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Table 2.1 PALM classication scale
PALM category 1 Severe anatomical
decit
2 Moderate
anatomical decit
2a Minor nonanatomical
2b Nonanatomical
3 Minor anatomical
decit
Can be used to classify patients and as such dene optimal treatment options for the individual OSA patient [5]
Category cut-off
P
> +2cm H2O Anatomical decit. Anatomical or
crit
−2cm H2O<P +2cm H2O
vulnerability
vulnerability
P
< −2cm H2O
crit
<
crit
Denition
mechanical intervention advised (e.g., CPAP)
Potential candidate for combination therapy
Anatomic interventions advised (e.g., CPAP, MAD, positional therapy)
Combination of anatomic and nonanatomical interventions (e.g., MAD + oxygen)
Nonanatomical interventions advised (e.g., oxygen)
S. Op de Beeck et al.
when the pharyngeal muscles are passive (i.e., not additionally activated). By deni­tion, active collapsibility is the ventilation that can be achieved at maximal ventila­tory drive (i.e., when ventilatory drive is at the arousal threshold and pharyngeal muscles are activated as much as possible). The upper airway gain, reecting upper airway muscle activation, is the slope of the line connecting V
passive
and V
active
. Stable breathing (orange) is achieved if the line representing “1/loop gain” and the line representing “upper airway gain” intersect. However, stable breathing can only be achieved if the ventilatory drive associated with this point is situated before (to the left of) the arousal threshold.
The goal in treating obstructive sleep apnea is to modify one or more of the traits (loop gain, arousal threshold, passive collapsibility or upper airway muscle com­pensation) to allow stable breathing without reaching the arousal threshold.
A potential patient classication scale is dened as the PALM scale [5] based on four pathophysiological traits: P
, Arousal threshold, Loop gain and Muscle
crit
responsiveness (Table2.1). According to this scale, OSA patients can be subdivided into three main categories The major determinant to dene the category of each individual patient is the upper airway collapsibility, based on P
[5]. Patients with
crit
moderate anatomical decits can be further subdivided into patients without non­anatomical vulnerability (group 2a) and patients with nonanatomical vulnerability (group 2b). Based on this classication scheme, optimal treatment actions can be dened for individual patients [5].
2.8 Association Between Treatment Outcome
andPathophysiological Traits
While the different traits will interact as shown in Fig.2.13, the relative importance of each trait affects treatment outcome of different OSA treatment modalities (Table2.2).
Site, pattern
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Table 2.2 The optimal treatment for OSA patients depends on the underlying pathophysiological trait distribution. Colored elds represent the most important traits for each OSA treatment. Importance of each trait is reected in the height of the colored bars
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Upper airway
collapsibility
Continuous
Positive Airway
Pressure (CPAP)
Mandibular
Advancement
Devices (MAD)
Hypoglossal
Nerve
Stimulation
Upper Airway
Surgery
Drug Therapy
and degree of
upper airway
collapse
Ventilatory
control stability
Muscle
responsiveness
Arousal
threshold
2.8.1 Continuous Positive Airway Pressure (CPAP)
CPAP treatment is characterized by a high efcacy across different patient cohorts. However, limited adherence might hamper overall efciency. Assessing the under­lying pathophysiology of patients and its associations with CPAP adherence might increase overall efciency. A recent study on patients with coronary artery disease showed that a greater adherence to CPAP was found in patients with a higher arousal threshold and average muscle compensation [61].
2.8.2 Mandibular Advancement Devices (MAD)
Regarding MAD treatment, all pathophysiological, both anatomical and physiologi­cal, traits play a role in selecting the best candidates.
Regarding the site of upper airway collapse, an increase in velopharyngeal cross­sectional area with MAD correlates with treatment response [62–66]. Furthermore, an improvement in upper airway patency during DISE using a simulation bite pre­dicts MAD response [63]. Recently, a posteriorly located tongue during natural sleep was also found to be associated with MAD treatment outcomes [67]. Similarly, tongue base collapse during DISE was found to be associated with increased odds of being a MAD responder. In contrast, CCCp and complete laterolateral oropha­ryngeal collapse were associated with increased odds for deteriorating during MAD treatment [68].
