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Role of Inflammation in the Cardiometabolic Co-Morbidities of Sleep Apnoea

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Role of Inflammation in the Cardiometabolic Co-Morbidities of Sleep Apnoea bs_bs_banner Sleep and Biological Rhythms 2015; 13 (Suppl. 1): 1–98 doi:10.1111/sbr.12132 Abstracts (UAMs) have a variety of different discharge patterns. These patterns 001 are found in all UAMs, although the distribution of different patterns ROLE OF INFLAMMATION IN THE differs from one muscle to another. UAM motor units may be divided CARDIOMETABOLIC CO-MORBIDITIES into two classes, the “Inspiratory System” which consists of inspiratory modulated motor units and the “tonic system” consisting of tonic and OF SLEEP APNOEA expiratory modulated motor units. The inspiratory system motor units WALTER MCNICHOLAS1,2 1 2 are recruited under conditions of elevated respiratory drive, such as at University College Dublin, Dublin, Ireland, UCD Conway Institute, arousal from sleep and during hypercapnia, their activity being coor- Dublin, Ireland dinated by a central drive mediated by the respiratory pattern gen- erator, referred to as common drive. Common drive to inspiratory Obstructive sleep apnoea syndrome (OSA) is strongly associated with motor units is pervasive subsuming inspiratory motor units both cardiovascular morbidity and mortality and there is increasing evi- within and between UAMs. This system is the main mechanism for dence for a link between OSA and metabolic dysfunction, in particular the defence of airway patency in the face of closing forces. The tonic insulin resistance and metabolic syndrome. The particular form of system, which consists of almost 50% of motor units in UAMs, intermittent hypoxia (IH) observed in OSA, with repetitive short responds only weakly to airway closure. Further, common drive to cycles of desaturation followed by rapid reoxygenation, plays a major tonic and expiratory modulated motor units within a muscle is less role in the development of cardiovascular co-morbidities. The patho- than to inspiratory system motor units and is non-existent between genesis is likely multifactorial and likely involves sympathetic nervous muscles. The heterogeneity of the tonic system suggests its function is system over activity, systemic inflammation and oxidative stress to fine tune airway configuration. Consistent with this suggestion is leading to endothelial dysfunction, and possibly metabolic dysfunction the observation that the motor units of the tonic system are often as the most important pathways. Inflammatory processes are central in inhibited in situations of high respiratory drive, such as sleep related this pathogenesis and there is evidence from both cell culture obstructions, or physical exercise. and in vivo models that IH selectively activates the transcription κ κ These observations have relevance to treatments of obstructive sleep factor nuclear factor-kappa B (NF- B). NF- B is a key player in apnoea that involve stimulation of the UAMs. inflammatory and innate immune responses and when chronically activated contributes to atherosclerosis through driving product- ion of inflammatory mediators such as tumour necrosis factor alpha (TNF-α), interleukin (IL)-8 and IL-6. Moreover, these mediators 003 have been found to be upregulated in OSA patients versus matched controls and effective CPAP therapy significantly lowers these EFFECTS OF EVENING VERSUS MORNING levels supporting the key role of NF-κB as driver of inflammation in ADMINISTRATION OF AN ACE-INHIBITOR ON OSA. 24 HOUR BLOOD PRESSURE CONTROL IN The main source organ of the IH-dependent release of inflammatory PATIENTS WITH OBSTRUCTIVE SLEEP APNOEA mediators in OSA is still unknown, but white adipose tissue (WAT) is a likely source given the close link between OSA and obesity. Moreover, AND HYPERTENSION: A DOUBLE BLIND obesity itself represents a low-grade inflammatory condition through the RANDOMISED CONTROLLED TRIAL secretion of pro-inflammatory mediators from WAT (termed YASAMAN DJAVADKHANI1, BRENDON J YEE1,3, PHILIP LEE1, adipokines). These include a variety of pro-inflammatory mediators KEITH K WONG1,3, PETER A CISTULLI2,4, HISATOMI ARIMA5,6, such as TNF-α and IL-6 that may represent a key link between obesity RONALD R GRUNSTEIN1,3, CRAIG L PHILLIPS1,4 and obesity-induced cardiovascular diseases. There is emerging evi- 1Sleep and Circadian Group, Centre for Integrated Research and dence that hypoxia is a key factor in modulating the production of Understanding of Sleep, Woolcock Institute of Medical Research, University inflammatory adipokines in obesity. As IH represents a stronger inflam- of Sydney, Sydney, NSW, Australia, 2Discipline of Sleep Medicine, Sydney matory stimulus than sustained hypoxia, this process may be potenti- Medical School, University of Sydney, Sydney, NSW, Australia, ated in diseases