Published date: July 1, 2025
The AHI and OSA grew up together, but the time may have come for them to part ways. The more we learn about OSA, the more we understand its complex nature and potentially severe consequences for patients and impact on research, diagnosis and treatment. But how did AHI gain such an important role in the first place?
Although the association between morbid obesity, hypersomnolence and respiratory failure was first fully described in 1956,1 it wasn’t until 1976 that Guilleminault, Tilkian and Dement introduced the concept of ‘sleep apnea syndromes’ and identified them as drivers of disease in their own right.2
Their research, based on laboratory findings, provided formal evidence that respiratory problems during sleep could account for previously unexplained medical conditions. It defined an apnea as a cessation of airflow lasting at least ten seconds and argued that sleep apnea syndrome should be diagnosed in patients suffering at least 30 apneas during the night of sleep.2
So far, so good. But in 1978, with no obvious rationale, Guilleminault and Dement proposed a new metric, the apnea index (AI), which measured the number of apneic events a patient suffered per hour of sleep. Formal comparative analyses of the merits of an hourly index versus a night-long total were not carried out due to a lack of data.3
The cut-off value for diagnosing sleep apnea—at least five events per hour—was derived from a limited cohort of patients and control subjects. The research underpinning the index has never been adequately reproduced or validated. At the same time that a clinically important condition had been discovered, the key way of understanding and quantifying it was taking a wrong turn.4
Concerns about the AHI were raised from the outset. Researchers worried that a simple measure of frequency might obscure the varied clinical picture of sleep apnea syndrome. They noted it was an inadequate metric to represent a heterogenous collection of respiratory disturbances and symptoms. They also indicated it did not capture important differences between men and women or between younger and older people in apneic events, desaturation and symptoms. They argued the cut-off score of five events per hour was arbitrary, implied a high risk of false-positive diagnoses and did not reliably predict clinically relevant disease.4
Nevertheless, for lack of an alternative, the AI became a shared standard, morphing into the AHI as the importance of hypopneas became recognized. Still the criticisms did not go away. In the 1990s, for example, researchers noted the weak correlation between AHI score and relevant clinical symptoms, the lack of a clear ‘dose-response’ relationship between AHI and clinical consequences of OSA, and methodological issues around the recording and scoring of hypopneas.4
In light of these criticisms and with the aim of developing a standardized approach to OSA research, efforts were made to refine and formalize OSA diagnosis and assessment. Results were mixed.
For example, AHI ≥30 was classified as severe disease due to research showing that an increased risk of systemic hypertension at this level. The cut-off for ‘moderate’ disease—an AHI ≥15—however, was just a convenient mid-point between 5 and 30. The importance of hypopnea was recognized and they were integrated into the index, but scoring systems and severity thresholds were not adjusted accordingly.4
Competing definitions of hypopneas were allowed even though ~20% of patients diagnosed under one definition would be OSA-free under another.5 The first Manual for the Scoring of Sleep and Associated Events, published by the American Academy of Sleep Medicine (AASM) in 2007, even insisted that digital filters be used to ensure that the results of new, digital PSG testing would be consistent with existing paper-based analogue tests.6
While the intention to reduce inaccuracy and improve research quality was good and gave the appearance of increasingly refined and standardized guidelines, the reality was undermined by circular definitions, a reliance on consensus rather than evidence, and the need to keep one eye on the realities of the US health insurance industry.
Over the years, the AHI has become the benchmark for diagnosing and assessing sleep disordered breathing and has even been codified in laws and regulations as a way to assess fitness for driving, medical reimbursements and more. But fundamental weaknesses, identified from the outset and exacerbated by later decisions, remain.
AHI fails to express relevant clinical features of OSA and does not necessarily reflect clinically relevant disease. It does not capture the heterogeneity of sleep disordered breathing or the true severity of disease. It doesn’t identify the risk or potential magnitude of systemic effects on patients’ bodies or the benefits those patients might receive from treatment. It risks over-diagnosing some populations, like the elderly, and under-diagnosing others who could benefit from treatment.7,8,9 It suffers from methodological issues regarding the recording, scoring and classification of events and fails to make effective use of extensive data collected during sleep trials.10 While AHI is an effective way to measure the frequency of apneic episodes, it is not adequate as a metric to diagnose OSA, measure its severity or assess treatment efficacy.