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S. Op de Beeck et al.
Regarding upper airway collapsibility, MAD treatment response is associated with a lower pharyngeal collapsibility, reected in a lower P
and lower optimal
crit
CPAP level [67, 69–72]. Using nite element modeling and during clinical studies, mandibular advancement was shown to lower P
in a dose-dependent way [21, 23,
crit,
24, 73–77].
Loop gain affects both upper airway surgery outcomes and MAD treatment out­comes. For both treatment modalities, a lower loop gain, reecting a more stable ventilatory control system, was associated with an increased probability of treat­ment response [52, 69].
Overall, using the noninvasive technique to assess the pathophysiological traits based on baseline PSG signals, a low loop gain proved to be the most critical physi­ological parameter [72]. However, lower collapsibility, higher arousal threshold, lower response to arousal and weaker muscle compensation were also favorable determinants [71].
2.8.3 Hypoglossal Nerve Stimulation
Complete concentric collapse at the level of the palate (CCCp), assessed during DISE, is a negative endotype and formal exclusion criterion for respiration­synchronized upper airway stimulation treatment [78, 79]. Furthermore, it has been shown that patients with complete anteroposterior or laterolateral palatal or epiglot­tic collapse might have increased odds for therapy failure [80].
Regarding the other traits, a recent study using the noninvasive methods described earlier showed that patients with a higher arousal threshold had increased odds of being a responder to HGNS treatment after 1 year [81]. Combining arousal thresh­old with the other physiological traits into one model showed that patients with a nonanatomical problem predisposing OSA (low arousal threshold, high loop gain, low pharyngeal compensation, mild collapsibility) tend to be nonresponders to HGNS treatment.
2.8.4 Upper Airway Surgery
Assessing the site of upper airway collapse is paramount before performing upper airway surgery. Therefore, DISE is routinely performed on each surgical candidate to dene and ne-tune the treatment plan [82, 83].
In contrast to HGNS or MAD treatment, maxillomandibular advancement (MMA) surgery was shown not to be affected by the presence of CCCp. In addition, MMA tended to resolve CCCp [84].
Regarding the other traits, especially loop gain was shown to affect upper airway surgery outcomes. A lower loop gain was associated with an increased probability of treatment response [52, 69].
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2.8.5 Pharmacological Treatment Options
Numerous drugs have been investigated, such as antidepressants, diuretics, antihy­pertensives, antiemetics, stimulants and sedatives, with some of them showing interesting properties [85].
Acetazolamide, a carbonic anhydrase inhibitor, may enhance respiratory drive by inducing metabolic acidosis, thus improving loop gain [86]. Other drugs have also been repurposed for the treatment of OSA.Spironolactone may improve upper airway collapsibility by reducing uid retention and edema [87]. Several studies tried to mitigate OSA by modifying the activity of dilatory upper airway muscles. Initially, it was thought that sleep-related changes in muscle activity were primarily due to the withdrawal of serotonin at the hypoglossal neurons [88, 89]. However, more recent data suggest that drops in noradrenaline levels also play a key role. Therefore, noradrenergic stimulants, such as protriptyline and desipramine, can increase muscle activity and reduce upper airway collapsibility [90, 91].
A nal potential target is the arousal threshold. Studies have indicated that seda­tives such as eszopiclone and zolpidem increase the arousal threshold by 20–30% [92–95].
Regarding oxygen therapy, a correlation between response and lower collaps­ibility at baseline was found [96]. Furthermore, oxygen therapy lowers loop gain [47]. Pharyngeal muscle compensation affects the response to oxygen therapy; patients with a higher muscle compensation show increased response [96].
As OSA is a multifactorial disease, recent studies have looked at combinations of drugs. One of the most exciting studies in this eld demonstrated that the combi­nation of atomoxetine (noradrenergic) and oxybutynin (antimuscarinic) lowers the AHI by 63% [97]. This improvement was attributed to drastic changes in collaps­ibility and muscle compensation [98]. Notably, both drugs were ineffective when administered separately. Another exciting combination, eszopiclone and supple­mental oxygen reduced the AHI by 43% via improvements in arousal threshold and loop gain [99].
