpO₂ values >95%.