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(Circulation. 1999;100:2332.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Nocturnal Continuous Positive Airway Pressure Decreases Daytime Sympathetic Traffic in Obstructive Sleep Apnea
From the Department of Internal Medicine (K.N., M.K., C.A.P., D.E.D., V.K.S.) and Division of Clinical and Administrative Pharmacy (B.G.P.), University of Iowa, Iowa City.
Correspondence to Virend K. Somers, MD, PhD, Department of Internal Medicine, Mayo Clinic, 200 First St SW, Rochester MD 55905. E-mail somers.virend{at}mayo.edu
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Abstract |
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Background—Patients with obstructive sleep apnea (OSA) have high levels of muscle sympathetic nerve activity (MSNA). We tested the hypothesis that long-term continuous positive airway pressure (CPAP) treatment will decrease MSNA in OSA patients.
Methods and Results—We measured blood pressure, heart rate, and MSNA in 11 normotensive, otherwise healthy patients with OSA who were treated with CPAP. The measurements were obtained at baseline and after 1 month, 6 months, and 1 year of CPAP treatment. These measurements were compared with those recorded in 9 otherwise healthy OSA patients who were not treated with CPAP for 1 year. In both untreated and treated patients, blood pressure and heart rate did not change over time. MSNA was similar during repeated measurements in the untreated group. By contrast, MSNA decreased significantly over time in patients treated with CPAP. This decrease was evident after both 6 months and 1 year of CPAP treatment (P=0.02 for both).
Conclusions—CPAP treatment decreases muscle sympathetic traffic in patients with OSA. This effect of CPAP is evident only after an extended duration of therapy.
Key Words: positive-pressure respiration • sleep apnea syndromes • sympathetic nervous system • therapeutics
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Introduction |
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Patients with obstructive sleep apnea (OSA) experience repetitive apneic events during sleep, with resulting hypoxia and hypercapnia. Hypoxia and hypercapnia, acting via the chemoreflexes, elicit increases in sympathetic nerve activity, with consequent increases in blood pressure.1 2 The increased sympathetic activity during sleep carries over into daytime wakefulness. Patients with OSA have high daytime levels of norepinephrine3 4 5 and elevated muscle sympathetic nerve activity (MSNA).1 6 The increased MSNA during normoxic wakefulness is evident whether or not patients are hypertensive,1 6 and is not explained by obesity.8
Acute treatment with continuous positive airway pressure (CPAP) results in a marked reduction in nocturnal sympathetic nerve traffic1 and blunts blood pressure surges during sleep.1 9 Autonomic responses to OSA result in increased left ventricular afterload,10 which is decreased by short-term CPAP therapy in patients with heart failure.11 These short-term effects are secondary to the attenuation of apneic episodes by CPAP.
Sympathetic nerve responses to CPAP treatment seem to depend on the duration of therapy. Marrone et al12 showed that high levels of catecholamines in OSA patients were not reduced after 1 night of CPAP treatment. After 1 month of CPAP treatment in 7 patients,13 a variable effect on sympathetic traffic was evident, with decreases in 4 patients and no change in 3 patients. Other studies of short-term CPAP treatment showed either a decrease5 (3 months of CPAP) or no change14 (7 days of CPAP) in plasma norepinephrine. After 1 to 2 years of CPAP treatment, however, Hedner et al4 reported a significant reduction in both plasma norepinephrine levels and catecholamine excretion. Untreated patients were not included in any of these studies. Nevertheless, taken together, these data suggest that any effect of CPAP treatment on sympathetic drive is evident only after an extended duration of therapy.
Therefore, we tested the hypothesis that long-term CPAP treatment will decrease MSNA in patients with OSA. We measured sympathetic traffic in normotensive, otherwise healthy patients with OSA who were treated with CPAP. Measurements were obtained at baseline and after 1 month, 6 months, and 1 year of CPAP treatment to provide some insight into the timing and stability of any response to therapy. These measurements were compared with those recorded at identical intervals in otherwise healthy OSA patients who were not treated with CPAP for 1 year.
