Affiliations: Mobile, AL
Dr. Broughton is associated with the USA Knollwood Park Sleep Disorders Center.
Correspondence to: William A. Broughton, MD, FCCP, USA Knollwood Park Sleep Disorders Center, 5644 Girby Rd, Mobile, AL 36693-3398; e-mail: email@example.com
The role of nasal resistance in the occurrence of snoring
and obstructive sleep apnea hypopnea syndrome (OSAHS) has been a matter
of speculation for years. In 1988, it was reported in a study of 16
patients that the use of a plastic internal nasal dilator (Nozovent;
Prevancure; Frölunda, Sweden) improved airflow by approximately
25%.1 It was speculated that such a device could
decrease the volume of snoring and the degree of OSAHS severity.
In the following years, the inventor of the device and his teams of
investigators published five studies supporting that contention. Four
of the studies reported purely or mostly subjective
data2–5; a fifth study6 reported objective
data regarding the effect of the device on OSAHS. Unfortunately, all of
these studies shared design weaknesses that left their findings far
from conclusive. Still, the studies suggested that the dilation of the
nasal valve could be beneficial for snorers and those with OSAHS, and
other investigators were sparked to examine those possibilities.
Studies have clearly verified that the placement of the Nozovent device
increases the cross-sectional area of the nasal valve (the nasal valve
is the narrowest segment of the nasal cavity, found at the junction of
the upper and lower lateral nasal cartilages) and lowers nasal
resistance. Most awake patients perceive improved nasal airflow that is
similar to the effect of a topical decongestant. Still, the
sleep-related findings of the initial investigators had not been
verified. In 1992, two Canadian studies using the Nozovent device
appeared that included nocturnal polysomnographic data.7–8
While the details of these data were minimal in one of the studies,
both of these investigators verified the aforementioned increase in
nasal patency, but could not demonstrate any change in apneas or
hemoglobin saturation associated with use of the nasal dilator. Only
one of the studies looked at snoring and it reported no change. The
original investigators had reported that people who use Nozovent felt
an improvement in sleep quality. One of these Canadian studies
indicated about a 20% decrease in nocturnal arousals that they
believed might account for that perception of an improvement in sleep
In this issue of CHEST, Schönhofer et al (see page
587) examined the effect of the Nozovent device on 26 consecutive
subjects with OSAHS. Their study included a more rigorous objective
investigation of the effect of the Nozovent device with nocturnal
polysomnographic conditions that were well defined using a standard
montage that included inductive plethysmography. Their subjective
outpatient snoring data were based on a standard 5-point system, and
perceived excessive daytime somnolence was estimated by the Epworth
Sleepiness Scale (ESS). Mild to severe OSAHS patients were represented.
The study found no improvement in apnea frequency, snoring, oxygen
saturation, or sleep parameters. A minimal improvement in the ESS
score was noted; in 25 patients, no change or only a mild
decrease in snoring was estimated by the bed partner.
This totals three independent investigations that have been unable to
verify the findings of the original investigative teams. These
independent studies appear to be better designed, with this most recent
being very well done. We must strongly consider the possibility that
the original reports may be incorrect. It may be that only a few
patients derive significant objective benefit from the Nozovent device.
So far, no way to identify those few patients has been found.
During the review process, the authors’ use of the traditional
definition of hypopnea was questioned (a ≥ 50% reduction
in the amplitude of oronasal airflow from baseline lasting at least
10 s, associated with a decrease in O2
saturation of ≥ 4%). It is true that thermal sensors detect apnea
well, but exhalations of 50 to 500 mL (hypopneas) might not exhibit
enough variance in temperature to accurately indicate a decrease in
volume. The decision to add a decrease in O2
saturation to the definition has helped ensure that hypoventilation has
actually occurred. However, if that definition were applied in the
clinical practice of sleep medicine, scores of patients might be sent
home without treatment for what is obvious OSAHS.
It may be time to reevaluate the “standard” definition of hypopnea.
Certainly O2 desaturation is a helpful adjunct
when interpreting a reduction of the thermal oronasal airflow tracing,
but the consideration of the following occurrences may also be helpful:
(1) associated arousal, (2) concurrent crescendo snoring (in the
snore-sensor graphic output channel), (3) associated decreases from
baseline snoring (in the snore-sensor graphic output channel), and/or
(4) a repetitive pattern of occurrence consistent with OSAHS.
Schönhofer et al used inductive plethysmography to assess
thoracoabdominal movement. This semiquantitative measure of air
movement should also have been adequate to assess whether or not
hypopnea had occurred without a requirement for a decrease in
O2 saturation. However, the authors’ preference
for the standard definition is understood. Still, it may be time to
consider rethinking the definition of hypopnea for future research.
With up to 45% of middle-aged adults reporting some form of snoring,
the authors correctly point out that the potential market for such
devices is very large. Many patients who report to a sleep disorders
center for evaluation have already tried these devices on their own.
Studies such as the article from Schönhofer et al and the other
investigators allow us to correctly advise our patients that these
devices may only help a few. Such advice might help lead to more prompt
evaluations of sleep-disordered breathing and to the savings of
millions of dollars on devices that, for most patients, have no
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