Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial.

AIMS: Obstructive sleep apnoea (OSA) is highly prevalent in patients with chronic heart failure (CHF) and may contribute to CHF progression. We aimed to determine whether treatment of OSA with continuous positive airway pressure (CPAP) would improve subjective and objective measures of heart failure severity in patients with CHF and OSA. METHODS AND RESULTS: Twenty-six patients with stable symptomatic CHF and OSA were randomized to nocturnal auto-titrating CPAP or sham CPAP for 6 weeks each in crossover design. Study co-primary endpoints were changes in peak VO(2) and 6 min walk distance. Secondary endpoints were changes in left ventricular ejection fraction, VE/VCO(2) slope, plasma neurohormonal markers, and quality-of-life measures. Twenty-three patients completed the study protocol. Mean CPAP and sham CPAP usage were 3.5 +/- 2.5 and 3.3 +/- 2.2 h/night, respectively (P = 0.31). CPAP treatment was associated with improvements in daytime sleepiness (Epworth Sleepiness Score 7 +/- 4 vs. 8 +/- 5, P = 0.04) but not in other quality-of-life measures. There were no changes in other study endpoints. CONCLUSION: In patients with CHF and OSA, auto-titrating CPAP improves daytime sleepiness but not other subjective or objective measures of CHF severity. These data suggest that the potential therapeutic benefits of CPAP in CHF are achieved by alleviation of OSA rather than by improvement in cardiac function.     

Inhibition of awake sympathetic nerve activity of heart failure patients with obstructive sleep apnea by nocturnal continuous positive airway pressure

OBJECTIVES: This study was designed to determine whether reductions in morning systolic blood pressure (BP) elicited by treatment of moderate to severe obstructive sleep apnea (OSA) in heart failure (HF) patients are associated with a reduction in sympathetic vasoconstrictor tone. BACKGROUND: Daytime muscle sympathetic nerve activity (MSNA) is elevated in HF patients with coexisting OSA. In our recent randomized trial in HF, abolition of OSA by continuous positive airway pressure (CPAP) increased left ventricular ejection fraction (LVEF) and lowered morning systolic BP. METHODS: Muscle sympathetic nerve activity, BP, and heart rate (HR) of medically treated HF patients (EF <45%) and OSA (apnea-hypopnea index > or =20/h of sleep) were recorded on the morning after overnight polysomnography, and again one month after patients were randomly allocated nocturnal CPAP treatment or no CPAP (control). RESULTS: In nine control patients, there were no significant changes in the severity of OSA, MSNA, systolic BP, or HR. In contrast, in the 8 CPAP-treated patients, OSA was attenuated, and there were significant reductions in daytime MSNA (from 58 +/- 4 bursts/min to 48 +/- 5 bursts/min; 84 +/- 4 bursts/100 heart beats to 72 +/- 5 bursts/100 heart beats; p < 0.001 and p = 0.003, respectively), systolic BP (from 135 +/- 5 mm Hg to 120 +/- 6 mm Hg, p = 0.03), and HR (from 69 +/- 2 min(-1) to 66 +/- 2 min(-1); p = 0.013). CONCLUSIONS: Treatment of coexisting OSA by CPAP in HF patients lowers daytime MSNA, systolic BP, and HR. Inhibition of increased central sympathetic vasoconstrictor outflow is one mechanism by which nocturnal CPAP reduces awake BP in HF patients with moderate to severe OSA.     

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.     

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.     