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Methods |
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Subjects
We studied 25 patients with newly diagnosed OSA. All patients were normotensive, free of any other known diseases, and receiving no medications. None of the patients had central sleep apnea. Ten of the 25 patients refused CPAP treatment and served as a control group. The remaining 15 patients began CPAP treatment after baseline measurements were obtained.
Four patients from the treated group and 1 untreated patient were lost to follow-up. Consequently, 1 year follow-up was completed in 11 patients treated with CPAP (10 men and 1 woman aged 46±8 years; mean body mass index, 33±5 kg/m2) and 9 untreated patients (8 men and 1 woman aged 49±13 years; mean body mass index, 30±4 kg/m2). Compliance with prescribed CPAP treatment was based on self-reported estimated use, expressed as average time with CPAP in relation to total time spent in bed.4 All treated patients reported >75% compliance with CPAP treatment.
Informed written consent was obtained from all subjects. The study was approved by the Institutional Human Subjects Review Committee.
Measurements
Heart rate was measured continuously by ECG. Blood pressure was
measured each minute by an automatic sphygmomanometer (Life Stat 200,
Physio-Control Corp). Sympathetic nerve activity to muscle was
recorded continuously by obtaining multiunit recordings of
postganglionic sympathetic activity to muscle blood vessels, and it was
measured from a muscle nerve fascicle in the peroneal nerve posterior
to the fibular head, as described previously.15
Protocol
Measurements of heart rate, blood pressure, and MSNA were
obtained during 10 minutes of undisturbed supine rest in carefully
standardized conditions. Studies were conducted in the same room and
3 hours after the last meal. In addition, all patients were asked to
void before the recordings. None of the subjects had apneas,
hypopneas, or oxygen desaturation during the study. In all 20 patients,
these recordings were repeated after 1 month, 6 months, and
1 year.
Analyses
A random code was given to the recordings so that all
data analyses were performed with the analyst completely
blinded to the identity of the subject and the session during which the
recording was performed. Sympathetic bursts were identified by
a careful inspection of the voltage neurogram. Sympathetic activity was
expressed as bursts/min. Statistical analysis consisted of
repeated-measures ANOVA with time as the within factor and group
(treated versus untreated) as the between factor. The key variable
was the group-by-time interaction. Data are presented as
mean±SEM. P<0.05 was considered significant.
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Results |
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Baseline Measurements
The mean baseline apnea-hypopnea index was 27±6 events/hour in patients who received treatment with CPAP and 23±5 events/hour in untreated OSA patients (P=NS). Baseline blood pressure, heart rate, and MSNA in the treated group were not different from those observed in the untreated group (Table
).
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Repeated Measurements
Both untreated and treated patients tended to gain weight over
time, and the weight gain in the treated group (2.5±2.0 kg at 6 months
and 1.4±1.6 kg at 1 year) was similar to that in the untreated group
(1.6±2.1 kg at 6 months and 1.2±1.9 kg at 1 year). In both untreated
and treated patients, blood pressure and heart rate did not change over
time (Table
). However, MSNA decreased significantly over time in
patients treated with CPAP (Figure 1;
Table). By contrast, MSNA was similar during repeated
measurements in the untreated group (Figure 2; Table).
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Figure 3 presents group data for the
MSNA changes over time. In the treated group, a decrease in MSNA after
1 month of CPAP was not significant (P>0.20). A significant
MSNA decrease was observed only after both 6 months and 1 year of CPAP
treatment (P=0.02 for both).
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Discussion |
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The novel finding of this study is that long-term CPAP treatment decreases muscle sympathetic traffic in normotensive patients with OSA. MSNA reduction during CPAP treatment is not paralleled by changes in blood pressure or heart rate.
