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Scottsdale, AZ
Correpondence to: Robert G. Hooper, MD, FCCP, PO Box 4100, Scottsdale, AZ 85261-4100
To the Editor:
The cause of most obstructive sleep apnea (OSA) is unknown. An imbalance between the negative inspiratory airway pressure and the ability of the upper-airway muscle to hold the airway open is believed to play a role. Nasal airflow obstruction has been proposed as one mechanism that will produce more negative inspiratory pressure and thus may cause OSA. Schonhofer et al1 (September 2000) report that a nasal dilator does not improve the polysomnogram in patients with OSA and suggest that nasal obstruction does not produce OSA.
Nasal obstruction can occur at the nasal valve, the turbinates, or in the posterior area of the nasal passage. Structural abnormalities or disease processes can lead to the obstruction. Treatment must be directed at the disease process and, if necessary, at the anatomic location of the obstruction to be successful. If nasal obstruction leads to OSA, then to improve OSA the treatment should relieve nasal obstruction.
A nasal dilator might be helpful in treating OSA, but only if a series of conditions are met. Nasal obstruction should be present at the nasal valve. The degree of obstruction must be significant enough to cause airway collapse during sleep and result in OSA. Finally, the nasal dilator employed must be effective in relieving the obstruction.
In the study by Schonhofer et al,1 a Nozovent nasal dilator (Prevancure AB; Västra Frölunda, Sweden) was used in patients with known OSA, and the effect of the dilator on the polysomnogram was examined. When 17 of 21 patients and the group as a whole showed no improvement, they concluded the nasal dilator was ineffective. There are several reasons to be concerned about their report. Nasal obstruction was not demonstrated in their patients. The effectiveness of the dilator at relieving obstruction was not demonstrated. The population studied was that of OSA, not the population of OSA secondary to nasal obstruction at the nasal valve. Of interest, 4 of 21 of the patients (19%) in their study apparently did demonstrate some improvement, but the authors did not describe the responders, a subgroup that might have met the necessary conditions.
The authors faced a major obstacle: the dilemma of how to define nasal airway obstruction. While no standardized technique is widely accepted, I have found the forced inspiratory nasal flow-volume curve an effective tool to measure the severity of nasal airflow obstruction.2 Comparing baseline nasal flow with flow after placing a nasal dilator on the nose can be helpful in identifying which patients have obstruction at the nasal valve. Certainly, methods for identifying the site and severity of nasal obstruction must be developed before the role of nasal obstruction in sleep apnea syndrome can be established or dismissed.
References
Grafschaft, Germany
Ume
, Sweden
Correspondence to: Bernd Schönhofer, MD, PhD, Krankenhaus Kloster Grafschaft, Zentrum für Pneumologie, Beatmungs-und Schlafmedizin, Annostrasse, Schmallenberg, Grafschaft, Germany D-57392; e-mail: Bernd.Schoenhofer@t-online.de
To the Editor:
Contrary to our findings published in CHEST (September 2000),1 Dr. Hooper argues that a subsample of patients with sleep apnea presenting with increased nasal resistance may benefit from a nasal dilator. As we noted,1 it has been reported that several devices, including the nasal-valve dilator, Nozovent (Prevancure AB; Västra Frölunda, Sweden), reduce nasal resistance and improve nasal breathing. The Nozovent inventors tested their device, and they have reported an excellent effect on nasal resistance, snoring, and sleep apneas in a number of articles. On the contrary, Metes et al2 did not find any effect on snoring, apneas, hypopneas, or oxygen saturation in a small sample of patients with sleep apnea, despite a reduction of nasal resistance in the same patients.
We aimed to investigate whether Nozovent had the effect on snoring and sleep apnea that was reported among patients suffering from obstructive sleep apnea. It was not the aim of our study to investigate or to define nasal airway obstruction. Thus, neither nasal obstruction nor nasal resistance was measured.
The main finding of our study was that objective measurements of snoring and apneas during sleep were almost unaffected by the nasal dilator. In 4 of 21 patients, a decrease in respiratory disturbance index was found with Nozovent. However, in another 17 of 21 patients, it deteriorated. Obviously, patients with obstructive sleep apnea in common will not benefit from this kind of treatment, and our findings support studies reporting that nasal resistance has no impact on the pathogenesis of obstructive sleep apnea.2 3 4 5
Based on the results of our study, we cannot contribute any new data on Dr. Hooper’s proposals that a decrease of nasal resistance after insertion of the nasal dilator predicts responders to this device. However, we refer to another study. Pevernagie et al6 did not observe any effect on apneas and quality of sleep using an external nasal dilator despite that snoring frequency was reduced among their patients who suffered from chronic rhinitis and confirmed nasal obstruction.
References
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