Impact of sleep apnea on sympathetic nervous system activity in heart failure

OBJECTIVES: To compare and establish the relevance of the relative degree of sympathetic nervous system activity (SNSA) in groups of patients with congestive heart failure (CHF) and obstructive sleep apnea (OSA), and in a control group. BACKGROUND: Elevated SNSA is a characteristic feature of CHF, as well as of OSA and nonhypercapnic central sleep apnea (CSA). OSA and CSA commonly occur with CHF; however, the relative contribution of apnea-related hypoxemia and sleep fragmentation to the SNSA of patients with CHF is not known. METHODS: This was a prospective, controlled, observational trial in which the overnight urinary norepinephrine (UNE) level, which is a measure of integrated overnight SNSA while asleep, was measured in 15 healthy male volunteers, 15 male OSA patients who did not have CHF, and 90 CHF patients (77 men). CHF patients also had right heart pressure measurements and then were grouped by the presence of sleep apnea. RESULTS: Compared with healthy individuals, the mean (+/- SD) UNE level was significantly elevated in the OSA group and was even further elevated in the CHF group (13.4 +/- 5.6 vs 19.7 +/- 12.3 vs 32.2 +/- 20.2 nmol/mmol creatinine, respectively; p < 0.001 [by analysis of variance]). Within the CHF group, the mean UNE levels were greatest in the CHF-CSA group compared with the CHF-OSA group and the CHF nonapnea group (43.9 +/- 24.1 vs 24.0 +/- 10.8 vs 22.4 +/- 8.9 nmol/mmol creatinine, respectively; p < 0.001). Using a multivariate regression model, the variance of the UNE level in the CHF group was predicted, in descending order, by pulmonary capillary wedge pressure (14% variance), rapid eye movement sleep (8%), and the mean sleep pulse oximetry level (7%). CONCLUSIONS: Overnight SNSA is significantly greater in CHF patients than in OSA patients. Moreover, the hemodynamic severity of CHF contributes to the elevation of SNSA in CHF patients to a greater degree than apnea-related hypoxemia.     

Blood pressure changes after automatic and fixed CPAP in obstructive sleep apnea: relationship with nocturnal sympathetic activity

Treatment of obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) usually causes a reduction in blood pressure (BP), but several factors may interfere with its effects. In addition, although a high sympathetic activity is considered a major contributor to increased BP in OSA, a relationship between changes in BP and in sympathetic nervous system activity after OSA treatment is uncertain. This study was undertaken to assess if, in OSA subjects under no pharmacologic treatment, treatment by CPAP applied at variable levels by an automatic device (APAP) may be followed by a BP reduction, and if that treatment is associated with parallel changes in BP and catecholamine excretion during the sleep hours. Nine subjects underwent 24-h ambulatory BP monitoring and nocturnal urinary catecholamine determinations before OSA treatment and 2 months following OSA treatment by APAP (Somnosmart2, Weinmann, Hamburg, Germany). Eight control subjects were treated by CPAP at a fixed level. After APAP treatment, systolic blood pressure (SBP) decreased during sleep (p < 0.05), while diastolic blood pressure (DBP) decreased both during wakefulness (p < 0.05) and sleep (p < 0.02). Similar changes were observed in subjects receiving fixed CPAP. Nocturnal DBP changes were correlated with norepinephrine (in the whole sample: r = .61, p < 0.02) and normetanephrine (r = .71, p < 0.01) changes. In OSA subjects under no pharmacologic treatment, APAP reduces BP during wakefulness and sleep, similarly to CPAP. A reduction in nocturnal sympathetic activity could contribute to the reduction in DBP during sleep following OSA treatment.     

Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study.

AIMS: We tested the hypothesis that: (i) obstructive sleep apnoea (OSA) by itself originates pulmonary hypertension (PH); and (ii) the application of continuous positive airway pressure (CPAP) can reduce pulmonary pressure. METHODS AND RESULTS: In this randomized and cross-over trial, 23 middle-aged OSA (apnoea-hypopnoea index, 44.1 +/- 29.3 h(-1)) and otherwise healthy patients and 10 control subjects were included. OSA patients randomly received either sham or effective CPAP for 12 weeks. Echocardiographic parameters, blood pressure recordings, and urinary catecholamine levels were obtained at baseline and after both treatment modalities. At baseline, OSA patients had higher pulmonary artery systolic pressure than control subjects (29.8 +/- 8.8 vs. 23.4 +/- 4.1 mmHg, respectively, P = 0.036). Ten out of 23 patients [43%, (95% CI: 23-64%)] and none of the control subjects had PH at baseline (P = 0.012). Two patients were removed from the study because of inadequate CPAP compliance. Effective CPAP induced a significant reduction in the values for pulmonary systolic pressure (from 28.9 +/- 8.6 to 24.0 +/- 5.8 mmHg, P < 0.0001). The reduction was greatest in patients with either PH or left ventricular diastolic dysfunction at baseline. CONCLUSION: Severe OSA is independently associated with PH in direct relationship with disease severity and presence of diastolic dysfunction. Application of CPAP reduces pulmonary systolic pressure levels.     

Acute and chronic effects of continuous positive airway pressure therapy on left ventricular systolic and diastolic function in patients with obstructive sleep apnea and congestive heart failure

BACKGROUND:

Obstructive sleep apnea (OSA) may contribute to the pathogenesis of congestive heart failure (CHF). Nocturnal continuous positive airway pressure (CPAP) therapy can alleviate OSA and may have a role in the treatment of CHF patients.

