CPAP therapy prevents increase in blood pressure after upper airway surgery for obstructive sleep apnoea

Objective

The aim of this study was to investigate the efficacy of continuous positive airway pressure (CPAP) therapy following uvulopalatopharyngoplasty (UPPP) to prevent blood pressure (BP) elevation during sleep.

Methods

Sixteen normotensive patients with OSA were subjected to UPPP with or without septoplasty. These patients were instrumented for 24 h of ambulatory BP recording, polysomnography, nocturnal urinary catecholamine and pain evaluation using a visual analogue scale in the day prior to surgery (D?1), following the surgery (D+1) and 30 days later (D+30). For the D+1, the patients were divided into two groups: the without CPAP therapy group and the with CPAP therapy group.

Results

The apnoea–hypopnoea index (AHI) significantly increased in the patients without CPAP therapy compared with the D?1 (74?±?23 vs. 35?±?6 times/h, p?<?0.05), and in the CPAP group, there was a significant reduction in the average AHI value to 14?±?6 times/h, p?<?0.01. During D+1, we observed an increase in the nocturnal systolic BP (10 %), diastolic BP (12 %) and heart rate (14 %) in the group without CPAP. These metrics were re-established in the CPAP group to values that were similar to those that were observed on the D?1. The absence of nocturnal dipping in the group without CPAP was followed by a significant increase in nocturnal norepinephrine (42?±?12 μg/l/12 h) and epinephrine (8?±?2 μg/l/12 h) levels compared with the D?1 (norepinephrine 17?±?3; epinephrine 2?±?0.3 μg/l/12 h, p?<?0.001). In the patients who used the CPAP treatment, the nocturnal catecholamine levels were similar to D?1. The effectiveness of intravenous analgesic therapy was verified by a significant decrease in the pain scores in patients both with and without CPAP therapy.

Conclusion

These data confirm an increase in the AHI on the night following UPPP with or without septoplasty. This increase promotes an absence of nocturnal dipping and a significant increase in urinary catecholamine levels. CPAP therapy was effective to prevent the transitory increase in BP.     

Leptin and ghrelin levels in patients with obstructive sleep apnoea: effect of CPAP treatment.

Serum leptin and ghrelin levels were investigated in patients with obstructive sleep apnoea (OSA) syndrome before and during continuous positive airways pressure (CPAP) treatment and compared with body mass index (BMI)-matched controls without OSA. Male patients (n=30) with OSA (apnoea/hypopnoea index=58+/-16, BMI=32.6+/-5.3 kg x m(-2)) underwent CPAP treatment. Fasting leptin and ghrelin were measured at baseline and 2 days, and in the case of leptin 2 months after initiation of treatment. Baseline plasma ghrelin levels were significantly higher in OSA patients than in controls. After 2 days of CPAP treatment, plasma ghrelin decreased in almost all OSA patients (n=9) to levels that were only slightly higher than those of controls (n=9). Leptin levels did not change significantly from baseline after 2 days of CPAP treatment, but were higher than in the control group. After 8 weeks, leptin levels decreased significantly, although the BMI of the patients showed no change. The decrease in leptin levels was more pronounced in patients with a BMI <30 kg x m(-2). These data indicate that the elevated leptin and ghrelin levels are not determined by obesity alone, since they rapidly decreased during continuous positive airways pressure therapy.     

Impact of CPAP on asthmatic patients with obstructive sleep apnoea.

