Effects of continuous positive airway pressure versus supplemental oxygen on 24-hour ambulatory blood pressure

Obstructive sleep apnea (OSA) is associated with recurrent episodes of nocturnal hypoxia and increased risk for development of systemic hypertension. Prior studies have been limited, however, in their ability to show reduction in blood pressure after continuous positive airway pressure (CPAP) therapy, and the effect of supplemental oxygen alone on blood pressure in OSA has not been evaluated. We performed a randomized, double-blind, placebo-controlled study comparing the effects of 2 weeks of CPAP versus sham-CPAP versus supplemental nocturnal oxygen on 24-hour ambulatory blood pressure in 46 patients with moderate-severe OSA. We found that 2 weeks of CPAP therapy resulted in a significant reduction in daytime mean arterial and diastolic blood pressure and nighttime systolic, mean, and diastolic blood pressure (all Ps <0.05). Although nocturnal supplemental oxygen therapy improved oxyhemoglobin saturation, it did not affect blood pressure. We conclude that CPAP therapy reduces both daytime and nighttime blood pressure in patients with OSA, perhaps through mechanisms other than improvement of nocturnal oxyhemoglobin saturation.     

Obstruktive Schlafapnoe bei Patienten mit Typ-2-Diabetes

In patients with type 2 diabetes obstructive sleep apnea (OSA) is in addition to obesity, hyperlipidemia and arterial hypertension a common comorbidity which is characterized by repetitive apnea, arousals from sleep and surges of heart rate and arterial blood pressure. Symptoms related to OSA include morning tiredness, daytime hypersomnolence, nocturnal dyspnea and nocturia and justify treatment of OSA. Patients with type 2 diabetes can profit from treatment of OSA in terms of symptom relief, blood pressure lowering effects and potential beneficial effects on lipid and glucose metabolism. Diagnostics of OSA with an ambulatory polygraphy is indicated in patients with type 2 diabetes and OSA-related symptoms or other typical clinical signs for OSA, such as arterial hypertension refractory to drug treatment or non-dipping in 24?h blood pressure monitoring.     

Effect of nocturnal nasal continuous positive airway pressure on blood pressure in obstructive sleep apnea

Obstructive sleep apnea (OSA) is a very common risk factor for hypertension, and continuous positive airway pressure (CPAP) has been widely used to treat OSA. We conducted a meta-analysis of randomized, controlled trials to evaluate the effects of CPAP on blood pressure, reported as either a primary or secondary end point, among patients with OSA. Studies were retrieved by searching Medline (January 1980 to July 2006), the Cochrane Database of Systematic Reviews, conference abstracts, and bibliographies of review and original articles. From 255 relevant reports, 16 randomized clinical trials were selected that compared CPAP to control among participants with OSA, had a minimum treatment duration of 2 weeks, and reported blood pressure changes during the intervention or control period. Data on sample size, participant characteristics, study design, intervention methods, duration, and treatment results were independently abstracted by 2 investigators using a standardized protocol. Data from 16 trials representing 818 participants were examined using a random-effects model. Mean net change in systolic blood pressure for those treated with CPAP compared with control was -2.46 mm Hg (95% CI: -4.31 to -0.62); mean net change in diastolic blood pressure was -1.83 mm Hg (95% CI: -3.05 to -0.61); and mean net change in mean arterial pressure was -2.22 mm Hg (95% CI: -4.38 to -0.05). Net reductions in blood pressure were not statistically different between daytime and nighttime. These results indicate that CPAP decreases blood pressure among those with OSA and may help prevent hypertension.     

Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex.