2.9 Conclusion
Overall, we can conclude that assessment of OSA pathophysiology holds promise for playing a pivotal role in coming to precision medicine for obstructive sleep apnea patients. While until recently, these traits could only be assessed using rigor­ous, often invasive, and overnight measurements. However, the newly developed noninvasive techniques can make this information available in routine clinical practice.
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Take-Home Message
• There are ve critical pathophysiological OSA traits: site(s) and pattern(s) of
upper airway collapse, upper airway collapsibility, ventilatory control stability
(loop gain), muscle responsiveness, and arousal threshold.
• All these traits can be measured using a gold standard technique involving over-
night measurements and/or upper airway pressure manipulations.
• OSA pathophysiological traits are helpful for treatment selection purposes.
Besides DISE, especially the non-invasive techniques, e.g., based on sleep study
data, hold promise as a patient selection tool.
References
1. Wenzel SE. Asthma phenotypes: the evolution from clinical to molecular approaches. Nat Med. 2012;18(5):716–25.
2. Edwards BA, Redline S, Sands SA, Owens RL.More than the sum of the respiratory events: personalized medicine approaches for obstructive sleep apnea. Am J Respir Crit Care Med. 2019;200(6):691–703.
3. Zinchuk AV, Gentry MJ, Concato J, Yaggi HK.Phenotypes in obstructive sleep apnea: a deni­tion, examples and evolution of approaches. Sleep Med Rev. 2017;35:113–23.
4. Wellman A, Eckert DJ, Jordan AS, Edwards BA, Passaglia CL, Jackson AC, etal. A method for measuring and modeling the physiological traits causing obstructive sleep apnea. J Appl Physiol (1985). 2011;110(6):1627–37.
5. Eckert DJ, White DP, Jordan AS, Malhotra A, Wellman A. Dening phenotypic causes of obstructive sleep apnea. Identication of novel therapeutic targets. Am J Respir Crit Care Med. 2013;188(8):996–1004.
6. Borowiecki B, Pollak CP, Weitzman ED, Rakoff S, Imperato J.Fibro-optic study of pharyn­geal airway during sleep in patients with hypersomnia obstructive sleep-apnea syndrome. Laryngoscope. 1978;88(8 Pt 1):1310–3.
7. Van den Bossche K, Van de Perck E, Kazemeini E, Willemen M, Van de Heyning PH, Verbraecken J, etal. Natural sleep endoscopy in obstructive sleep apnea: a systematic review. Sleep Med Rev. 2021;60:101534.
8. De Vito A, Carrasco Llatas M, Ravesloot MJ, Kotecha B, De Vries N, Hamans E, et al. European position paper on drug-induced sleep endoscopy: 2017 update. Clin Otolaryngol. 2018;43(6):1541–52.
9. De Vito A, Carrasco Llatas M, Vanni A, Bosi M, Braghiroli A, Campanini A, etal. European position paper on drug-induced sedation endoscopy (DISE). Sleep Breath. 2014;18(3):453–65.
10. Saruddin F, Koutsourelakis I, de Vries N.Analysis of the inuence of head rotation during drug-induced sleep endoscopy in obstructive sleep apnea. Laryngoscope. 2014;124(9):2195–9.
11. Vroegop AV, Vanderveken OM, Boudewyns AN, Scholman J, Saldien V, Wouters K, etal. Drug­induced sleep endoscopy in sleep-disordered breathing: report on 1249 cases. Laryngoscope. 2014;124(3):797–802.
12. Vroegop A. Drug-induced sleep endoscopy in patients with sleep-disordered breathing: a patient selection tool for surgical and mandibular advancement therapies. Antwerpen: Universiteit Antwerpen; 2013.
13. Verbruggen AER, Vroegop AVMT, Dieltjens M, Wouters K, Kastoer C, De Backer WA, etal. Predicting therapeutic outcome of mandibular advancement device treatment in obstruc­tive sleep apnoea (PROMAD): study design and baseline characteristics. J Dent Sleep Med. 2016;03(04):119–38.
2 Pathophysiology ofObstructive Sleep Apnea
https://t.me/medicina_free
14. Park D, Kim JS, Heo SJ.Obstruction patterns during drug-induced sleep endoscopy vs natural sleep endoscopy in patients with obstructive sleep apnea. JAMA Otolaryngol Head Neck Surg. 2019;145(8):730–4.