The impact of continuous positive airway pressure (CPAP) treatment on the airway responsiveness of asthmatic subjects with obstructive sleep apnoea (OSA) has scarcely been studied. A prospective study was performed comparing the changes in airway responsiveness and quality of life in stable asthmatic OSA patients, before and 6 weeks after their nocturnal CPAP treatment. A total of 20 subjects (11 males and nine females) participated in the study. With the nocturnal CPAP treatment, the apnoea/hypopnoea index dropped from 48.1 +/- 23.6 x h(-1) to 2.6 +/- 2.5 x h(-1). There were no significant changes in airway responsiveness after CPAP treatment (provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV(1); PC(20) 2.5 mg x mL(-1) (1.4-4.5)) compared with baseline (PC(20) 2.2 mg x mL(-1) (1.3-3.5)). There was no significant change in FEV(1) either. However, the asthma quality of life of the subjects improved from 5.0 +/- 1.2 at baseline to 5.8 +/- 0.9 at the end of the study. In conclusion, nocturnal continuous positive airway pressure treatment did not alter airway responsiveness or forced expiratory volume in one second in subjects with stable mild-to-moderate asthma and newly diagnosed obstructive sleep apnoea. However, nocturnal continuous positive airway pressure treatment did improve asthma quality of life.     

Hunter's syndrome and associated sleep apnoea cured by CPAP and surgery.

A 42-yr-old male with Hunter's syndrome presented with severe obstructive sleep apnoea syndrome (OSAS) and daytime respiratory failure. Continuous positive airway pressure (CPAP) therapy was initially ineffective and produced acute respiratory distress. Extensive Hunter's disease infiltration of the upper airway with a myxoma was confirmed. Following surgery to remove the myxoma at the level of the vocal cords, CPAP therapy was highly effective and well tolerated. This report demonstrates the necessity of evaluating fully the upper airway in patients with unusual variants of OSAS, particularly where the disease is not adequately controlled by CPAP.     

CPAP treatment for obstructive sleep apnoea in heart failure: expectations unmet.

Heart failure (HF) is an epidemic, increasing in prevalenceas the population ages. The Rotterdam Study shows that personswho live to age 55 have a one in three chance of eventuallydeveloping HF.¹ The staggering prevalence estimate of more thanfive million currently living with HF in the United States mayunderestimate the overall problem, since population-based studiesfind that a substantial proportion of those with systolic dysfunctionare asymptomatic, although still at increased mortality risk.^2,3Despite advances in treatment with drugs, lifestyle modifications,and therapeutic devices, mortality from HF continues to rise,fuelling interest in alternative methods of treatment. One suchtarget of therapy has been obstructive sleep apnoea (OSA). HF and OSA are closely linked by their strong associations withageing and obesity, and frequently     

Long-term effects of CPAP on daytime functioning in patients with sleep apnoea syndrome.

Daytime sleepiness, impaired cognitive performance and dysphoric mood are often present in patients with obstructive sleep apnoea syndrome (SAS). This prospective controlled study evaluates the effects of treatment with continuous positive airway pressure (CPAP) during 1 yr on daytime functioning in a large group of patients with SAS. The authors studied 80 patients (mean+/-sem 49+/-1 yrs) with SAS with a mean apnoea-hypopnoea index of 60+/-2 h-1, and 80 healthy control subjects matched for sex and age (46+/-1 yrs.). Measurements were obtained at the beginning of the study and 12+/-1 months later, and included: daytime sleepiness (Epworth scale), depression and anxiety (Beck tests), vigilance (Steer-Clear) and reaction time (Psychometer Vigilance Test 192). Drug, coffee and alcohol intake, as well as the sleep schedule, were also recorded. Results showed that, before treatment, patients were more somnolent (p<0.001), anxious (p<0.01) and depressed (p<0.001) than control subjects. Also, they had a longer reaction time (p<0.05) and poorer vigilance (p<0.01). The use of CPAP improved significantly the levels of somnolence (p<0.0001) and vigilance (p<0.01), but failed to modify anxiety and depression. Reaction time changes were minor. Variables with a potential confounding effect did not change during the study. These results provide firm evidence to substantiate the use of continuous positive airway pressure in patients with sleep apnoea syndrome.     

Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.     