This study was undertaken to determine whether abolition of obstructive sleep apnoea (OSA) by continuous positive airway pressure (CPAP) could reduce blood pressure (BP) in patients with refractory hypertension. In 11 refractory hypertensive patients with OSA, the acute effects of CPAP on nocturnal BP were studied during sleep and its longer term effects on 24-h ambulatory BP after 2 months. During a single night's application, CPAP abolished OSA and reduced systolic BP in stage 2 sleep from 138.3 +/- 6.8 to 126.0 +/- 6.3 mmHg. There was also a trend towards a reduction in average diastolic BP (from 77.7 +/- 4.5 to 72.9 +/- 4.5). CPAP usage for 2 months was accompanied by an 11.0 +/- 4.4 mmHg reduction in 24-h systolic BP. In addition, both the nocturnal and daytime components of systolic BP fell significantly by 14.4 +/- 4.4 and 9.3 +/- 3.9 mmHg, respectively. Diastolic BP was reduced significantly at night by 7.8 +/- 3.0 mmHg. In patients with refractory hypertension, acute abolition of obstructive sleep apnoea by continuous positive airway pressure reduces nocturnal blood pressure. These data also suggest that continuous positive airway pressure may reduce nocturnal and daytime systolic blood pressure chronically. Randomised trials are needed to confirm the latter results.     

Obstruktive Schlafapnoe und kardiovaskuläre Komorbidität

Obstructive sleep apnea (OSA) is the most common entity of sleep-disordered breathing in Germany. OSA is independently associated with an increased risk of cardiovascular disease. It predisposes to arterial hypertension in particular, but also to coronary artery disease, cardiac arrhythmias and atrial fibrillation. OSA has been established as an independent risk factor for arterial hypertension, and treatment of OSA with continuous positive airway pressure (CPAP) causes a significant and persistent drop in blood pressure. Long-term CPAP treatment reduces the rate of important cardiovascular comorbidities.     

Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea

BACKGROUND: Patients with obstructive sleep apnea (OSA) are at increased risk for hypertension. The mechanisms responsible for the development of hypertension are controversial. We hypothesized that patients with OSA had an abnormal 24-h blood pressure (BP) and an abnormal activity in vasoactive hormones, and that both BP and hormones were normalized during treatment with long-term nasal continuous positive airway pressure (CPAP). METHODS: The 24-h BP and plasma levels of the vasoactive hormones (renin, angiotensin II, aldosterone, atrial natriuretic peptide, brain natriuretic peptide, vasopressin, and endothelin-1) were measured in 24 patients with OSA and in 18 control subjects. Thirteen patients with OSA were reexamined after 14 months of CPAP therapy. RESULTS: Patients with OSA had significantly increased BP and heart rate and a reduced nocturnal BP drop. Both angiotensin II (13.3 +/- 1.6 v 7.8 +/- 1.0 pmol/L) and aldosterone (94.0 +/- 9.4 v 62.2 +/- 4.5 pmol/L) were significantly higher in OSA than in control subjects. Positive correlations were found between angiotensin II and daytime BP (systolic: r = 0.49, P <.01; diastolic: r = 0.52, P <.01). The CPAP therapy resulted in a decrease in BP, and this CPAP-induced reduction in BP was correlated with a decrease in both plasma renin (r = 0.76 to 0.92, all P <.01) and plasma angiotensin II concentration (r = 0.58 to 0.81, all P <.05). CONCLUSIONS: Plasma angiotensin II and aldosterone were elevated in OSA, and plasma angiotensin II was correlated with BP. Long-term CPAP reduced BP, and this decrease in BP was correlated with the reductions in plasma renin and angiotensin II levels. We suggest that OSA mediates hypertension, at least in part, via a stimulation of angiotensin II production.     

Resistant hypertension, obstructive sleep apnoea and aldosterone

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.     

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.     

Nasal CPAP continues to improve sleep-disordered breathing and daytime oxygenation over long-term follow-up of occlusive sleep apnea syndrome.