15. Genta PR, Sands SA, Butler JP, Loring SH, Katz ES, Demko BG, etal. Airow shape is associ­ated with the pharyngeal structure causing OSA.Chest. 2017;152(3):537–46.
16. Op de Beeck S, Van de Perck E, Vena D, Kazemeini E, Dieltjens M, Willemen M, etal. Flow­identied site of collapse during drug-induced sleep endoscopy: feasibility and preliminary results. Chest. 2021;159(2):828–32.
17. Azarbarzin A, Marques M, Sands SA, Op de Beeck S, Genta PR, Taranto-Montemurro L, et al. Predicting epiglottic collapse in patients with obstructive sleep apnoea. Eur Respir J. 2017;50(3):1700345.
18. Azarbarzin A, Sands SA, Marques M, Genta PR, Taranto-Montemurro L, Messineo L, etal. Palatal prolapse as a signature of expiratory ow limitation and inspiratory palatal collapse in patients with obstructive sleep apnoea. Eur Respir J. 2018;51(2):1–11.
19. Op de Beeck S, Vena D, Mann D, Azarbarzin A, Gell L, Van de Perck E, etal. Polysomnographic airow shapes and site of collapse during drug-induced sleep endoscopy. In: ATS international conference. San Francisco; 2022.
20. Sforza E, Bacon W, Weiss T, Thibault A, Petiau C, Krieger J.Upper airway collapsibility and cephalometric variables in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2000;161(2 Pt 1):347–52.
21. Schwartz AR, Gold AR, Schubert N, Stryzak A, Wise RA, Permutt S, etal. Effect of weight loss on upper airway collapsibility in obstructive sleep apnea. Am Rev Respir Dis. 1991;144(3 Pt 1):494–8.
22. Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt S, Smith PL.Upper airway col­lapsibility in snorers and in patients with obstructive hypopnea and apnea. Am Rev Respir Dis. 1991;143(6):1300–3.
23. Penzel T, Moller M, Becker HF, Knaack L, Peter JH.Effect of sleep position and sleep stage on the collapsibility of the upper airways in patients with sleep apnea. Sleep. 2001;24(1):90–5.
24. Ong JS, Touyz G, Tanner S, Hillman DR, Eastwood PR, Walsh JH.Variability of human upper airway collapsibility during sleep and the inuence of body posture and sleep stage. J Sleep Res. 2011;20(4):533–7.
25. Boudewyns A, Punjabi N, Van de Heyning PH, De Backer WA, O'Donnell CP, Schneider H, et al. Abbreviated method for assessing upper airway function in obstructive sleep apnea. Chest. 2000;118(4):1031–41.
26. Issa FG, Sullivan CE.Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol Respir Environ Exerc Physiol. 1984;57(2):520–7.
27. Carberry JC, Jordan AS, White DP, Wellman A, Eckert DJ.Upper airway collapsibility (Pcrit) and pharyngeal dilator muscle activity are sleep stage dependent. Sleep. 2016;39(3):511–21.
28. Rowley JA, Zhou X, Vergine I, Shkoukani MA, Badr MS.Inuence of gender on upper airway mechanics: upper airway resistance and Pcrit. J Appl Physiol (1985). 2001;91(5):2248–54.
29. Jordan AS, Wellman A, Edwards JK, Schory K, Dover L, MacDonald M, etal. Respiratory control stability and upper airway collapsibility in men and women with obstructive sleep apnea. J Appl Physiol (1985). 2005;99(5):2020–7.
30. Wellman A, Genta PR, Owens RL, Edwards BA, Sands SA, Loring SH, etal. Test of the Starling resistor model in the human upper airway during sleep. J Appl Physiol (1985). 2014;117(12):1478–85.
31. Schwartz AR, Smith PL. CrossTalk proposal: the human upper airway does behave like a Starling resistor during sleep. J Physiol. 2013;591(9):2229–32.
32. Schwartz AR, Smith PL, Wise RA, Gold AR, Permutt S.Induction of upper airway occlu­sion in sleeping individuals with subatmospheric nasal pressure. J Appl Physiol (1985). 1988;64(2):535–42.
33. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S.Upper airway pressure-ow relation­ships in obstructive sleep apnea. J Appl Physiol (1985). 1988;64(2):789–95.
37
38
https://t.me/medicina_free
34. Permutt S, Riley RL.Hemodynamics of collapsible vessels with tone: the vascular waterfall. J Appl Physiol. 1963;18:924–32.
35. Butler JP, Owens RL, Malhotra A, Wellman A.CrossTalk opposing view: the human upper airway during sleep does not behave like a Starling resistor. J Physiol. 2013;591(9):2233–4.
36. Owens RL, Edwards BA, Sands SA, Butler JP, Eckert DJ, White DP, et al. The classical Starling resistor model often does not predict inspiratory airow patterns in the human upper airway. J Appl Physiol (1985). 2014;116(8):1105–12.
37. Osman AM, Carberry JC, Burke PGR, Toson B, Grunstein RR, Eckert DJ.Upper airway col­lapsibility measured using a simple wakefulness test closely relates to the pharyngeal critical closing pressure during sleep in obstructive sleep apnea. Sleep. 2019;42(7):zsz080.
38. Malhotra A, Pillar G, Fogel R, Beauregard J, Edwards J, White DP.Upper-airway collapsibil­ity: measurements and sleep effects. Chest. 2001;120(1):156–61.
39. Landry SA, Joosten SA, Eckert DJ, Jordan AS, Sands SA, White DP, etal. Therapeutic CPAP level predicts upper airway collapsibility in patients with obstructive sleep apnea. Sleep. 2017;40(6):zsx056.
40. Genta PR, Schorr F, Edwards BA, Wellman A, Lorenzi-Filho G.Discriminating the severity of pharyngeal collapsibility in men using anthropometric and polysomnographic indices. J Clin Sleep Med. 2020;16(9):1531–7.
41. Kazemeini E, Van de Perck E, Dieltjens M, Willemen M, Verbraecken J, Op de Beeck S, etal. Critical to know Pcrit: a review on pharyngeal critical closing pressure in obstructive sleep apnea. Front Neurol. 2022;13:775709.
42. Condos R, Norman RG, Krishnasamy I, Peduzzi N, Goldring RM, Rapoport DM.Flow limi­tation as a noninvasive assessment of residual upper-airway resistance during continuous positive airway pressure therapy of obstructive sleep apnea. Am J Respir Crit Care Med. 1994;150(2):475–80.
43. Wellman A, Edwards BA, Sands SA, Owens RL, Nemati S, Butler J, etal. A simplied method for determining phenotypic traits in patients with obstructive sleep apnea. J Appl Physiol (1985). 2013;114(7):911–22.
44. Kazemeini E, Van de Perck E, Dieltjens M, Willemen M, Verbraecken J, Sands SA, et al. Critical closing pressure of the pharyngeal airway during routine drug-induced sleep endos­copy: feasibility and protocol. J Appl Physiol (1985). 2022;132(4):925–37.
45. Azarbarzin A, Sands SA, Taranto-Montemurro L, Oliveira Marques MD, Genta PR, Edwards BA, etal. Estimation of pharyngeal collapsibility during sleep by peak inspiratory airow. Sleep. 2017;40(1):zsw005.
46. Sands SA, Edwards BA, Terrill PI, Taranto-Montemurro L, Azarbarzin A, Marques M, et al. Phenotyping pharyngeal pathophysiology using polysomnography in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2018;197(9):1187–97.
47. Wellman A, Malhotra A, Jordan AS, Stevenson KE, Gautam S, White DP. Effect of oxygen in obstructive sleep apnea: role of loop gain. Respir Physiol Neurobiol. 2008;162(2):144–51.
48. Dempsey JA, Veasey SC, Morgan BJ, O'Donnell CP.Pathophysiology of sleep apnea. Physiol Rev. 2010;90(1):47–112.
49. Messineo L, Taranto-Montemurro L, Azarbarzin A, Oliveira Marques MD, Calianese N, White DP, etal. Breath-holding as a means to estimate the loop gain contribution to obstructive sleep apnoea. J Physiol. 2018;596(17):4043–56.