Increased incidence of nonfatal cardiovascular events in stroke patients with sleep apnoea: effect of CPAP treatment

Obstructive sleep apnoea (OSA) is a risk factor for stroke, but little is known about the effect of OSA and continuous positive airway pressure (CPAP) on the incidence of long-term, nonfatal cardiovascular events (CVE) in stroke patients. A prospective observational study was made in 223 patients consecutively admitted for stroke. A sleep study was performed on 166 of them. 31 had an apnoea/hypopnoea index (AHI) <10 events · h(-1); 39 had an AHI between 10 and 19 events · h(-1) and 96 had an AHI ≥ 20 events · h(-1). CPAP treatment was offered when AHI was ≥ 20 events · h(-1). Patients were followed up for 7 yrs and incident CVE data were recorded. The mean ± SD age of the subjects was 73.3 ± 11 yrs; mean AHI was 26 ± 16.7 events · h(-1). Patients with moderate-to-severe OSA who could not tolerate CPAP (AHI ≥ 20 events · h(-1); n = 68) showed an increased adjusted incidence of nonfatal CVE, especially new ischaemic strokes (hazard ratio 2.87, 95% CI 1.11-7.71; p = 0.03), compared with patients with moderate-to-severe OSA who tolerated CPAP (n = 28), patients with mild disease (AHI 10-19 events · h(-1); n = 36) and patients without OSA (AHI <10 events · h(-1); n = 31). Our results suggest that the presence of moderate-to-severe OSA is associated with an increased long-term incidence of nonfatal CVE in stroke patients and that CPAP reduces the excess of incidence seen in these patients.     

Nocturnal blood pressure during apnoeic and ventilatory periods in patients with obstructive sleep apnoea.

The exact nature of asleep blood pressure in relation to awake blood pressure is still unclear in patients with obstructive sleep apnoea. This study aimed: 1) to investigate the asleep blood pressure in both apnoeic and ventilatory periods; 2) to determine the diurnal and nocturnal factors correlated with the changes in blood pressure from apnoea to ventilatory periods during sleep. Thirty-two patients, newly diagnosed as moderate to severe obstructive sleep apnoea with a standard nocturnal polysomnography, were enrolled. The blood pressure was monitored by using the noninvasive continuous monitoring method during polysomnographic study. The mean blood pressures in ventilatory periods during nonrapid eye movement (NREM) and rapid eye movement (REM) sleep were 117.5+/-17.9 mm Hg and 128.8+/-21.9 mm Hg, and those in apnoea periods were 94.5+/-15.4 mm Hg and 102.7+/-19.0 mm Hg. The average blood pressure during NREM sleep (103.0+/-16.1 mm Hg) was higher than the awake blood pressure (97.0+/-15.7 mm Hg). The blood pressure during REM sleep was greater than that during NREM sleep. The changes in the nocturnal blood pressure from apnoea to ventilatory periods were inversely correlated with the age and nocturnal mean nadir saturation. In conclusion, patients with obstructive sleep apnoea have higher asleep blood pressure than awake blood pressure.     

Pituitary reactivity, androgens and catecholamines in obstructive sleep apnoea. Effects of continuous positive airway pressure treatment (CPAP).

We studied the effects of chronic nocturnal hypoxaemia due to obstructive sleep apnoea syndrome (OSAS) on the hypothalamic-pituitary-thyroid and hypothalamic-pituitary-testicular axes and on catecholamine and cortisol secretion. We investigated whether hormones other than catecholamines may serve as markers for chronic hypoxic stress and the possible effects of nasal continuous positive airway pressure (nCPAP) treatment on endocrine status. Nocturnal oximetry was performed in 16 male patients with OSAS diagnosed by polysomnography, immediately before nCPAP treatment and in 11 of the patients the oximetry was repeated after 7 months of nCPAP therapy. Plasma and urinary catecholamines, luteinizing hormone (LH) testosterone, cortisol, thyroid stimulating hormone (TSH), prolactin (PRL), and the response of TSH and PRL to a thyroid releasing hormone (TRH) challenge test were measured immediately before and after 7 months of nCPAP treatment. Subnormal LH and TSH and elevated serum cortisol as well as increased nocturnal urinary norepinephrine levels were found in patients prior to treatment; otherwise endocrine values were normal. There was a significant correlation between low pretreatment nocturnal arterial oxygen saturation and high plasma and urinary norepinephrine levels. The nCPAP treatment caused significant reduction in serum prolactin and TSH, and significant reduction in plasma epinephrine and urinary norepinephrine. The reduction in serum TSH and urinary norepinephrine was most pronounced in the subjects with the worst pretreatment nocturnal hypoxaemia. No other significant changes were found in basal hormone levels. The response to TRH challenge was normal before and after treatment and was not influenced by CPAP therapy. OSAS is associated with elevated catecholamine and cortisol and decreased TSH and LH levels but a normal response to TRH challenge and a normal androgen status. Apart from catecholamines, none of the hormones studied is likely to serve as a specific marker for chronic hypoxic stress.     

