Roughly half of patients with obstructive sleep apnea (OSA) do not tolerate continuous positive airway pressure (CPAP); thus, the need for CPAP alternatives is abundantly clear. While the pneumatic stenting action of CPAP results in highly efficacious treatment, the success of CPAP alternatives (eg, oral appliance therapy and upper airway surgery) is reduced due to relatively localized manipulation of the upper airway. Upper airway anatomy remains a rightful obsession for sleep surgeons and dentists as airway phenotype has proven an important predictor of CPAP alternative therapy success.1–3
In this issue of Journal of Clinical Sleep Medicine, Amali et al.4 conducted a randomized, clinical trial comparing 2 techniques for treatment of OSA. In looking at the baseline cohort data, one will appreciate that this is an anatomically favorable patient population with an average body mass index of 28 kg/m2 and greater than 80% of patients with Friedman tongue position 1/2, an uncommon combination in an American sleep medicine clinic. Surgical group 1 underwent modified radiofrequency tissue ablation (RFTA) which included RFTA of soft palate and tonsils plus mucosal resection of the palatal and uvular tissue. Surgical group 2 underwent uvulopalatalopharyngoplasty (UPPP) which involved resection of uvulopalatal tissues +/− tonsillectomy. With surgical success defined as a reduction of apnea-hypopnea index (AHI) greater than 50%, the UPPP and RFTA demonstrated a 73% and 40% success rate, respectively. On subjective measures, both groups improved comparably on the Epworth Sleepiness Scale; however, the Sleep Apnea Quality of Life Index (SAQLI) showed greater improvement in the RFTA group.
Firstly, the authors should be commended for successfully conducting a randomized, controlled sleep surgery trial as the execution of such a trial bears several intrinsic challenges. The authors also utilized validated sleepiness and quality of life measures which, one might argue, bear more importance than polysomnographic outcomes in a mild-moderate OSA population. I do not, however, concur with the conclusion that “…[modified radiofrequency tissue ablation] can be considered as the first surgical treatment option in patients with mild OSA who have velopharyngeal or oropharyngeal lateral wall obstruction,” as the study is hampered by a relatively short follow-up period of 6 months. The expectant nasal regurgitation and voice changes of traditional UPPP often require 6 months for full recovery. I suspect a 1-year assessment would no longer demonstrate superior SAQLI scores for the modified RFTA group. Nonetheless, one should wonder why the success rates (“success” liberally defined as 50% reduction in AHI) of this anatomically favorable group for UPPP were only 73%. In other words, why did 1 out of 4 of these highly selected patients fail? Answer: anatomy is not the only culprit in OSA. As surgeons, it is our anatomy “fetish” acquired over years of surgical training that represents our Achilles' heel in sleep medicine. Anatomy is tangible, as one can readily assess the facial skeleton and related soft tissues. However, there exists a litany of other factors implicated in OSA pathophysiology, such as neuromuscular tone, rostral fluid shift, airway edema, loop gain, arousal threshold. These factors have remained relatively elusive given our inability to quantify these variables in clinical practice.
For this reason, it is with great enthusiasm that I read Li et al.'s study5—also published in this issue of Journal of Clinical Sleep Medicine. In this study, the authors attempt to create a comprehensive physiological model, incorporating both anatomical and nonanatomical traits, to predict response to surgical therapy. This was a retrospective cohort study in which 31 adult Chinese patients underwent baseline polysomnography and primary velopharyngeal surgery followed by postoperative polysomnography. The preoperative polysomnography was retrospectively analyzed for loop gain using ventilatory fluctuations in non-REM sleep. The arousal threshold was calculated using a regression equation from polysomnography variables, a surrogate for epiglottic pressure. Several prediction models for estimating postoperative AHI were were developed, including a model incorporating the following physiological measures: anatomy, arousals, control of breathing, and muscle responsiveness.
Using the polysomnography data from the 31 patients, the authors successfully derive an equation that can explain 61% of the variance in postoperative AHI using physiological measures. Loop gain and arousal threshold, two well-known entities in the mechanism of OSA, are highlighted within this equation. For example, high loop gain is positively correlated (r = 0.47, P < .01) with postoperative AHI while low arousal threshold is negatively correlated (r = −0.45, P = .011) with postoperative AHI. While the positive association with high loop gain and postoperative AHI is expected, the negative association of low arousal threshold with postoperative AHI is counterintuitive. One must be aware that the authors used “fraction of events that were hypopnea” rather than epiglottic pressure to represent arousal threshold. In this way, their measurement of “arousal threshold” more likely serves as a proxy for “airway collapsibility,” explaining their negative correlation with postoperative AHI.
In any case, this important work by Li et al. represents the latest frontier in personalized treatment of the sleep apnea patient. Earlier this year, Joosten et al.6 produced similar findings in which low loop gain predicted favorable response to upper airway surgery. As we begin to look beyond the anatomy of our sleep surgery patients, we will further our understanding and ability to quantify other metrics of importance such as loop gain, arousal threshold, and airway collapsibility. While an accurate, comprehensive, pathophysiology-based assessment tool for surgeons is currently not available; the importance of non-anatomic factors in sleep surgery outcomes is no longer in question. Continued research efforts into the diversity of OSA endotypes will allow better matching of CPAP alternative therapy—from oral appliance therapy to hypoglossal nerve stimulation to upper airway surgery—to achieve our vision of personalized sleep medicine.
The author reports no conflicts of interest.
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Li Y, Ye J, Han D, et al. Physiology-based modeling may predict surgical treatment outcome for obstructive sleep apnea. J Clin Sleep Med. 2017;13(9):1029–1037.
Joosten SA, Leong P, Landry SA, et al. Loop gain predicts the response to upper airway surgery in patients with obstructive sleep apnoea: ventilatory control abnormalities predict surgical responsiveness. Sleep. 2017;40(7):zsx094.