OBJECTIVES:

To investigate the acute and chronic effects of CPAP therapy on left ventricular systolic function, diastolic function and filling pressures in CHF patients with OSA.

METHODS:

Twelve patients with stable CHF (New York Heart Association II or III, radionuclide ejection fraction lower than 40%) underwent overnight polysomnography to detect OSA. In patients with OSA (n=7), echocardiography was performed at baseline (awake, before and during acute CPAP administration) and after 6.9±3.3 weeks of nocturnal CPAP therapy. Patients without OSA (n=5) did not receive CPAP therapy, but underwent a baseline and follow-up echocardiogram.

RESULTS:

In CHF patients with OSA, acute CPAP administration resulted in a decrease in stroke volume (44±15 mL versus 50±14 mL, P=0.002) and left ventricular ejection fraction ([LVEF] 34.8±5.0% versus 38.4±3.3%, P=0.006) compared with baseline, but no change in diastolic function or filling pressures (peak early diastolic mitral annular velocity [Ea]: 6.0±1.6 cm/s versus 6.3±1.6 cm/s, P not significant; peak early filling velocity to peak late filling velocity [E/A] ratio: 1.05±0.74 versus 1.00±0.67, P not significant; E/Ea ratio: 10.9±4.1 versus 11.3±4.1, P not significant). In contrast, chronic CPAP therapy resulted in a trend to an increase in stroke volume (59±19 mL versus 50±14 mL, P=0.07) and a significant increase in LVEF (43.4±4.8% versus 38.4±3.3%, P=0.01) compared with baseline, but no change in diastolic function or filling pressures (Ea: 6.2±1.2 cm/s versus 6.3±1.6 cm/s, P not significant; E/A ratio: 1.13±0.61 versus 1.00±0.67, P not significant; E/Ea ratio: 12.1±2.7 versus 11.3±4.1, P not significant). There was no change in left ventricular systolic function, diastolic function or filling pressures at follow-up in CHF patients without OSA.

CONCLUSIONS:

Acute CPAP administration decreased stroke volume and LVEF in stable CHF patients with OSA. In contrast, chronic CPAP therapy for seven weeks improved left ventricular systolic function, but did not affect diastolic function or filling pressures. The potential clinical implications of the discrepant effects of CPAP therapy on left ventricular systolic and diastolic function in CHF patients with OSA warrant further study.     

Left ventricular ejection fraction in obstructive sleep apnea. Effects of long-term treatment with nasal continuous positive airway pressure

The effects of treatment with nasal continuous positive airway pressure (CPAP) on left ventricular ejection fraction (LVEF) were assessed in 29 patients with obstructive sleep apnea (OSA) in a prospective study using multiple gated equilibrium radionuclide angiocardiography. All patients were evaluated before CPAP treatment was initiated and were reevaluated after one year (mean +/- SE, 415 +/- 6 days), of home treatment with nasal CPAP. The mean LVEF increased from 59 +/- 1 percent to 63 +/- 1 percent (p less than 0.005). The degree of improvement in LVEF was correlated with baseline LVEF (r = 0.54; p less than 0.003), meaning that the lower the baseline value, the greater the increase with treatment. The changes were not different when subgroups of medicated and unmedicated patients were considered separately. These results show that long-term nasal CPAP treatment results in improved left ventricular function in OSA.     

Decreased right and left ventricular myocardial performance in obstructive sleep apnea

BACKGROUND: Obstructive sleep apnea (OSA) may predispose patients to congestive heart failure (CHF), suggesting a deleterious effect of OSA on myocardial contractility. METHODS: A cross-sectional study of 85 subjects with suspected OSA who had undergone their first overnight polysomnogram, accompanied by an echocardiographic study. Patients were divided according to the apnea-hypopnea index as follows: < 5 (control subjects); 5 to 14 (mild OSA); and >or= 15 (moderate-to-severe OSA). Right and left ventricular function was evaluated using the myocardial performance index (MPI) and other echocardiographic parameters. For the right ventricle analyses, we excluded patients with a Doppler pulmonary systolic pressure of >or= 45 mm Hg, while for the left ventricle we excluded patients with an ejection fraction of 相似文献   

The effects of continuous positive airway pressure on myocardial energetics in patients with heart failure and obstructive sleep apnea.

