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AbstractDO.05.13 Flicker-induced retinal vasodilatation in patients with diabetes, patients with systemic hypertension and/or hypercholesterolemia, and healthy control subjects Garhöfer G.1, Pemp B.1, Weigert G.1, Schmetterer L.1,2
1Department of Clinical Pharmacology, 2Center for Biomedical Engineering and Physics, Medical University of Vienna, Austria Objective: A number of studies indicate that patients with diabetes show an abnormal retinal vessel response to flicker stimulation. The mechanism behind this reduced vasodilator capacity is unclear. It has, however, been hypothesized that this phenomenon may be related to endothelial dysfunction, because the retinal flicker response has been shown to be nitric oxide dependent. In the present study we tried to gain more insight into this question by comparing the flicker responses in different groups with well established endothelial dysfunction.
Methods: In the present study 20 patients with insulin dependent diabetes, no or mild non-proliferative diabetic retinopathy, and serum cholesterol levels <250 mg/dl, 40 patients with systolic blood pressure between 140 and 159 mmHg and diastolic blood pressure between 90 and 99 mmHg and/or serum cholesterol plasma levels >250 mg/dl and 20 healthy control subjects were included. The response of retinal arteries to flicker stimulation was measured using the Imedos Dynamic Retinal Vessel Analyzer. The retinal vessel response between the three groups was compared by an ANOVA model.
Results: The response in retinal arterial diameter to flicker stimulation was 2.9 ± 0.6 % in patients with diabetes, 4.1 ± 0.4 % patients with systemic hypertension and/or hypercholesterolemia, and 7.6 ± 0.5 % in healthy control subjects (p<0.001). There was, however, no difference in the flicker-induced vasodilatation between patients with diabetes and patients with systemic hypertension and/or hypercholesterolemia.
Conclusions: The present study shows that different groups of patients with well established endothelial dysfunction have reduced flicker responses in the human retina. This supports the concept that flicker-induced vasodilatation is endothelium dependent.
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