Prior studies of CPAP have shown either a decrease4 5 13 or no change in sympathetic activity.12 14 This inconsistent effect of CPAP on sympathetic drive may be linked to the duration of CPAP treatment, as discussed earlier. Other potential explanations may include the presence of diabetic13 and hypertensive4 13 14 patients in some studies and the absence of an untreated control group. Hypertension16 17 and the dosage and timing of vasoactive medications18 19 may influence measurements of heart rate, blood pressure, and sympathetic activity. Furthermore, the presence of untreated sleep apneic patients is crucial to minimizing the effects of repeated measurements or regression to the mean as causes of apparent decreases in sympathetic drive in OSA patients on CPAP therapy.
An important strength of the present study is that all patients
were free of any diseases other than OSA and they were receiving no
medications. Thus, we eliminated confounding effects of other disease
states or pharmacological intervention on sympathetic traffic. Another
unique feature of our study is the inclusion of patients who remained
untreated. Furthermore, all analyses were conducted blinded to
subject and session. Potential limitations also exist. One is the lack
of randomization of patients to therapy. In mitigation, CPAP treatment
has been shown to improve daytime sleepiness, cognition, mood, quality
of life, work performance, and concentration
ability.20 21 Therefore, for reasons of subject safety,
the untreated group included only those patients who refused CPAP
treatment. Another potential limitation is that compliance with
prescribed CPAP treatment was determined on the basis of self-reported
estimated use. Self-reported compliance may represent 
15%
overestimation of true use.4 22 Overestimation of CPAP use
may, therefore, have underestimated the effects of CPAP on sympathetic
traffic.
We could not demonstrate a decrease in MSNA after 1 month of CPAP treatment. However, we found a significant decrease in sympathetic traffic after both 6 months and 1 year of treatment. Thus, long-term CPAP therapy is required to attenuate the sympathetic activation observed in patients with OSA. Increased sympathetic drive may be implicated in atherosclerotic vascular disease and adverse cardiovascular events.23 24 Patients with sleep apnea have both high levels of sympathetic activity and an increased risk of cardiovascular disease.25 26 The increased sympathetic drive in patients with OSA may predispose them to cardiovascular morbidity, perhaps by mechanisms such as enhanced platelet activation.27 CPAP treatment in otherwise healthy patients with OSA may conceivably reduce their cardiovascular risk through the reduction of sympathetic activity. In OSA patients with heart failure, attenuated sympathetic drive induced by long-term CPAP therapy may contribute to the reported increases in ejection fraction.28 However, our data do not speak directly to any effects of CPAP on cardiovascular morbidity because we studied OSA patients who were otherwise healthy and at less cardiovascular risk than the sleep apneic patient population at large.
The effect of CPAP on daytime blood pressure is controversial; some studies report a reduction in blood pressure,14 29 30 31 and others find no change.4 13 In the present study, long-term CPAP treatment did not affect blood pressure. This may be explained by our selection criteria. To eliminate the potential influence of other diseases and of medications, we studied only normotensive patients. Those studies reporting a significant decrease in blood pressure included mostly hypertensive patients with OSA. Thus, a reduction in blood pressure may be evident only in hypertensive patients with OSA. The absence of significant blood pressure change, despite a decrease in MSNA, may be secondary to maintenance of sympathetic drive in other vascular beds, because MSNA does not necessarily reflect overall level of sympathetic nerve traffic. Alternatively, a lack of significant blood pressure decrease during CPAP treatment may be explained by the effects of atrial natriuretic peptide. Untreated patients with OSA have high levels of atrial natriuretic peptide, resulting in increased diuresis and natriuresis.32 33 34 CPAP treatment reduces atrial natriuretic peptide secretion and sodium excretion.32 34 35 Thus, the pressor effects of increased sodium retention might oppose the expected blood pressure–lowering effects of reduced sympathetic activity.
