Obstructive Sleep Apnoea in people with Primary Open-angle Glaucoma: prevalence, associations and the impact of Continuous Positive Airway Pressure on Intraocular Pressure

Introduction: Obstructive sleep apnoea (OSA) has been proposed as a contributing factor in the development and progression of primary open-angle glaucoma (POAG) but there is insufficient evidence to confirm or refute this hypothesis. The prevalence of OSA among people with POAG is unknown. To complicate the picture further, concerns have been raised that continuous positive airway pressure (CPAP) increases nocturnal intraocular pressure (IOP), currently the only treatable risk factor for POAG. Objectives: The objective of this thesis was to assess whether the prevalence of OSA among patients with POAG is different from that in people without glaucoma and to examine for associations between apnoea-hypopnea index (AHI) and markers of functional and structural changes in POAG. In addition, the thesis examined whether POAG patients with untreated OSA have faster rates of retinal nerve fibre layer (RNFL) loss than those without OSA. The impact of CPAP on IOP and ocular microvasculature were investigated. Methods: In order to examine the thesis’ questions, studies with the following methodology were conducted: a cross-sectional observational study with a control group, a retrospective longitudinal data analysis, a prospective longitudinal study examining the effect of intervention and a physiological experiment. Results: Based on data from 235 POAG patients and 160 controls the prevalence of OSA was 58% and 54%, respectively. After statistical matching, the proportion of participants diagnosed with OSA was not different between the groups (p=0.91). The AHI was not associated with the severity of visual field defect or RNFL thinning after adjustment for confounders in a cross-sectional study but, in a longitudinal study, people with OSA had almost twice faster rates of RNFL loss than those without OSA (-1.1±1.5 μm/year vs -0.6 ±1 μm/year, respectively, p=0.013) and this was independent of other risk factors. CPAP significantly raised nocturnal IOP in people with (+2.2±2.2mmHg) and without POAG (+3.2±2.2mmHg) but a diurnal application of CPAP at different levels in awake subjects was not associated with IOP elevation. A short-term treatment with CPAP did not alter the optic disc and retinal microvasculature. Conclusions: The burden of OSA among POAG patients is not higher than in people without glaucoma but OSA may be an independent progression risk factor in those with established POAG. CPAP raises IOP and the long-term impact of this on POAG progression should be investigated in future studies.