To assess the effects of long-term nasal continuous positive airway pressure (CPAP) in occlusive sleep apnea syndrome (OSA), 17 patients with severe symptomatic OSA had repeated spirometry, arterial blood gases, and nocturnal polysomnograms off nasal CPAP after 3 to 46 months of treatment with nasal CPAP. Without loss of weight or change in respiratory mechanics, the ventilatory disturbance index fell from a mean of 87 events per hour to 57 events per hour (p < 0.0001), correlating with an improvement in mean nocturnal desaturation with sleep-disordered breathing events (r = 0.54, p = 0.03). Moreover, the daytime PaO2 rose significantly from a mean of 69 mm Hg to a mean of 82 mm Hg (P = 0.0001) at follow-up. The rise in daytime PaO2 was not only due to the alleviation of daytime hypercapnea observed in eight of nine hypercapneic subjects since the P(A-a)O2 gradient also decreased significantly. The improvement in PaO2 correlated significantly with the number of months of CPAP therapy, suggesting a continuing effect over time (r = 0.58, p = 0.015). These results indicate that there is a reversible element of the severity of OSA and suggest a result of nasal CPAP therapy may be to reverse the adverse and time-dependent effects of hypoxemia and sleep fragmentation on ventilatory control in severe OSA.     

Obstructive Sleep Apnea and Hypertension

Obstructive sleep apnea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure. However, these studies do indicate a wide variation in the blood pressure effects of CPAP, with some patients, on an individual basis, manifesting a large antihypertensive benefit. OSA is particularly common in patients with resistant hypertension. The reason for this high prevalence of OSA is not fully explained, but data from our laboratory suggest that it may be related to the high occurrence of hyperaldosteronism in patients with resistant hypertension. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid in the neck, which then contributes to increased upper airway resistance.     

Obstructive sleep apnea and cardiovascular disease - time to act!

Sleep related breathing disorders are common and their potential to disrupt sleep leading to daytime fatigue and hypersomnolence is widely acknowledged. In the future, obstructive sleep apnoea (OSA) may become even more important because obesity as a main risk factor is increasingly prevalent. Apart from disturbing sleep, OSA has also been recognised as a risk factor for hypertension, acute cardiovascular events and metabolic disturbance such as insulin resistance. Several randomised controlled trials demonstrated a positive effect of nasal continuous positive airway pressure (CPAP) treatment on arterial blood pressure, leading the "Joint National Council on High Blood Pressure" to list obstructive sleep apnoea as the first identifiable cause of arterial hypertension. Recently, a growing body of evidence demonstrated also a risk reduction of fatal and non-fatal cardiovascular events by treatment of obstructive sleep apnoea. A beneficial effect of treatment of OSA was also shown for patients with heart failure, or heart rhythm disturbance. Obstructive sleep apnoea may no longer be seen as a cause for daytime sleepiness and impaired quality of life only, but also as an independent risk factor, at least for the occurrence of hypertension but probably for any cardiovascular and cerebrovascular disease. While prospective controlled trials to document a reduction of cardiovascular morbidity and mortality are awaited, therapeutic nihilism seems no longer appropriate. With effective treatment available, subgroups that may profit best remain to be identified.     

Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics.

BACKGROUND: Limited information exists regarding the development of pulmonary hypertension in patients with obstructive sleep apnea (OSA) in the absence of lung and heart comorbidity. OBJECTIVES: The aims of this study were to investigate whether OSA patients without any other cardiac or lung disease develop pulmonary hypertension, and to assess the effect of continuous positive airway pressure (CPAP) treatment on pulmonary artery pressure (P(PA)). METHODS: Twenty-nine patients aged 51 +/- 10 years with OSA and 12 control subjects were studied with pulsed-wave Doppler echocardiography for estimation of P(PA) before and after 6-month effective treatment with CPAP. RESULTS: A significantly higher mean P(PA) was found in OSA patients as compared to control subjects (17.2 +/- 5.2 vs. 12.1 +/- 1.9 mm Hg, p < 0.001). Six out of the 29 OSA patients had mild pulmonary hypertension (P(PA) > or = 20 mm Hg). Significant differences were observed between pulmonary hypertensive and normotensive OSA patients with respect to age (62 +/- 4 vs. 48 +/- 15 years, respectively, p < 0.05), body mass index (41 +/- 7 vs. 32 +/- 4 kg/m(2), p < 0.02) and daytime P(a)O(2) (81 +/- 9 vs. 92 +/- 9 mm Hg, p < 0.05). CPAP treatment was effective in reducing mean P(PA) in both groups of pulmonary hypertensive and normotensive OSA patients (decreases in P(PA) from 25.6 +/- 4.0 to 19.5 +/- 1.5 mm Hg, p < 0.001; from 14.9 +/- 2.2 to 11.5 +/- 2.0 mm Hg, respectively, p < 0.001). CONCLUSIONS: A proportion (20.7%) of OSA patients without any other lung or heart disease and characterized by older age, greater obesity and lower daytime oxygenation develop mild pulmonary hypertension which has been partially or completely reversed after 6-month CPAP treatment. In conclusion, OSA alone constitutes an independent risk factor for the development of pulmonary hypertension.     

