The Association among Blood Pressure, Blood Pressure Medications, and Glaucoma in a Nationwide Electronic Health Records Database.

PURPOSE: To measure the association among blood pressure (BP), BP medications, and glaucoma using the All of Us Research Program database.

DESIGN

A retrospective, longitudinal cohort study leveraging a national electronic health record (EHR) database administered by the National Institutes of Health.

PARTICIPANTS

Eye patients in the All of Us Research Program database with at least 15 months of follow-up and 1 BP measurement.

METHODS

Univariable and multivariable Cox regression models predicted the risk of developing incident open-angle glaucoma (OAG). Mean arterial pressure (MAP) and the number of BP medication classes were entered as time-varying predictors to account for changes over time.

MAIN OUTCOME MEASURES: The risk of developing incident OAG, as defined by billing diagnosis codes.

RESULTS

Of 20 815 eligible eye patients who qualified for this study, 462 developed OAG. Low BP (MAP < 83.0 mmHg) was associated with increased risk of developing OAG (hazard ratio [HR], 1.32; 95% confidence interval [CI], 1.04-1.67). High BP (MAP > 101.3 mmHg) and the number of BP medication classes were not associated with OAG after adjustment for covariates. Other risk factors associated with OAG included being Black (HR, 3.31, 95% CI, 2.63-4.17), Hispanic or Latino (HR, 2.53, 95% CI, 1.94-3.28), Asian (HR, 2.22, 95% CI, 1.24-3.97), older in age (80+ years, HR, 20.1, 95% CI, 9.10-44.5), and diabetic (HR, 1.32, 95% CI, 1.04-1.67). Female gender was associated with decreased hazard of developing OAG (HR, 0.66, 95% CI, 0.55-0.80). No significant interaction was observed between MAP and the number of BP medications on the risk of developing OAG.

CONCLUSIONS

We found that low BP is associated with increased risk of developing OAG in a national longitudinal EHR database. We did not find evidence supporting a differential effect of medically treated and untreated low BP. This study adds to the body of literature implicating vascular dysregulation as a potential etiology for the development of OAG, particularly emphasizing the lack of influence of BP medications on this relationship.