50. Messineo L, Taranto-Montemurro L, Azarbarzin A, Marques M, Calianese N, White DP, et al. Loop gain in REM versus non-REM sleep using CPAP manipulation: a pilot study. Respirology. 2019;24(8):805–8.
51. Terrill PI, Edwards BA, Nemati S, Butler JP, Owens RL, Eckert DJ, et al. Quantifying the ventilatory control contribution to sleep apnoea using polysomnography. Eur Respir J. 2015;45(2):408–18.
52. Joosten SA, Leong P, Landry SA, Sands SA, Terrill PI, Mann D, et al. Loop gain pre­dicts the response to upper airway surgery in patients with obstructive sleep apnea. Sleep. 2017;40(7):zsx094.
53. Carberry JC, Hensen H, Fisher LP, Saboisky JP, Butler JE, Gandevia SC, etal. Mechanisms contributing to the response of upper-airway muscles to changes in airway pressure. J Appl Physiol (1985). 2015;118(10):1221–8.
S. Op de Beeck et al.
2 Pathophysiology ofObstructive Sleep Apnea
https://t.me/medicina_free
54. Berry RB, Gleeson K.Respiratory arousal from sleep: mechanisms and signicance. Sleep. 1997;20(8):654–75.
55. Berry RB, Kouchi K, Bower J, Prosise G, Light RW.Triazolam in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 1995;151(2 Pt 1):450–4.
56. Phillipson EA, Sullivan CE.Arousal: the forgotten response to respiratory stimuli. Am Rev Respir Dis. 1978;118(5):807–9.
57. Edwards BA, Eckert DJ, McSharry DG, Sands SA, Desai A, Kehlmann G, etal. Clinical pre­dictors of the respiratory arousal threshold in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2014;190(11):1293–300.
58. Sands SA, Terrill PI, Edwards BA, Taranto Montemurro L, Azarbarzin A, Marques M, et al. Quantifying the arousal threshold using polysomnography in obstructive sleep apnea. Sleep. 2018;41(1):zsx183.
59. Sforza E, Krieger J, Petiau C.Arousal threshold to respiratory stimuli in OSA patients: evi­dence for a sleep-dependent temporal rhythm. Sleep. 1999;22(1):69–75.
60. Younes M. Contributions of upper airway mechanics and control mechanisms to severity of obstructive apnea. Am J Respir Crit Care Med. 2003;168(6):645–58.
61. Zinchuk A, Yaggi HK, Liang J, Chu J, de Beeck SO, Stepnowsky C, etal. Physiologic traits predict therapeutic pressure requirements and residual respiratory events among patients with coronary artery disease and obstructive sleep apnea. Am J Respir Crit Care. 2020;201:2.
62. Chan AS, Sutherland K, Schwab RJ, Zeng B, Petocz P, Lee RW, etal. The effect of mandibular advancement on upper airway structure in obstructive sleep apnoea. Thorax. 2010;65(8):726–32.
63. Vroegop AV, Vanderveken OM, Dieltjens M, Wouters K, Saldien V, Braem MJ, etal. Sleep endoscopy with simulation bite for prediction of oral appliance treatment outcome. J Sleep Res. 2013;22(3):348–55.
64. Chan AS, Lee RW, Srinivasan VK, Darendeliler MA, Grunstein RR, Cistulli PA.Nasopharyngoscopic evaluation of oral appliance therapy for obstructive sleep apnoea. Eur Respir J. 2010;35(4):836–42.
65. Okuno K, Sasao Y, Nohara K, Sakai T, Pliska BT, Lowe AA, etal. Endoscopy evaluation to predict oral appliance outcomes in obstructive sleep apnoea. Eur Respir J. 2016;47(5):1410–9.
66. Vanderveken OM, Van de Heyring PH, Braem MJ. Nasopharyngoscopy during wakefulness for predicting treatment outcome of OSA with mandibular advancement splints. Breathe. 2010;7(1):94–5.
67. Marques M, Genta PR, Azarbarzin A, Taranto-Montemurro L, Messineo L, Hess LB, et al. Structure and severity of pharyngeal obstruction determine oral appliance efcacy in sleep apnoea. J Physiol. 2019;597(22):5399–410.
