PS-C12-4: OPEN-ANGLE GLAUCOMATOUS OPTIC DAMAGE ASSOCIATED WITH DAYTIME AND NOCTURNAL DIPS IN BLOOD PRESSURE

Abstract

Background: Impaired ocular perfusion pressure via systemic hypoperfusion plays a pivotal role in the pathogenesis of open-angle glaucoma (OAG). Extreme dips in mean arterial pressure (MAP) during 24-h are associated with OAG, however, whether this is driven by diurnal or nocturnal dips remains undocumented. We aimed this study to investigate the association of OAG damage with daytime and nocturnal dips in MAP. Methods: We conducted a retrospective longitudinal study that included 110 primary OAG patients who underwent 24-h ambulatory blood pressure monitoring. OAG damage was defined as changes in mean deviation (MD) of visual field tests during follow-up. MAP variability independent of the mean (VIMmap) was computed for daytime and nighttime. Dips were the five daytime and three nighttime lowest drops in MAP. We also calculated the night-to-day ratio and defined low diurnal and nocturnal MAP levels. We applied mixed models to evaluate changes in MD (expressed as decibels [dB]) during follow-up in relation to diurnal and nocturnal variability and dips in MAP. Results: The mean age was 64.0y (53% women). The median follow-up was nine years. In adjusted mixed models, every + 3 mmHg increase in daytime VIMmap was associated with a -2.57 dB longitudinal change in MD (P < 0.001). The longitudinal changes in MD associated with daytime dip measures ranged from -2.56 dB (95% confidence interval [CI], -3.61 to -1.51; P < 0.001) to -3.19 dB (95% CI, -4.53 to -1.84; P < 0.001). For nighttime measures, the MD changed -0.71 dB (CI, -1.24 to -0.17; P = 0.009) per every -5 decrease in the nighttime MAP level. Nocturnal MAP level < 74 mmHg and every 0.05 decrease in the night-to-day ratio were related to -7.23 (P = 0.003) and -0.96 (P = 0.011) changes in MD. Nighttime VIMmapP and nocturnal dips were not associated with changes in MD (P > 0.097). Conclusions: Extreme daytime dips in MAP relate to OAG damage independently of the MAP level. Whereas, the association between OAG damage and nocturnal measures is driven by the nocturnal MAP level rather than variability or dips in MAP. The assessment of diurnal patterns in MAP might offer an opportunity to understand the pathogenesis of OAG. This is also critical as the perfusion pressure to the eyes is physiological 30% lower than at the brachial level in the standing or sitting positions. Therefore, a physiological lower perfusion pressure combined with extreme diurnal dips in MAP would exacerbate the hypoperfusion state in the optic nerve, leading to further glaucoma damage.