OBJECTIVES: We sought to examine the short-term and longer term (6-week) effects of continuous positive airway pressure (CPAP) on myocardial energetics. BACKGROUND: Obstructive sleep apnea (OSA) and heart failure (HF) are both states of increased afterload and metabolic demand. Treatment with CPAP may initially reduce stroke volume but subsequently improves left ventricular function. However, it is not clear whether CPAP therapy favorably affects myocardial energetics and hence improves cardiac efficiency. METHODS: Twelve patients with HF were divided into two groups: 7 patients with OSA were treated with CPAP (group I), and 5 patients without OSA served as a control group (group II). Oxidative metabolism was measured using the mono-exponential fit of the myocardial [(11)C] acetate positron emission tomography time-activity curve (k-mono). Myocardial efficiency was derived using the work metabolic index (WMI = [heart rate x stroke volume index x systolic blood pressure]/k-mono) measured at baseline, during short-term CPAP, and after 6 +/- 3 weeks of CPAP. RESULTS: In group I, short-term CPAP tended to reduce SVI (p = 0.063) and reduced oxidative metabolism (p = 0.031). Work metabolic index did not change. However, longer term CPAP improved left ventricular ejection fraction (38.4 +/- 3.3% to 43.4 +/- 4.8%, p = 0.031), tended to reduce oxidative metabolism (0.047 +/- 0.012 to 0.040 +/- 0.008 min(-1), p = 0.078), and improved WMI (7.13 +/- 2.82 x 10(6) to 8.17 +/- 3.06 x 10(6) mm Hg.ml/m(2), p = 0.031). In group II (control), these parameters did not change. CONCLUSIONS: In this cohort of patients with HF and OSA, short-term CPAP decreased oxidative metabolism and tended to decrease SVI, but did not alter cardiac efficiency. Longer term CPAP improved cardiac efficiency, indicating an energy-sparing effect. These effects may contribute to the benefits of CPAP therapy.     

Effects of continuous positive airway pressure on Cheyne-Stokes breathing in congestive heart failure]

To investigate the effects of a continuous positive airway pressure (CPAP) of 5 cmH2O for three months on sleep disordered breathing and cardiac function in congestive heart failure (CHF), we performed physiological tests before and after the CPAP treatment in six male patients with stable CHF, whose echocardiographic left ventricular ejection fraction (LVEF) was below 30%. The control polysomnography revealed that all six had Cheyne-Stokes breathing (with central sleep apnea in four, and central sleep hypopnea in two). Prior to the CPAP, the number of episodes of apnea/hypopnea per hour of sleep, the contribution of slow wave sleep to total sleep time, LVEF and the cardio-thoracic ratio were 34.7 +/- 21.4, 4.1 +/- 1.5%, 24.4 +/- 2.3% and 58.4 +/- 3.7% (mean +/- SD), respectively. After the CPAP, these values changed to 6.0 +/- 7.0, 16.5 +/- 8.3%, 34.3 +/- 3.3% and 55.0 +/- 4.2%, respectively, all of which changes showed a statistical significance (p < 0.05). We conclude that CPAP is an effective treatment for CHF with Cheyne-Stokes breathing, improving sleep disordered breathing, sleep quality and cardiac function, and providing a new non-pharmacological approach for CHF.     

Advances in the management of sleep-disordered breathing in heart failure

Obstructive (OSA) and central sleep apnea (CSA) are very common in patients with congestive heart failure (CHF). This is clearly a risk factor for worsening the prognosis of patients. Treatment of sleep apnea in these patients may stop disease progression. Modern therapy, primarily central sleep apnea, is provided by adaptive servoventilation (ASV). Short-term randomized trials have demonstrated that treatment with ASV increased ejection fraction (EF), reduces sympathetic activity and blood pressure. Unfortunately, there is not enough data on whether there are effects on mortality and morbidity. Studies of this issue, such as SERVE-HF and ADVENT-HF, are currently in progress and results are expected. There are other forms of therapy of OSA like CPAP, oxygen, theophylline, acetazolamide, heart synchronisation therapy and transplantation. In patients with a predominance of OSA, in addition to previous methods, there are other recommended forms of therapy like appropriate weight loss, orthodontic appliances and surgical treatment.     

Assisted ventilation for heart failure patients with Cheyne-Stokes respiration.