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 Role of Obesity and Obstructive Sleep Apnea in the Pathogenesis and Treatment of Resistant Hypertension

The incidence of resistant hypertension, obesity, and obstructive sleep apnea (OSA), three highly prevalent conditions in the United States, is rising. Approximately one in three adults in the US has hypertension, and a significant proportion of these individuals have hypertension that is difficult to treat, or resistant. Obesity and OSA are well-established risk factors for resistant hypertension, a condition that portends significant cardiovascular risk. Awareness of the various mechanisms by which obesity and OSA impact systemic blood pressure is essential to better understand how best to effectively care for patients with resistant hypertension. In this review, we discuss the clinical and pathophysiologic associations between obesity, OSA, and resistant hypertension. Furthermore, we will explore the effect of continuous positive airway pressure therapy (CPAP) and other therapeutic interventions on blood pressure control in patients with resistant hypertension. Key Points ? Obesity, obstructive sleep apnea, and resistant hypertension are highly prevalent conditions, with increasing overall incidence [1–3]. ? Both obesity and obstructive sleep apnea are independent risk factors for the development of resistant hypertension. ? OSA is characterized by a physiologic cascade of collapse of the upper airway, which can lead to intermittent hypoxia, hypercapnia, significant negative intra-thoracic pressure, and increased SNS output. ? Intermittent hypoxia leads to activation of the endothelin system [17, 18, 19?], which can lead to the development of resistant hypertension. ? Intermittent hypoxia can lead to the over activation of the SNS, which can also contribute to the development of resistant hypertension [20, 21]. ? OSA leads to state of elevated adrenergic tone, which in turn may contribute to resistant hypertension [25–27]. ? OSA patients have a higher incidence of “non-dipping” of nocturnal systolic blood pressure, a marker of increased adrenergic tone. This potentially represents a risk factor for hypertensive end organ disease [31, 32]. ? The prevalence of OSA is significantly higher in patients predisposed to fluid accumulation: including kidney disease, heart failure and resistant hypertension [33]. ? Interventions (such as the daytime use of compression stocking) which reduce daytime lower extremity fluid accumulation can significantly reduce the severity of OSA, particularly in patients with comorbid resistant hypertension [35, 36]. ? CPAP therapy can significantly reduce blood pressure in patients with comorbid hypertension and OSA. The treatment effect is most pronounced in those with resistant hypertension and OSA [16??, 38–42].     

Nocturnal pulse rate and symptomatic response in patients with obstructive sleep apnoea treated with continuous positive airway pressure for one year

Background

Obstructive sleep apnoea (OSA) is the most common form of sleep-disordered breathing and a known risk factor for cardiovascular disease. We hypothesised that in patients with OSA the characteristics of nocturnal pulse rate (PR) are associated with changes in blood pressure and daytime sleepiness, following commencement of continuous positive airway pressure (CPAP) therapy.

Methods

Pulse oximetry data, demographics, daytime sleepiness and blood pressure were recorded at baseline and at one year follow up. Patients with OSA were grouped according to positive and negative changes in the PR (ΔPR) response during the first night of pulse oximetry before commencement of CPAP.

