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Editors Selection IGR 9-1
Miscellaneous: Sleep apnea and POAG
Comment by Jost Jonas on:
81817 Obstructive Sleep Apnea in Patients With Primary-open Angle Glaucoma: No Role for a Screening Program, Wozniak D; Bourne R; Peretz G et al., Journal of Glaucoma, 2019; 28: 668-675
Obstructive sleep apnea (OSA) has long been debated to be primarily or secondarily be associated with the pathogenesis of glaucomatous optic neuropathy, in particular in patients with so-called normal-(IOP)pressure glaucoma. Wozniak and colleagues re-addressed that question and examined a relatively large group of unselected patients with primary openangle glaucoma (POAG) (n = 235) and a control group of unselected non-glaucomatous individuals (n = 160). All study participants underwent a nocturnal multichannel cardiorespiratory monitoring. Wozniak and associates found that the prevalence of OSA did not differ significantly between the glaucoma group (58%; 95% confidence interval [CI], 52-65%) and the control group (54%; 95% CI, 47-62%). In a similar manner, the prevalence of moderate and severe OSA did not vary significantly between the glaucoma group and the control group (22% (95% CI, 16-27%) versus 16% (95% CI, 11-22%). By the same token, the apnea-hypopnea index was not significantly associated with the degree of glaucomatous optic nerve damage in a multivariable analysis. The study showed that OSA, despite being common among patients with POAG, was not associated with POAG and may thus have no value for a screening examination and may not give clues for the elucidation of the pathogenesis of glaucomatous optic neuropathy.
The severity of glaucomatous optic nerve damage was not related with the degree of OSA
The study by Wozniak is important since it addressed a clinically and scientifically important topic with a sound study design and since it included a larger study population than most previous investigations addressing the same topic did. The finding that the severity of glaucomatous optic nerve damage was not related with the degree of OSA supports the conclusions and contradicts a potential bias by the selection of study participants. In conclusion, OSA may not play a major role for the pathogenesis and diagnosis of POAG.
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