Patients with chronic congestive cardiac failure (CCF) frequently suffer from central sleep apnoea syndrome (CSAS). Continuous positive airway pressure (CPAP) has been suggested as a treatment. The authors hypothesised that bilevel ventilation might be easier to initiate and superior to CPAP at correcting the sleep-related abnormality of breathing in patients with CCF. After excluding those with a history suggestive of obstructive sleep apnoea, 35 patients with CCF (left ventricular ejection fraction <35%) were screened with overnight oximetry and the diagnosis of CSAS was established with polysomnography in 18. Two 14-day cycles of CPAP (0.85 kPa (8.5 mbar)) or bilevel ventilation (0.85/0.3 kPa (8.5/3 mbar)) in random order, were compared in a crossover study. Sixteen patients (13 males), mean age 62.0+/-7.4 yrs completed the study. The pretreatment apnoea/hypopnoea index of 26.7+/-10.7 was significantly reduced by CPAP and bilevel ventilation to 7.7+/-5.6 and 6.5+/-6.6, respectively. The arousal index fell from 31.1+/-10.0 per hour of sleep to 15.7+/-5.4 and 16.4+/-6.9, respectively. Significant and equal improvements with CPAP and bilevel ventilation were found for sleep quality, daytime fatigue, circulation time and New York Heart Association class. The authors conclude that continuous positive airway pressure and bilevel ventilation equally and effectively improve Cheyne-Stokes respiration in patients with congestive cardiac failure.     

Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function. Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP. A significantly lower LVEF was found in OSA patients, compared to control subjects, (53+/-7 versus 61+/-6%) along with a reduced LVPER (2.82+/-0.58 versus 3.82+/-0.77 end-diastolic volumes x s(-1)). Furthermore, OSA patients had significantly lower LVPFR (2.67+/-0.71 versus 3.93+/-0.58 end-diastolic volumes x s(-1)) and delayed TPFR (0.19+/-0.04 versus 0.15+/-0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR. In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.     

Obstructive sleep apnea syndrome: more insights on structural and functional cardiac alterations, and the effects of treatment with continuous positive airway pressure.

OBJECTIVES: We studied structural and functional cardiac alterations in obstructive sleep apnea (OSA), their relationship to the severity of OSA, and the effects of treatment with continuous positive airway pressure (CPAP). BACKGROUND: Obstructive sleep apnea may influence the cardiac function by several mechanisms in the awake patient. METHODS: Left and right ventricular morphology and function were studied using echocardiography before and after treatment with CPAP in symptomatic patients (Epworth sleepiness score, 10 +/- 4.8) with severe OSA (apnea-hypopnea index [AHI], 42 +/- 24). The patients (n = 43, 32 men) had no known cardiac disease and were obese (body mass index, 31.6 +/- 5.4 kg/m2). The same echocardiographic parameters were studied in age-matched overweight patients (n = 40; body mass index, 26.4 +/- 2.3 kg/m2). RESULTS: The patients were hypertensive (systolic blood pressure, 153 +/- 25 mm Hg), with a higher resting heart rate (77 +/- 10 beats/min, p = 0.008) compared with age-matched control patients (n = 40). There was right ventricular dilatation, hypertrophic interventricular septum, reduced left ventricular stroke volume, tissue Doppler-determined systolic and diastolic velocities of the left and right ventricle, and normal pulmonary artery pressure. The structural and functional parameters were significantly associated with AHI (p < 0.004). Multiple stepwise regression showed the interventricular septum thickness, right ventricular free wall, and mitral annulus tissue Doppler systolic velocities to be predictive of a higher AHI (p < 0.001). Six months after treatment with CPAP, significant improvements were observed in the symptoms and hemodynamics, as well as left and right ventricular morphology and function. CONCLUSIONS: The structural and functional consequences of OSA on the heart are influenced by the severity of AHI. These effects are reversible if the apneic episodes are abolished.     

Overnight decrease in hematocrit after nasal CPAP treatment in patients with OSA

To clarify the paradox of a decrease in urine and sodium excretion occurring along with the elimination of peripheral edema when patients with obstructive sleep apnea (OSA) are treated with nasal continuous positive airway pressure (CPAP), we investigated the immediate effects of this treatment on the hematocrit and red blood cell count in eight patients with OSA. The hematocrit decreased in all patients, from a mean of 45.6 +/- 1.2 percent to 43.0 +/- 1.4 percent, with a parallel decrease in the red blood cell count from 4.777 +/- 0.168 millions/cu mm to 4.577 +/- 0.174 millions/cu mm (p less than 0.0005, one-tailed, in both cases). These results suggest that nasal CPAP treatment causes a hemodilution in patients with OSA, and are compatible with the hypothesis of an atrial natriuretic peptide-induced fluid shift from the intravascular to the extravascular volume in untreated patients with OSA. The reversal of these changes with CPAP treatment could explain the simultaneous decrease in sodium and urine excretion and the reduction of peripheral edema.     