The mechanism underlying the decrease in MSNA after long-term CPAP treatment is not known. Tonic activation of excitatory chemoreflex afferents may contribute to increased efferent sympathetic activity to muscle circulation in untreated patients with OSA.36 It is possible that attenuation of apneic events by CPAP decreases chemoreflex sensitivity and tonic chemoreflex activation, with consequent decreases in sympathetic traffic. Other potentially beneficial effects of CPAP also need evaluation. These include effects on sleep architecture, REM sleep deprivation, and humoral vasoactive substances, each of which may also influence levels of sympathetic traffic.
In conclusion, we showed that long-term CPAP treatment decreases muscle sympathetic traffic in patients with OSA. This effect of CPAP is evident only after an extended duration of therapy, and it may have implications for the prevention of cardiovascular disease in this patient population.
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Acknowledgments |
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Dr Narkiewicz was a visiting research scientist from the Department of Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland, and the recipient of an International Research John E. Fogarty Fellowship (NIH 3F05 TW05200) and a Perkins Memorial Award from the American Physiological Society. These studies were also supported by National Institutes of Health grants HL61560 and HL14388. Dr Somers is an Established Investigator of the American Heart Association and a Sleep Academic Awardee of the National Institutes of Health.
Received May 25, 1999; revision received July 20, 1999; accepted July 20, 1999.
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J. Spaak, Z. J. Egri, T. Kubo, E. Yu, S.-I. Ando, Y. Kaneko, K. Usui, T. D. Bradley, and J. S. Floras Muscle Sympathetic Nerve Activity During Wakefulness in Heart Failure Patients With and Without Sleep Apnea Hypertension, December 1, 2005; 46(6): 1327 - 1332. [Abstract] [Full Text] [PDF]
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V. K. Somers Sleep -- A New Cardiovascular Frontier N. Engl. J. Med., November 10, 2005; 353(19): 2070 - 2073. [Full Text] [PDF]
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 S. M. Caples, A. S. Gami, and V. K. Somers Obstructive Sleep Apnea Focus, October 1, 2005; 3(4): 557 - 567. [Full Text] [PDF]
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M. A. Martinez-Garcia, R. Galiano-Blancart, P. Roman-Sanchez, J.-J. Soler-Cataluna, L. Cabero-Salt, and E. Salcedo-Maiques Continuous Positive Airway Pressure Treatment in Sleep Apnea Prevents New Vascular Events After Ischemic Stroke Chest, October 1, 2005; 128(4): 2123 - 2129. [Abstract] [Full Text] [PDF]
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C M Ryan, K Usui, J S Floras, and T D Bradley Effect of continuous positive airway pressure on ventricular ectopy in heart failure patients with obstructive sleep apnoea Thorax, September 1, 2005; 60(9): 781 - 785. [Abstract] [Full Text] [PDF]
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G. Grassi, A. Facchini, F. Q. Trevano, R. Dell'Oro, F. Arenare, F. Tana, G. Bolla, A. Monzani, M. Robuschi, and G. Mancia Obstructive Sleep Apnea-Dependent and -Independent Adrenergic Activation in Obesity Hypertension, August 1, 2005; 46(2): 321 - 325. [Abstract] [Full Text] [PDF]
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 M. A. Arias, F. Garcia-Rio, A. Alonso-Fernandez, O. Mediano, I. Martinez, and J. Villamor Obstructive Sleep Apnea Syndrome Affects Left Ventricular Diastolic Function: Effects of Nasal Continuous Positive Airway Pressure in Men Circulation, July 19, 2005; 112(3): 375 - 383. [Abstract] [Full Text] [PDF]
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 V. K. Somers, A. S. Gami, and L. J. Olson Treating Sleep Apnea in Heart Failure Patients: Promises But Still No Prizes J. Am. Coll. Cardiol., June 21, 2005; 45(12): 2012 - 2014. [Full Text] [PDF]
