Retinal Vessel Signs and 10-Year Incident Age-Related Maculopathy: The Blue Mountains Eye Study

Abstract

To examine whether retinal vessel signs are independent predictors of the long-term development of age-related maculopathy (ARM). Prospective population-based cohort study. Blue Mountains Eye Study participants aged > or =49 years (n = 3654) were examined during 1992 through 1994; 2335 (75% of survivors) were reexamined after 5 years and 1952 (76% of survivors) were reexamined after 10 years. Baseline focal arteriolar narrowing and arteriovenous (AV) nicking were assessed and vessel calibers were measured from retinal photographs. A side-by-side grading method was used to assess ARM incidence. Eye-specific data were analyzed using generalized estimating equation models, adjusting for age, gender, smoking, and blood pressure. Incident early ARM (soft indistinct or reticular drusen or combined soft distinct drusen and retinal pigment abnormality) was defined in eyes free of both early and late ARM at baseline. Incident late ARM (either geographic atrophy or neovascular macular degeneration) was defined in eyes free of these 2 lesions at baseline. Over a 10-year period, incident late ARM developed in 106/4745 eyes at risk of late ARM (2.2%). Eyes with mild (2.7%) or severe (4.6 %) AV nicking were more likely to develop late ARM than eyes without this sign (1.5%). The adjusted odds ratio (OR) was 1.4, 95% confidence interval (CI) 0.8 to 2.4 for mild and OR 2.6, 95% CI 1.2 to 5.5 for severe AV nicking. Eyes with focal narrowing were also more likely to develop late ARM (7.6% vs. 1.8%), adjusted OR 2.2, 95% CI 1.1 to 4.1. Incident early ARM developed in 398/4490 eyes at risk of early ARM (8.9%). Severe AV nicking, but not focal arteriolar narrowing, was associated with an increased long-term risk of early ARM (13.6% vs. 8.2%; OR 1.5; 95% CI 1.0-2.3). Neither arteriolar nor venular caliber was significantly associated with the incidence of either early or late ARM. These 10-year incidence data confirm our previous observation that structural retinal arteriolar changes may either contribute to ARM progression or share common pathologic pathways with ARM, independent of traditional vascular risk factors.