Cardiovascular Implications in the Treatment of Obstructive Sleep Apnea

Epidemiological studies provide strong evidence that obstructive sleep apnea (OSA) is associated with cardiovascular complications such as systemic hypertension, congestive heart failure, and atrial fibrillation. Successful OSA treatment with continuous positive airway pressure (CPAP) has resulted in coincident reductions in systemic hypertension, improvements in left ventricular systolic function, and reductions in sympathetic nervous activity. These data suggest that successful treatment of OSA may reduce cardiovascular morbidity in such patients. Although CPAP is the more successful treatment for OSA when used properly and consistently, its clinical success is often limited by poor patient and partner acceptance, which leads to suboptimal compliance. Oral appliances or upper airway surgeries are considered a second line of treatment for patients with mild to moderate OSA who do not comply with or refuse long-term CPAP treatment. Oral devices such as mandibular repositioning appliances were recently shown to improve arterial hypertension in OSA patients. Electrical stimulation of the hypoglossal nerve is a new investigational therapy for patients with moderate to severe OSA. This new treatment option, if proven effective, may provide cardiovascular benefits secondary to treating OSA.     

Quality of life in bed partners of patients with obstructive sleep apnea or hypopnea after treatment with continuous positive airway pressure

OBJECTIVE: Obstructive sleep apnea (OSA) has been shown to affect the quality of life (QOL) in patients, and QOL improves after treatment with nasal continuous positive airway pressure (CPAP). However, the effects on the bed partner of the patient with OSA have received little attention. We studied QOL in patients with OSA and their bed partners, and the effect of CPAP therapy on QOL. DESIGN: Fifty-four patients and their bed partners who had been seen for evaluation of OSA, had undergone polysomnography, and subsequently had received treatment with CPAP. Patients and bed partners completed the Epworth sleepiness scale (ESS) and QOL questionnaires before and after the patients' therapy. SETTING: Sleep disorders center in an academic medical center. PARTICIPANTS: Patients with documented OSA and regular bed partners. INTERVENTIONS: Both individuals completed the 36-item short-form health survey (SF-36), the ESS, and the Calgary sleep apnea quality of life index (SAQLI). At about 6 weeks after CPAP therapy, patients and their bed partners completed the same set of questionnaires again. RESULTS: Of the 54 subjects who completed the study, the mean (+/- SD) apnea-hypopnea index was 48.4 +/- 33.3. For the subjects, the mean ESS decreased from 12.9 +/- 4.4 to 7.3 +/- 4.0 (p < 0.001) after treatment with CPAP. For the bed partners, the mean ESS decreased from 7.4 +/- 6.1 to 5.8 +/- 4.7 (p = 0.02). The mean scores on the SAQLI were 4.1 +/- 1.0 for the subjects and 4.5 +/- 1.3 for the bed partners. Following CPAP therapy, the SAQLI increased in the subjects to 4.9 +/- 1.2 (p < 0.001), and in the bed partners to 5.1 +/- 0.9 (p = 0.002). The SF-36 showed positive changes in both the subjects and the bed partners. Significant improvements were observed in the subjects in role-physical, vitality, social functioning, role-emotional, and mental health domains. In the bed partners, significant changes in the SF-36 were observed in role-physical, vitality, social functioning, and mental health domains. CONCLUSION: OSA results in impaired QOL in both the patients and their bed partners. Treatment with CPAP improves QOL, as measured by the SF-36 and the SAQLI.     

阻塞性睡眠呼吸暂停患者持续正压通气治疗前后自主神经 …

目的 研究阻塞性睡眠呼吸暂停（ＯＳＡ）患者夜间睡眠时自主神经功能的状态，以及有效的持续正压通气治疗对自主神经张力的影响。方法 对５６例重度ＯＳＡ患者持续正压通气（ＣＰＡＰ）治疗前和治疗中进行夜间７小时多导睡眠图（ＰＳＧ）及动态心电图监测，另择３０名正常受试者作为对照。采用心率功率谱分析法（ＨＲＰＳＡ）定量分析ＯＳＡ患者治疗前后夜间自主神经功能的变化。结果 ＯＳＡ组夜间睡眠时伴随着反复的呼吸暂停和低