Use of heated humidification during nasal CPAP titration in obstructive sleep apnoea syndrome.

Nasal symptoms associated with the use of nasal continuous positive airway pressure (nCPAP) in obstructive sleep apnoea (OSA) can adversely impact on patients' tolerance, acceptance and adherence to nCPAP therapy. Regular use of heated humidification is effective in alleviating these symptoms and improve patient comfort. In a randomised, parallel, double-blinded, controlled study, the present authors examined the use of heated humidification during a single night laboratory nCPAP titration in untreated OSA patients and its effect on nasal symptoms, nasal airway resistance (NAR), effective pressure and treatment tolerability and acceptance. Baseline characteristics of subjects (n=70) receiving placebo and humidification were (mean+/-sem): age 51.2+/-2.2 versus 50.6+/-1.6 yrs; body mass index 33.6+/-0.9 versus 35.2+/-0.9 kg.m-2; Epworth Sleepiness Scale 10.8+/-1.0 versus 11.3+/-0.7; and apnoea-hypopnoea index 43.5+/-4.6 versus 44.4+/-4.1 events.h-1. Total inspiratory NAR, before (0.36+/-0.09 (placebo) versus 0.33+/-0.09 kPa.L-1.s-1) and after nCPAP (0.47+/-0.11 versus 0.29+/-0.04 kPa.L-1.s-1) were not significantly different between the groups. No difference was found in the frequency and severity of nasopharyngeal symptoms, therapeutic pressure and subjective response to nCPAP. In conclusion, heated humidification during the initial nasal continuous positive airway pressure titration offers no additional benefit in nasal physiology, symptoms or subjective response to nasal continuous positive airway pressure, and, therefore, should not be routinely recommended.     

Effect of continuous positive airway pressure on ambulatory blood pressure in patients with obstructive sleep apnoea

OBJECTIVES: Previous reports on the effects of continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea (OSA) on blood pressure has shown contradictory results. Accordingly, we have investigated the effects of CPAP on blood pressure and on the potential reversal of the diagnosis of hypertension in patients with OSA evaluated repeatedly by ambulatory blood pressure monitoring. METHODS: We studied 122 patients (104 men and 18 women), 55.1+/-10.5 years of age, with diagnosis of OSA corroborated by overnight polysomnography at the clinic. Among those patients, 83 were treated with CPAP after their first evaluation, while 39 remained without CPAP for the duration of the trial. Blood pressure was measured by ambulatory monitoring at 20-min intervals during the day and at 30-min intervals at night for 48 consecutive hours, at baseline and after 2 and 4 months of intervention. RESULTS: There was a small, but not statistically significant, reduction in ambulatory blood pressure in patients treated with CPAP (0.7 and 1.5 mmHg in 24-h mean of systolic and diastolic blood pressure after 2 months of therapy; 2.0 and 2.3 mmHg after 4 months; P>0.239). The blood pressure reduction was very similar in patients with OSA followed for 4 months without CPAP (1.9 and 2.2 mmHg in 24-h mean of systolic and diastolic blood pressure, respectively; P=0.543). We found a high (77%) prevalence of hypertension among the patients participating in this study, although only 37% were receiving antihypertensive medication at the time of recruitment. The prevalence of hypertension was slightly but not significantly reduced to just 74% after 4 months of treatment with CPAP. CONCLUSIONS: The small reduction in blood pressure for consecutive profiles of ambulatory monitoring can probably be explained by the documented 'ABPM pressor effect' on patients using the ambulatory device for the first time. The high prevalence of hypertension among patients with OSA is not significantly reduced by treatment with CPAP. These results suggest that patients with OSA should always be properly evaluated for diagnosis of hypertension, and provided, if needed, with antihypertensive treatment apart from the recommended CPAP.     