68. Op de Beeck S, Dieltjens M, Verbruggen AE, Vroegop AV, Wouters K, Hamans E, et al. Phenotypic labelling using drug-induced sleep endoscopy improves patient selection for mandibular advancement device outcome: a prospective study. J Clin Sleep Med. 2019;15(8):1089–99.
69. Edwards BA, Andara C, Landry S, Sands SA, Joosten SA, Owens RL, et al. Upper-airway collapsibility and loop gain predict the response to oral appliance therapy in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2016;194(11):1413–22.
70. Tsuiki S, Kobayashi M, Namba K, Oka Y, Komada Y, Kagimura T, etal. Optimal positive airway pressure predicts oral appliance response to sleep apnoea. Eur Respir J. 2010;35(5):1098–105.
71. Bamagoos AA, Cistulli PA, Sutherland K, Madronio M, Eckert DJ, Hess L, et al. Polysomnographic endotyping to select patients with obstructive sleep apnea for oral appli­ances. Ann Am Thorac Soc. 2019;16(11):1422–31.
72. Op de Beeck S, Dieltjens M, Azarbarzin A, Willemen M, Verbraecken J, Braem MJ, et al. Mandibular advancement device treatment efcacy is associated with polysomnographic endotypes. Ann Am Thorac Soc. 2021;18(3):511–8.
73. Bamagoos AA, Cistulli PA, Sutherland K, Ngiam J, Burke PGR, Bilston LE, et al. Dose­dependent effects of mandibular advancement on upper airway collapsibility and muscle func­tion in obstructive sleep apnea. Sleep. 2019;42(6):zsz049.
74. Huang Y, White DP, Malhotra A. The impact of anatomic manipulations on pharyngeal collapse: results from a computational model of the normal human upper airway. Chest. 2005;128(3):1324–30.
39
40
https://t.me/medicina_free
75. Inazawa T, Ayuse T, Kurata S, Okayasu I, Sakamoto E, Oi K, etal. Effect of mandibular posi­tion on upper airway collapsibility and resistance. J Dent Res. 2005;84(6):554–8.
76. Ng AT, Gotsopoulos H, Qian J, Cistulli PA.Effect of oral appliance therapy on upper airway collapsibility in obstructive sleep apnea. Am J Respir Crit Care Med. 2003;168(2):238–41.
77. Schwartz AR, Schubert N, Rothman W, Godley F, Marsh B, Eisele D, etal. Effect of uvulopal­atopharyngoplasty on upper airway collapsibility in obstructive sleep apnea. Am Rev Respir Dis. 1992;145(3):527–32.
78. Van de Heyning PH, Badr MS, Baskin JZ, Cramer Bornemann MA, De Backer WA, Dotan Y, etal. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope. 2012;122(7):1626–33.
79. Vanderveken OM, Maurer JT, Hohenhorst W, Hamans E, Lin HS, Vroegop AV, etal. Evaluation of drug-induced sleep endoscopy as a patient selection tool for implanted upper airway stimu­lation for obstructive sleep apnea. J Clin Sleep Med. 2013;9(5):433–8.
80. Ong AA, Murphey AW, Nguyen SA, Soose RJ, Woodson BT, Vanderveken OM, etal. Efcacy of upper airway stimulation on collapse patterns observed during drug-induced sedation endoscopy. Otolaryngol Head Neck Surg. 2016;154(5):970–7.
81. Op de Beeck S, Wellman A, Dieltjens M, Strohl KP, Willemen M, Van de Heyning PH, etal. Endotypic mechanisms of successful hypoglossal nerve stimulation for obstructive sleep apnea. Am J Respir Crit Care Med. 2021;203(6):746–55.
82. Koutsourelakis I, Saruddin F, Ravesloot M, Zakynthinos S, de Vries N.Surgery for obstructive sleep apnea: sleep endoscopy determinants of outcome. Laryngoscope. 2012;122(11):2587–91.
83. Green KK, Kent DT, D'Agostino MA, Hoff PT, Lin H-S, Soose RJ, et al. Drug-induced sleep endoscopy and surgical outcomes: a multicenter cohort study. Laryngoscope. 2019;129(3):761–70.
