The retina is increasingly being explored as a source of biomarkers for cardiovascular and cerebrovascular health. Now, a prospective seven-year study suggests that retinal imaging may also reveal the long-term vascular effects of treating obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP).
Researchers at Macquarie Medical School and The University of Sydney Save Sight Institute, New South Wales, Australia, followed participants from an earlier OSA cohort in which disease severity had been linked to retinal arteriolar narrowing and reduced retinal pulse amplitude. At two years, patients with severe untreated OSA showed progressive retinal arterial narrowing, whereas CPAP appeared to attenuate the change. The latest study asked whether that apparent protective effect persisted at seven years.
Of 79 participants eligible from the two-year follow-up, 39 completed the seven-year assessment. They underwent medical review, OCT, and retinal vessel imaging, with researchers evaluating central retinal artery equivalent (CRAE), central retinal vein equivalent (CRVE), arteriovenous ratio, and retinal nerve fiber layer (RNFL) thickness. Participants were stratified by OSA severity and CPAP adherence.
The strongest signals emerged in severe OSA. Mean CRAE was 161.0 in CPAP-treated patients compared with 143.2 in those not using CPAP, while mean CRVE was 200.9 versus 186.9, respectively. Although between-group comparisons were not statistically significant after Bonferroni correction, the longitudinal data suggested slower retinal vascular narrowing among CPAP users. Over seven years, severe OSA patients on CPAP showed a smaller decline in CRAE than untreated patients, while CRVE also appeared better preserved.
A similar pattern was seen in the RNFL. Global thinning rates did not differ significantly between groups, but the superotemporal RNFL was observably thicker in patients with severe OSA using CPAP than in untreated counterparts.
The findings are intriguing because retinal arterial narrowing has previously been associated with cardiovascular and cerebrovascular disease. In this cohort, hypertension was also more common among non-CPAP users, while stroke or transient ischemic attack occurred only in participants not using CPAP – although the numbers were too small for formal statistical analysis.
That small sample is the study’s major limitation. Almost half of the original cohort was lost to follow-up, several subgroups contained very few participants, and researchers could not perform multivariable adjustment for major vascular comorbidities. CPAP adherence was also assessed using data from only the 90 days preceding the ophthalmic visit rather than continuously over seven years.
The study authors therefore frame the results as exploratory rather than definitive. Still, the long-term trends support the possibility that CPAP may attenuate retinal vascular damage in severe OSA, and strengthen the case for retinal imaging as a potentially useful oculomic marker of systemic vascular health.