Comparison of empirical continuous positive airway pressure (CPAP) treatment versus initial portable sleep monitoring followed by CPAP treatment for patients with suspected obstructive sleep apnoea

Background: Polysomnography is labour‐intensive for diagnosing obstructive sleep apnoea (OSA). We compared two algorithms for initiating continuous positive airway pressure (CPAP) treatment for patients with suspected OSA. Methods: Symptomatic OSA patients were randomised into either algorithm I or II. Algorithm I consisted of an empirical CPAP trial whereas algorithm II utilised an Apnea Risk Evaluation System, a wireless device applied on the forehead, for establishing a diagnosis before a CPAP trial for 3 weeks. Primary outcome was success of CPAP trial, defined as CPAP usage > 4 h/night and willingness to continue CPAP. Subjective usefulness of CPAP, accuracy of Apnea Risk Evaluation System versus polysomnography and CPAP adherence at 6 months were secondary end‐points. Results: Altogether 138 patients in algorithm I and 110 patients in algorithm II completed the CPAP trial. There were no significant differences between these algorithms with respect to the primary end‐point. The sensitivity and specificity of algorithm I versus II as a diagnostic test for OSA were 0.3, 0.8 versus 0.31, 1.00 respectively. In predicting CPAP adherence at 6 months, the likelihood ratio positive for algorithms I and II was 2.7 and 5.27 respectively. The mean (SE) time taken from the first consultation to the end of CPAP trial in algorithm I and algorithm II was 60 (2) and 98 (5) days, respectively, P < 0.01. Conclusion: An ambulatory approach with portable sleep monitoring for diagnosing OSA before a CPAP trial can identify more patients who would adhere to CPAP at 6 months than empirical CPAP treatment alone.     

High prevalence of unrecognized sleep apnoea in drug-resistant hypertension.

OBJECTIVES: To determine the prevalence of obstructive sleep apnoea (OSA) in adult patients with drug-resistant hypertension, a common problem in a tertiary care facility. DESIGN: Cross-sectional study. SETTING: University hypertension clinic. PATIENTS AND METHODS: Adults with drug-resistant hypertension, defined as a clinic blood pressure of > or = 140/90 mmHg, while taking a sensible combination of three or more antihypertensive drugs, titrated to maximally recommended doses. Each of the 41 participants completed an overnight polysomnographic study and all but two had a 24 h ambulatory blood pressure measurement. RESULTS: Prevalence of OSA, defined as an apnoea-hypopnoea index of > or = 10 obstructive events per hour of sleep, was 83% in the 24 men and 17 women studied. Patients were generally late middle-aged (57.2 +/- 1.6 years, mean +/- SE), predominantly white (85%), obese (body mass index, 34.0 +/- 0.9 kg/m2) and taking a mean of 3.6 +/- 0.1 different antihypertensive medications daily. OSA was more prevalent in men than in women (96 versus 65%, P = 0.014) and more severe (mean apnoea-hypopnoea index of 32.2 +/- 4.5 versus 14.0 +/- 3.1 events/h, P = 0.004). There was no gender difference in body mass index or age. Women with OSA were significantly older and had a higher systolic blood pressure, lower diastolic blood pressure, wider pulse pressure and slower heart rate than women without OSA. CONCLUSIONS: The extraordinarily high prevalence of OSA in these patients supports its potential role in the pathogenesis of drug-resistant hypertension, and justifies the undertaking of a randomized controlled trial to corroborate this hypothesis.