84. Kastoer C, Op de Beeck S, Dom M, Neirinckx T, Verbraecken J, Braem MJ, et al. Drug­induced sleep endoscopy upper airway collapse patterns and maxillomandibular advancement. Laryngoscope. 2020;130(4):E268–E74.
85. Gaisl T, Haile SR, Thiel S, Osswald M, Kohler M.Efcacy of pharmacotherapy for OSA in adults: a systematic review and network meta-analysis. Sleep Med Rev. 2019;46:74–86.
86. Edwards BA, Sands SA, Eckert DJ, White DP, Butler JP, Owens RL, etal. Acetazolamide improves loop gain but not the other physiological traits causing obstructive sleep apnoea. J Physiol. 2012;590(5):1199–211.
87. Fiori CZ, Martinez D, Montanari CC, Lopez P, Camargo R, Sezerá L, etal. Diuretic or sodium­restricted diet for obstructive sleep apnea—a randomized trial. Sleep. 2018;41(4):zsy016.
88. Kubin L, Davies RO, Pack AI.Control of upper airway motoneurons during REM sleep. News Physiol Sci. 1998;13:91–7.
89. Sood S, Liu X, Liu H, Nolan P, Horner RL. 5-HT at hypoglossal motor nucleus and respi­ratory control of genioglossus muscle in anesthetized rats. Respir Physiol Neurobiol. 2003;138(2–3):205–21.
90. Taranto-Montemurro L, Sands SA, Edwards BA, Azarbarzin A, Marques M, de Melo C, etal. Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation. Eur Respir J. 2016;48(5):1340–50.
91. Taranto-Montemurro L, Edwards BA, Sands SA, Marques M, Eckert DJ, White DP, et al. Desipramine increases genioglossus activity and reduces upper airway collapsibility during non-REM sleep in healthy subjects. Am J Respir Crit Care. 2016;194(7):878–85.
92. Eckert DJ, Owens RL, Kehlmann GB, Wellman A, Rahangdale S, Yim-Yeh S, etal. Eszopiclone increases the respiratory arousal threshold and lowers the apnoea/hypopnoea index in obstruc­tive sleep apnoea patients with a low arousal threshold. Clin Sci (Lond). 2011;120(12):505–14.
93. Carberry JC, Grunstein RR, Eckert DJ.The effects of zolpidem in obstructive sleep apnea—an open-label pilot study. J Sleep Res. 2019;28:e12853.
94. Carberry JC, Fisher LP, Grunstein RR, Gandevia SC, McKenzie DK, Butler JE, etal. Role of common hypnotics on the phenotypic causes of obstructive sleep apnoea: paradoxical effects of zolpidem. Eur Respir J. 2017;50(6):1701344.
S. Op de Beeck et al.
2 Pathophysiology ofObstructive Sleep Apnea
https://t.me/medicina_free
95. Carter SG, Berger MS, Carberry JC, Bilston LE, Butler JE, Tong BK, etal. Zopiclone increases the arousal threshold without impairing genioglossus activity in obstructive sleep apnea. Sleep. 2016;39(4):757–66.
96. Sands SA, Edwards BA, Terrill PI, Butler JP, Owens RL, Taranto-Montemurro L, et al. Identifying obstructive sleep apnoea patients responsive to supplemental oxygen therapy. Eur Respir J. 2018;52(3):1800674.
97. Taranto-Montemurro L, Messineo L, Sands SA, Azarbarzin A, Marques M, Edwards BA, etal. The combination of atomoxetine and oxybutynin greatly reduces obstructive sleep apnea severity. A randomized, placebo-controlled, double-blind crossover trial. Am J Respir Crit Care Med. 2019;199(10):1267–76.
98. Taranto-Montemurro L, Messineo L, Azarbarzin A, Vena D, Hess L, Calianese N, etal. Effects of the combination of atomoxetine and oxybutynin on obstructive sleep apnea endotypic traits. Chest. 2020;157:1626.
99. Edwards BA, Sands SA, Owens RL, Eckert DJ, Landry S, White DP, etal. The combination of supplemental oxygen and a hypnotic markedly improves obstructive sleep apnea in patients with a mild to moderate upper airway collapsibility. Sleep. 2016;39(11):1973–83.
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