associated with IH such as OSA. 3Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, NSW, Australia, 4Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, Sydney, NSW, Australia, 5George Institute for Global Health, Sydney, NSW, Australia, 6Sydney Medical 002 School, Sydney, NSW, Australia HOW THE BRAIN CONTROLS UPPER AIRWAY Introduction: In patients with essential hypertension, ingesting antihy- MUSCLES TO MAINTAIN AIRWAY PATENCY pertensive medication in the evening (PM) instead of in the morning JOHN TRINDER (AM) substantially improves 24-hour blood pressure (24BP) control. University of Melbourne, Melbourne, VIC, Australia This chronotherapeutic effect has not been robustly tested in patients with obstructive sleep apnoea and hypertension (OSA-HT) where there Airway patency is dependent on the activity of upper airway muscles is potential to improve 24BP by greater than twice the effect of Con- such as Genioglossus and Tensor Palatini. Motor neurons originating tinuous Positive Airway Pressure (CPAP) treatment. We sought to deter- in brain stem motor nuclei and innervating upper airway muscles mine whether PM versus AM administration of an ACE-Inhibitor has a © 2015 Japanese Society of Sleep Research 1 Sleep, Science and Research superior effect on 24 hour BP control in OSA-HT patients. We also Results: 1137 arousals were analysed from 24 participants. The median examined whether the addition of CPAP conferred an additional BP end-arousal CO2 was 0.72 mmHg below waking CO2 (range = benefit. −8.8 mmHg to 11.5 mmHg). There was a significant (p < 0.05) negative Methods: In this double-blind randomised placebo-controlled association that approximated an exponential function between end- cross-over trial, we studied 85 patients with OSA-HT (oxygen arousal CO2 and peak EMGgg on all breaths (except breath 4) following desaturation index ≥15/hr, HT based on 24BP). Patients with severe the return to sleep (see Figure 1 for an example). A 1 mmHg decrease in or resistant HTN or aged ≥65 yo were excluded. Patients were end-arousal CO2 was associated with a 2% increase in peak EMGgg, randomised to 6 weeks each of PM or AM perindopril 10 mg with with the lowest CO2 arousals having the highest EMGgg. matching placebo. CPAP therapy was then added at the end of the Tonic EMGgg was similar. second treatment arm. Outcomes were collected at the end of each treatment phase. Results: 85 patients were randomised, 79 completed AM and PM dosing,72 patients have thus far completed the final CPAP arm. Baseline values were: male/female 69/16, age 54 ± 8, BMI 34 ± 7 kg/m2, ESS 10 ± 5; ODI 42 ± 25/hr, AHI 48 ± 23/hr, minimum SaO2 76 ± 12%; 24BP: Wake 147/90 mmHg, Sleep 128/77 mmHg, 37% were non- dippers. Wake and sleep BP were significantly decreased from baseline after both AM and PM dosing (SBP −7.1 to −9.9 mmHg and DBP −3.7 to −5.2 mmHg, all p < 0.001). Sleep SBP (primary outcome) and DBP did not differ between AM and PM dosing. However, AM dosing lowered wake BP more than PM dosing [by −2.0(0.9)/−1.1(0.6) mmHg, both p < 0.05].Nocturnal dipping increased with medication independ- Figure 1 End arousal CO2 and peak EMGgg on breath 5 ent of ingestion time. Furthermore, addition of CPAP to AM but not PM dosing lowered sleep SBP/DBP (−4.3/−4.0 mmHg). Discussion: This is the first RCT to explore the role of chronotherapy in Conclusion: Arousal induced hypocapnia does not reduce upper OSA-HT patients. In contrast to patients with essential hypertension airway dilator muscle activity. Rather, arousals with low end-arousal who have lower sleep BP with PM dosing, our OSA patients had CO2 had increased genioglossus activity. Therefore, arousals are unlikely lower wake BP from AM dosing. Adding CPAP to AM dosing signifi- to perpetuate OSA via reduced dilator muscle activity as commonly cantly lowered sleep BP. Given that sleep BP strongly predicts cardio- stated in the arousal literature. vascular mortality, combining OSA and anti-hypertensive treatment is essential. 005 ZOPICLONE INCREASES THE RESPIRATORY 004 AROUSAL THRESHOLD WITHOUT IMPAIRING GENIOGLOSSUS MUSCLE ACTIVITY IN AROUSAL INDUCED HYPOCAPNIA IS NOT OBSTRUCTIVE SLEEP APNOEA DETRIMENTAL TO GENIOGLOSSUS MUSCLE SOPHIE CARTER1,2, MICHAEL BERGER1,2, JAYNE CARBERRY1,2, ACTIVITY FOLLOWING THE RETURN TO SLEEP LYNNE BILSTON1,2, JANE BUTLER1,2, BENJAMIN TONG1,2, IN OBSTRUCTIVE SLEEP APNEA RODRIGO MARTINS1,2, LAUREN FISHER1,2, DAVID MCKENZIE3, JENNIFER CORI1,2, THERESE THORNTON1,2, PETER ROCHFORD2, RONALD GRUNSTEIN4,5, DANNY ECKERT1,2 FERGAL O’DONOGHUE1,2, JOHN TRINDER1, AMY JORDAN1,2 1Neuroscience Research Australia, Sydney, NSW, Australia, 2The University 1The University of Melbourne, Parkville, Vic, Australia, 2The Institute of of New South Wales, Sydney, NSW, Australia, 3Prince of Wales Hospital, Breathing and Sleep, Heidelberg, Vic, Australia Sydney, NSW, Australia, 4Woolcock
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