Results

A total of 115 patients (58 with OSA and 57 matched subjects without OSA) were identified and included in the analysis. The scale of improvement in daytime sleepiness could be predicted by a negative or positive ΔPR, as recorded in the initial screening pulse oximetry [ΔESS –5.8 (5.1) vs. –0.8 (7.2) points, P<0.05]. A negative correlation was observed between mean nocturnal PR and changes in systolic blood pressure (SBP) after one year of CPAP treatment (r=–0.42, P<0.05).

Conclusions

Mean nocturnal PR prior to CPAP initiation was associated with changes in SBP at one year follow up. A descending nocturnal PR in patients with OSA, prior to CPAP initiation, might help to identify a symptomatic response from long term CPAP treatment.     

Blood pressure variability in obstructive sleep apnea: role of sympathetic nervous activity and effect of continuous positive airway pressure

BACKGROUND: Many studies support a link between obstructive sleep apnea (OSA), increased blood pressure (BP) and/or BP variability, and sympathetic nervous system (SNS) activity. We assessed the relationship between SNS activity and 24-h BP variability in patients with OSA, and the effect of continuous positive airway pressure (CPAP) on BP variability. DESIGN: Forty-one patients with a respiratory disturbance index (RDI) > 15 were randomized into CPAP or CPAP placebo groups for a 1-week trial. METHODS: Ambulatory BP, 24-h urine norepinephrine (NE) and polysomnography were measured prior to treatment and after 1 and 7 days of treatment. RESULTS: Neither RDI nor 24-h urine NE levels were related to 24-h mean BP levels. While RDI was associated only with night-time BP variability, daytime urine NE levels were associated with both night-time and daytime BP variability. After treatment, the BP variability decreased significantly but equally in both active and placebo CPAP groups. CONCLUSIONS: Obstructive sleep apnea is more related to BP variability than BP. Sympathetic nervous activity, as inferred from daytime urine NE, is related to changes in BP variability in OSA patients. BP variability is not specifically affected by CPAP.     

Obstructive sleep apnea and cardiovascular disease

Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension, arrhythmias, and atherosclerosis. Obesity is strongly linked to an increased risk of OSA, and weight loss can reduce the severity of OSA. The current standard treatment for OSA-nasal continuous positive airway pressure (CPAP)-eliminates apnea and the ensuing acute hemodynamic changes during sleep. Long-term CPAP treatment studies have shown a reduction in nocturnal cardiac ischemic episodes and improvements in daytime blood pressure levels and left ventricular function. Despite the availability of effective therapy, OSA remains an underdiagnosed and undertreated condition. A lack of physician awareness is one of the primary reasons for this deficit in diagnosis and treatment.     

Pulmonary hypertension and sleep-related breathing disorders

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).     

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.     

Obesity, sleep apnea, and hypertension

Obesity has a high and rising prevalence and represents a major public health problem. Obstructive sleep apnea (OSA) is also common, affecting an estimated 15 million Americans, with a prevalence that is probably also rising as a consequence of increasing obesity. Epidemiologic data support a link between obesity and hypertension as well as between OSA and hypertension. For example, untreated OSA predisposes to an increased risk of new hypertension, and treatment of OSA lowers blood pressure, even during the daytime. Possible mechanisms whereby OSA may contribute to hypertension in obese individuals include sympathetic activation, hyperleptinemia, insulin resistance, elevated angiotensin II and aldosterone levels, oxidative and inflammatory stress, endothelial dysfunction, impaired baroreflex function, and perhaps by effects on renal function. The coexistence of OSA and obesity may have more widespread implications for cardiovascular control and dysfunction in obese individuals and may contribute to some of the clustering of abnormalities broadly defined as the metabolic syndrome. From the clinical and therapeutic perspectives, the presence of resistant hypertension and the absence of a nocturnal decrease in blood pressure in obese individuals should prompt the clinician to consider the diagnosis of OSA, especially if clinical symptoms suggestive of OSA (such as poor sleep quality, witnessed apnea, excessive daytime somnolence, and so forth) are also present.