Other diagnostic tools exist and more are in the pipeline. A better, more complete, more considered approach to diagnosing and quantifying OSA is both possible and necessary, for the sake of clinicians, researchers and patients alike.
Bickelmann AG, Burwell CS, Robin ED, Whaley RD. Extreme obesity associated with alveolar hypoventilation; a Pickwickian syndrome. Am J Med. 1956 Nov;21(5):811-8. doi: 10.1016/0002-9343(56)90094-8. PMID: 13362309. https://www.amjmed.com/article/0002-9343(56)90094-8/abstract
Guilleminault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu Rev Med. 1976;27:465-84. doi: 10.1146/annurev.me.27.020176.002341. PMID: 180875. https://www.annualreviews.org/content/journals/10.1146/annurev.me.27.020176.002341
Guilleminault C, Hill MW, Simmons FB, Dement WC. Obstructive sleep apnea: electromyographic and fiberoptic studies. Exp Neurol. 1978 Oct;62(1):48-67. doi: 10.1016/0014-4886(78)90040-7. PMID: 729676. https://www.sciencedirect.com/science/article/abs/pii/0014488678900407?via%3Dihub
Pevernagie DA, Gnidovec-Strazisar B, Grote L, Heinzer R, McNicholas WT, Penzel T, Randerath W, Schiza S, Verbraecken J, Arnardottir ES. On the rise and fall of the apnea-hypopnea index: A historical review and critical appraisal. J Sleep Res. 2020 Aug;29(4):e13066. doi: 10.1111/jsr.13066. Epub 2020 May 14. PMID: 32406974.https://onlinelibrary.wiley.com/doi/10.1111/jsr.13066
Stevens, Damien R et al. Scoring of hypopneas by 3% vs 4% criteria using different home sleep test devices. CHEST, Volume 166, Issue 4, A6167 https://journal.chestnet.org/article/S0012-3692(24)04453-2/fulltext
Iber C., Ancoli-Israel S., Chesson A., et al. (2007) The AASM manual for the scoring of sleep and associated events: Rules, terminology and technical specifications. 1st Edition, American Academy of Sleep medicine. Westchester https://www.researchgate.net/publication/285881487_The_AASM_Manual_for_the_Scoring_of_Sleep_and_Associated_Events_Rules_Terminology_and_Technical_Specifications
Wimms A, Woehrle H, Ketheeswaran S, Ramanan D, Armitstead J. Obstructive Sleep Apnea in Women: Specific Issues and Interventions. Biomed Res Int. 2016;2016:1764837. doi: 10.1155/2016/1764837. Epub 2016 Sep 6. PMID: 27699167; PMCID: PMC5028797. https://pmc.ncbi.nlm.nih.gov/articles/pmid/27699167/
Wimms AJ, Kelly JL, Turnbull CD, McMillan A, Craig SE, O'Reilly JF, Nickol AH, Hedley EL, Decker MD, Willes LA, Calverley PMA, Benjafield AV, Stradling JR, Morrell MJ, & MERGE trial investigators. Continuous positive airway pressure versus standard care for the treatment of people with mild obstructive sleep apnoea (MERGE): a multicentre, randomised controlled trial. The Lancet 2022. Respiratory medicine, 8(4), 349–358. https://doi.org/10.1016/S2213-2600(19)30402-3
Wimms AJ, Kelly JL, Turnbull CD, McMillan A, Craig SE, O'Reilly JF, Nickol AH, Decker MD, Willes LA, Calverley PMA, Benjafield AV, Stradling JR, Morrell MJ, & MERGE Trial Investigators. Mild obstructive sleep apnoea in females: post hoc analysis of the MERGE randomised controlled trial. ERJ Open Research 2024, 10(1), 00574-2023. https://doi.org/10.1183/23120541.00574-2023
Martinez-Garcia MA, Sánchez-de-la-Torre M, White DP, Azarbarzin A. Hypoxic Burden in Obstructive Sleep Apnea: Present and Future. Arch Bronconeumol. 2023 Jan;59(1):36-43. English, Spanish. doi: 10.1016/j.arbres.2022.08.005. Epub 2022 Sep 5. PMID: 36115739. https://www.archbronconeumol.org/en-linkresolver-hypoxic-burden-in-obstructive-sleep-S03002896220129
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