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 S. M. Caples, A. S. Gami, and V. K. Somers Obstructive Sleep Apnea Ann Intern Med, February 1, 2005; 142(3): 187 - 197. [Full Text] [PDF]
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P Gordon and M H Sanders Sleep {middle dot} 7: Positive airway pressure therapy for obstructive sleep apnoea/hypopnoea syndrome Thorax, January 1, 2005; 60(1): 68 - 75. [Abstract] [Full Text] [PDF]
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L. J. Olson, E. J. Olson, and V. K. Somers Obstructive Sleep Apnea and Platelet Activation: Another Potential Link Between Sleep-Disordered Breathing and Cardiovascular Disease Chest, August 1, 2004; 126(2): 339 - 341. [Full Text] [PDF]
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A. S Gami and V. K Somers Obstructive sleep apnoea, metabolic syndrome, and cardiovascular outcomes Eur. Heart J., May 1, 2004; 25(9): 709 - 711. [Full Text] [PDF]
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D. S. Hui, F. W. Ko, J. P. Fok, M. C. Chan, T. S. Li, B. Tomlinson, and G. Cheng The Effects of Nasal Continuous Positive Airway Pressure on Platelet Activation in Obstructive Sleep Apnea Syndrome Chest, May 1, 2004; 125(5): 1768 - 1775. [Abstract] [Full Text] [PDF]
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I. Fietze, D. Romberg, M. Glos, S. Endres, H. Theres, C. Witt, and V. K. Somers Effects of positive-pressure ventilation on the spontaneous baroreflex in healthy subjects J Appl Physiol, March 1, 2004; 96(3): 1155 - 1160. [Abstract] [Full Text] [PDF]
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T. L. Goodfriend and D. A. Calhoun Resistant Hypertension, Obesity, Sleep Apnea, and Aldosterone: Theory and Therapy Hypertension, March 1, 2004; 43(3): 518 - 524. [Abstract] [Full Text] [PDF]
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S. Javaheri, W. T. Abraham, C. Brown, H. Nishiyama, R. Giesting, and L. E. Wagoner Prevalence of obstructive sleep apnoea and periodic limb movement in 45 subjects with heart transplantation Eur. Heart J., February 1, 2004; 25(3): 260 - 266. [Abstract] [Full Text] [PDF]
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D. A. Calhoun, M. K. Nishizaka, M. A. Zaman, and S. M. Harding Aldosterone Excretion Among Subjects With Resistant Hypertension and Symptoms of Sleep Apnea Chest, January 1, 2004; 125(1): 112 - 117. [Abstract] [Full Text] [PDF]
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 A. S. M. Shamsuzzaman, B. J. Gersh, and V. K. Somers Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease JAMA, October 8, 2003; 290(14): 1906 - 1914. [Abstract] [Full Text] [PDF]
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D. D. Sin Sleep-Disordered Breathing: A Heart-Changing Experience? Chest, September 1, 2003; 124(3): 778 - 780. [Full Text] [PDF]
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J. o-D. L. Lattimore, D. S. Celermajer, and I. Wilcox Obstructive sleep apnea and cardiovascular disease J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1429 - 1437. [Abstract] [Full Text] [PDF]
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T. D. Bradley and J. S. Floras Sleep Apnea and Heart Failure: Part I: Obstructive Sleep Apnea Circulation, April 1, 2003; 107(12): 1671 - 1678. [Full Text] [PDF]
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O. Marrone, A. Salvaggio, M.R. Bonsignore, G. Insalaco, and G. Bonsignore Blood pressure responsiveness to obstructive events during sleep after chronic CPAP Eur. Respir. J., March 1, 2003; 21(3): 509 - 514. [Abstract] [Full Text] [PDF]
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A.G. Logan, R. Tkacova, S.M. Perlikowski, R.S. Leung, A. Tisler, J.S. Floras, and T.D. Bradley Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex Eur. Respir. J., February 1, 2003; 21(2): 241 - 247. [Abstract] [Full Text] [PDF]
