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American Journal of Respiratory and Critical Care Medicine Vol 170. pp. 716, (2004)
© 2004 American Thoracic Society


Correspondence

Pharyngeal Anatomy and Severity of Obstructive Apnea

To the Editor:

An exchange of letters (1, 2) indicates confusion about interpretation of some data from a study I published recently (3). I believe clarification is in order. In this study (3), passive collapsibility of the upper airway was determined from the minimum flow observed after dial-down of continuous positive airway pressure. Passive collapsibility accounted for 28% of the variability in the apnea–hypopnea index (r2 = 0.28, Table 5 [3]). I concluded that nonanatomic factors account for much of the variability in obstructive sleep apnea (OSA) severity. To determine whether differences in control mechanisms related to age, sex, body mass index, body position, and sleep state contribute to the residual (nonanatomic) variability, these five variables were added to the regression between passive collapsibility and the apnea–hypopnea index. Although the correlation improved, r2 remained low (0.40, Table 7 [3]), indicating that variability in OSA severity is largely related to factors other than passive properties and the five variables mentioned above.

In an accompanying editorial (4), Naughton proposed that much of the residual variability is likely due to differences in bony and soft tissue structure. In fact, the study was criticized for ignoring these variables. This was quite disappointing. How can differences in anatomy affect OSA severity if not through changes in the passive properties? It is possible that differences in anatomy may do so by altering the effectiveness of pharyngeal dilators (i.e., anatomy may influence the effectiveness of compensatory mechanisms). However, I am not aware of any such evidence, and if that were what Naughton had in mind he should have mentioned it. Accordingly, I attributed Naughton's statement to an oversight, namely that he did not appreciate the fact that differences in passive properties were also included in the regression examining the effects of the five other variables.

An alert reader (Braidy) detected the inconsistency between Naughton's statement (4) and the findings in my paper (3), and wrote a letter to the editor (1). I was offered a chance to respond. But, considering that Braidy was taking issue with the editorial, not with my paper, I saw no point in responding. I had hoped that, prompted by this letter, Naughton would recognize the oversight on the first round and correct the error. Unfortunately, he did not (2). Unless Naughton provides a compelling explanation, his statement that differences in bony and soft tissue structure likely account for most of the variance in OSA severity should be discounted.

Magdy Younes

St. Michael's Hospital Toronto, Ontario, Canada

FOOTNOTES

Conflict of Interest Statement: M.Y. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter.

Dr. Naughton was given an opportunity to respond to this letter but declined to do so.

REFERENCES

  1. Braidy J. Control, upper airway, and sleep apnea [letter]. Am J Respir Crit Care Med 2004;169:1259.[Free Full Text]
  2. Naughton MT. Control, upper airway, and sleep apnea: reply [letter]. Am J Respir Crit Care Med 2004;169:1259–1260.
  3. Younes M. Contributions of upper airway mechanics and control mechanisms to severity of obstructive apnea. Am J Respir Crit Care Med 2003;168:645–658.[Abstract/Free Full Text]
  4. Naughton MT. Cycling sleep apnea: the balance of compensated and decompensated breathing [editorial]. Am J Respir Crit Care Med 2003;168:624–625.[Free Full Text]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2004 American Thoracic Society