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Dr. Littner is Chief, Pulmonary/Critical Care Medicine, Sepulveda VAMC.
Correspondence to: Michael Littner, MD, FCCP, Chief, Pulmonary/Critical Care Medicine, Sepulveda VAMC 111-P, 16111 Plummer St, Sepulveda, CA 91343-2036; e-mail: mlittner{at}ucla.edu
In this issue of CHEST (see page 353), Le Bon et al report the largest series to date of consecutive polysomnograms (PSGs) in patients suspected of having the obstructive sleep apnea-hypopnea syndrome (OSAHS). The authors conclude that a single negative PSG does not exclude a diagnosis of OSAHS. The evidence provided plus a review of the literature strongly supports this conclusion for any apnea-hypopnea index (AHI) that is considered to be clinically relevant below an AHI of 20.
According to a recent recommendation, an AHI of 5 to 15 is consistent with mild OSAHS.1 Furthermore, it is important to recognize such patients, since they may benefit from therapy such as continuous positive airway pressure (CPAP) with improvement in subjective daytime sleepiness and quality of life.2
In determining the diagnostic accuracy of the PSG to measure AHI, its sensitivity should be assessed. For the purposes of this analysis, I will accept the authors’ view that the highest AHI is the one to be used for diagnostic purposes. That is, a positive test on either night 1 or night 2 is 100% specific. This approach is designed, in part, to include symptomatic patients who may benefit from intervention. I will also confine most of my analysis to AHI thresholds of 5 and 10, since both have been recommended for clinical purposes.1 3
For the most part, I have analyzed the authors’ data to include only
the 142 patients with 2 nights of data in which the first night had an
AHI < 20. I have done this for several reasons. First, this is the
only group in which consecutive unselected nights were performed.
Second, it is the variability of AHI in patients with borderline or low
AHIs that presents diagnostic problems.4
5
6
7
8
9
10
In this
group, the sensitivity of the first night for an AHI 
5 was 75% (85
of 113 patients); for an AHI 10, it was 53.6% (37 of 69 patients).
Since performing a second night involves more expense and
inconvenience, it is important to examine the diagnostic yield of 2
nights in the face of a negative first night. For an AHI of < 5, the
diagnostic yield of a second night was 49.1% (28 of 57 patients); for
an AHI of < 10 it was 30.4% (32 of 105 patients). The yield is
greater and the number of repeat PSGs is less when using an AHI of
5. This concept is further supported since the AHI on night 1 did
not predict the AHI on night 2. For example, the 25 patients with an
AHI 
20 on night 1 and 20 on night 2 had AHIs on night 1 that
ranged from near 0 to near 20.
This analysis of the current study plus the potential for clinical
intervention supports an AHI 5, in an appropriate clinical setting,
to be consistent with a diagnosis of OSAHS. A recommendation has been
made to standardize such a clinical setting.1
Typically,
such patients are sleepy during the day and snore at night.
The current study also provides perspective for the relative number of
patients that are underdiagnosed with 1 night of polysomnography using
AHIs of 5 and 10 as thresholds. The percentage of total patients
presenting (in the current study) with an AHI < 5 and who had an
increase to > 5 was 11.5% (28 of 243 patients); for an increase from
< 10 to 10, it was 13.2% (32 of 243 patients).
The current study can be compared to limited data in the literature for
consecutive night studies. The diagnostic yield of combining the
studies of both nights, combining all patients,4
7
11
for
an AHI of 5 was 48.3% (14 of 29 patients); for an AHI 10, it
was 32.6% (14 of 43 patients).5
7
9
The percentage who
were underdiagnosed using an AHI of 5 is 14% (31 of 218
patients)4
6
7
8
9
; for an AHI of 10, it was 7.7% (12 of 155
patients).4
7
9
In general, the results of the current
study by Le Bon et al are consistent with data in the literature.
The reason for the variability between the 2 nights with a greater yield on the second night is not defined. The current study controlled the sleeping environment, standardized the method of scoring the record, and accounted for the patients’ sleeping position. One issue that may have impacted the results is the routine of waking patients at 7:00 AM, regardless of their usual waking time. However, the authors recognized this and made efforts to analyze this effect that did not appear to affect the results. The authors attempts to define a predictive relationship, including variables of sleep staging, between subject characteristics and a higher AHI on the second night were unrewarding.
One possible explanation for the relatively greater increase in AHI in this study in patients with lower AHI may be regression to the mean of the AHI combined with the fact that the lower values can increase more than decrease. This may occur since there is no "ceiling" on the increase but there is a "floor," namely an AHI of 0, on the decrease.
I have confined my comments to the use of AHI to define respiratory disturbance during sleep. In addition, recent information indicates that more subtle respiratory disturbances may lead to arousals, symptoms, and response to therapy such as CPAP consistent with OSAHS.3 12 These respiratory effort-related arousals1 are increasingly being incorporated in scoring of the PSG. How adding these events to the total will affect the threshold for a study to be consistent with OSAHS is currently undefined.
Future research in this area should focus on correlating respiratory events with symptoms and response to therapy. This will ideally produce an approach to combining pretest probability with posttest AHI and predicted response to therapy to estimate the likelihood that a patient has clinically relevant OSAHS. Only by putting the recommended OSAHS syndrome definition to the test of clinical science will validation or refinement of the recommended threshold of five respiratory events per hour of sleep1 be possible.
References
This article has been cited by other articles:
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  K. D. Pereira, J. C. Roebuck, and L. Howell The Effect of Body Position on Sleep Apnea in Children Younger Than 3 Years Arch Otolaryngol Head Neck Surg, November 1, 2005; 131(11): 1014 - 1016. [Abstract] [Full Text] [PDF]
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 D Schlosshan and M W Elliott Sleep * 3: Clinical presentation and diagnosis of the obstructive sleep apnoea hypopnoea syndrome Thorax, April 1, 2004; 59(4): 347 - 352. [Abstract] [Full Text] [PDF]
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 W. W. Flemons, M. R. Littner, J. A. Rowley, P. Gay, W. M. Anderson, D. W. Hudgel, R. D. McEvoy, and D. I. Loube Home Diagnosis of Sleep Apnea: A Systematic Review of the Literature: An Evidence Review Cosponsored by the American Academy of Sleep Medicine, the American College of Chest Physicians, and the American Thoracic Society Chest, October 1, 2003; 124(4): 1543 - 1579. [Full Text] [PDF]
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 L. Gianotti, S. Pivetti, F. Lanfranco, F. Tassone, F. Navone, E. Vittori, R. Rossetto, C. Gauna, S. Destefanis, S. Grottoli, et al. Concomitant Impairment of Growth Hormone Secretion and Peripheral Sensitivity in Obese Patients with Obstructive Sleep Apnea Syndrome J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 5052 - 5057. [Abstract] [Full Text] [PDF]
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