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C. P. O'Donnell, L. Allan, P. Atkinson, and A. R. Schwartz The Effect of Upper Airway Obstruction and Arousal on Peripheral Arterial Tonometry in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 965 - 971. [Abstract] [Full Text]
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K. M. Hla, J. B. Skatrud, L. Finn, M. Palta, and T. Young The Effect of Correction of Sleep-Disordered Breathing on BP in Untreated Hypertension Chest, October 1, 2002; 122(4): 1125 - 1132. [Abstract] [Full Text] [PDF]
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D. S.C. Hui, D. K.L. Choy, L. K.S. Wong, F. W.S. Ko, T. S.T. Li, J. Woo, and R. Kay Prevalence of Sleep-Disordered Breathing and Continuous Positive Airway Pressure Compliance* : Results in Chinese Patients With First-Ever Ischemic Stroke Chest, September 1, 2002; 122(3): 852 - 860. [Abstract] [Full Text] [PDF]
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M. R. Bonsignore, G. Parati, G. Insalaco, O. Marrone, P. Castiglioni, S. Romano, M. Di Rienzo, G. Mancia, and G. Bonsignore Continuous Positive Airway Pressure Treatment Improves Baroreflex Control of Heart Rate during Sleep in Severe Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., August 1, 2002; 166(3): 279 - 286. [Abstract] [Full Text] [PDF]
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M. Elam, D. McKenzie, and V. Macefield Mechanisms of sympathoexcitation: single-unit analysis of muscle vasoconstrictor neurons in awake OSAS subjects J Appl Physiol, July 1, 2002; 93(1): 297 - 303. [Abstract] [Full Text] [PDF]
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 V. Belozeroff, R. B. Berry, C. S. H. Sassoon, and M. C. K. Khoo Effects of CPAP therapy on cardiovascular variability in obstructive sleep apnea: a closed-loop analysis Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H110 - H121. [Abstract] [Full Text] [PDF]
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R. S. T. LEUNG and T. DOUGLAS BRADLEY Sleep Apnea and Cardiovascular Disease Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2147 - 2165. [Full Text] [PDF]
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M. G. Ziegler, P. J. Mills, J. S. Loredo, S. Ancoli-Israel, and J. E. Dimsdale Effect of Continuous Positive Airway Pressure and Placebo Treatment on Sympathetic Nervous Activity in Patients With Obstructive Sleep Apnea Chest, September 1, 2001; 120(3): 887 - 893. [Abstract] [Full Text] [PDF]
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M. C. K. KHOO, V. BELOZEROFF, R. B. BERRY, and C. S. H. SASSOON Cardiac Autonomic Control in Obstructive Sleep Apnea . Effects of Long-term CPAP Therapy Am. J. Respir. Crit. Care Med., September 1, 2001; 164(5): 807 - 812. [Abstract] [Full Text] [PDF]
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Z. Tahawi, N. Orolinova, I. G. Joshua, M. Bader, and E. C. Fletcher Physiological and Genomic Consequences of Intermittent Hypoxia: Selected Contribution: Altered vascular reactivity in arterioles of chronic intermittent hypoxic rats J Appl Physiol, May 1, 2001; 90(5): 2007 - 2013. [Abstract] [Full Text] [PDF]
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J. F. FACCENDA, T. W. MACKAY, N. A. BOON, and N. J. DOUGLAS Randomized Placebo-controlled Trial of Continuous Positive Airway Pressure on Blood Pressure in the Sleep Apnea-Hypopnea Syndrome Am. J. Respir. Crit. Care Med., February 1, 2001; 163(2): 344 - 348. [Abstract] [Full Text]
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J. M. Samet, F. Javier Nieto, and N. M. Punjabi Sleep-disordered Breathing and Hypertension: More Research Is Still Needed Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1409 - 1411. [Full Text]
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