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Risk for the development and progression of retinopathy
Ophthalmologists are well aware of the strong association between longstanding hyperglycaemia and the microvascular manifestations of diabetic retinopathy.1,2 The relation between macrovascular large vessel disease and diabetic retinopathy is less well understood, and is the subject of Klein et al's paper in this issue of the BJO (p 84). These authors seek to shed light on the association between arteriosclerotic cardiovascular disease and diabetic retinopathy in a cohort of patients from the Cardiovascular Health Study (CHS).
In their paper, Klein et al found an association between cardiovascular disease, elevated plasma LDL cholesterol and gross proteinuria, and diabetic retinopathy. These associations were independent of age, sex, race, blood sugar, and duration of diabetes. They did not, as one might expect, find an association between internal carotid artery wall abnormalities or subclinical atherosclerosis and diabetic retinopathy. Although there was a significant association between elevated systolic blood pressure and retinopathy in the univariate analysis, this relation lost significance in the multivariate analysis. In contrast, elevated blood pressure has been found to be significantly associated with diabetic retinopathy in various large prospective and cross sectional studies.3,4 Klein et al found a significant relation between elevated plasma LDL cholesterol and retinopathy, which is consistent with other studies.5,6 This finding will be more definitively answered in ongoing prospective randomised controlled clinical trials of lipid lowering drugs. Finally, the association between gross proteinuria and diabetic retinopathy found by Klein et al corroborates the findings of other investigators.7,8
As the authors point out, there are some limitations to their study. Firstly, and probably most significantly, is the fact that only about one half of the patients with diabetes, 296 out of 558 people classified as having diabetes in the CHS, were evaluated. The diabetic participants excluded from the study were in general older and sicker than the participants who were studied. Therefore, the younger and healthier diabetic participants in the study were not representative of the entire cohort of diabetic people in the CHS. Secondly, the cohort of diabetic participants studied is relatively small. Finally, the non-mydriatic non-stereoscopic fundus photograph of one eye of each participant probably underreported the prevalence of diabetic retinopathy and macular oedema in the participants.
More definitive demonstration of the relation of atherosclerotic cardiovascular disease and diabetic retinopathy will require long term prospective studies begun at or before the onset of diabetes. Until these studies are actualised, Klein et al's findings provide us with tantalising evidence of an association between atherosclerosis and diabetic retinopathy. If their results are confirmed by future studies, diabetic patients with evidence of atherosclerosis may have a higher risk for the development and progression of retinopathy and may require more frequent examinations and interventions.
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Risk for the development and progression of retinopathy