Purpose:
To describe the relationship of intima-media layer thickness (IMT) and the presence of plaque in the carotid artery, two measures of subclinical atherosclerosis, to the 10-year cumulative incidence of early and late age-related macular degeneration (AMD) in a population-based study.
Methods:
Mean and maximum IMT and presence of plaque were assessed using B-mode ultrasonography of the carotid artery. AMD was determined by grading stereoscopic color fundus photographs using the Wisconsin Age-Related Maculopathy Grading System. Analyses included 1972 persons 53-96 years of age participating in both the Epidemiology of Hearing Loss Study and the Beaver Dam Eye Study at the 1998-2000 examination and with photographs at a 5- and/or 10-year follow-up.
Results:
The 10-year cumulative incidence of early AMD in either eye was 15.7%, for late AMD it was 4.0%, and for progression of AMD it was 39.5%. While controlling for age, sex, smoking status, vitamin supplement use, body mass index, history of statin use, serum total cholesterol or serum HDL-cholesterol, serum C-reactive protein, CFH (rs1061170), ARMS2 (rs10490924) and AMD lipid pathways genes (ApoE, LIPC [rs7163555], LPL [rs263], CETP [rs11508026] and CETP [rs3764261]), mean IMT was associated (presented as odds ratio per 0.1 mm IMT, p value) with the 10-year incidence of early AMD (1.11, 1.00-1.23, p=0.05) and late AMD (1.35, 1.10-1.65, p=0.001), but not progression of AMD (1.04, 0.88-1.06, p=0.61). Mean IMT was associated with the 10-year incidence of pure geographic atrophy (4.12, 1.18-14.4, p=0.03) but not exudative AMD (0.94, 0.75-1.17, p=0.57). Similar associations were found for maximum IMT. The number of sites with plaque was not related to the 10-year incidence of any AMD outcome. There was no relation of a history of angina, myocardial infarction or stroke to any incident AMD outcome.
Conclusions:
These population-based data show a relationship of subclinical atherosclerosis to the incidence of AMD, independent of systemic and genetic risk factors. It remains to be seen whether early interventions directed at inflammatory or lipid pathways known to be associated with the pathogenesis of atherosclerosis will affect the incidence of AMD.