Abstract
Abstract: :
Purpose: To evaluate whether open–angle glaucoma (OAG) is associated with 9–year mortality after accounting for potential confounders. Methods: The Blue Mountains Eye Study examined 3654 persons (82.4% of eligible residents) during 1992–4. OAG was diagnosed from congruous typical visual field changes (30–2 fields) and optic disc cupping (stereo optic disc photographs). Demographic information from baseline participants was matched with Australian National Death Index data to obtain the number and causes of deaths. Cox proportional hazards regression analysis, controlling for age, male gender, diabetes, hypertension, current smoking history and alcohol use, were used to assess hazard ratios for vascular mortality (cardiovascular or cerebrovascular events). Adjustments for all–cause mortality also included history of heart attack, stroke, and cancer. Results: At baseline, OAG was diagnosed in 108 subjects (3.0%). Of 873 deaths (23.9%) before January 2002, 408 people (11.2%) died from vascular causes. Crude vascular mortality among subjects with OAG (33 subjects; 30.6%) was 3–times higher than in persons without OAG (375 subjects; 10.6%), p<0.0001. Increased crude all–cause mortality in OAG subjects was also found; 47.2% with vs. 23.2% without OAG, p<0.0001. After controlling for potential confounders of vascular mortality, OAG subjects had a non–significant 40% increased risk of vascular death (relative risk (RR) 1.4; 95% confidence intervals (CI) 0.95–2.01), which was borderline non–significant. However, a statistically significant increased vascular mortality risk was found among subjects with previously diagnosed OAG (RR 1.7; CI 1.10–2.71) compared with normal subjects, but not for newly diagnosed cases (RR 1.0; CI 0.55–1.85). Similarly, high–tension glaucoma cases (based on two IOP readings on separate days) had a 60% increased vascular mortality risk (RR 1.6; CI 1.06–2.47), not found in normal tension glaucoma cases (RR 1.0; CI 0.47–1.95). The increased vascular mortality risk associated with OAG was stronger among subjects <75 years (RR 2.2; CI 0.95–5.00) than persons ≥75 years (RR 1.3; CI 0.82–1.89), and in persons without diabetes (RR 1.4; CI 0.96–2.10) than with diabetes (RR 1.0; CI 0.29–3.25). OAG was not statistically related to all–cause mortality after controlling for confounders (RR 1.0; CI 0.77–1.40). No associations were found between all–cause or vascular mortality and ocular hypertension. Conclusions: Although OAG was not associated with all–cause mortality, our data suggest a possible association between OAG and vascular mortality, consistent with findings from the National Health Interview Survey.
Keywords: clinical (human) or epidemiologic studies: prevalence/incidence • clinical (human) or epidemiologic studies: risk factor assessment