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Athanasios Bezatis, Eva Becker, Christian Brinkmann, Steffen Schmitz-Valckenberg, Rolf Fimmers, Monika Fleckenstein, Frank Holz; Enhanced Depth Imaging Optical Coherence Tomography of the Choroid in eyes with Geographic Atrophy secondary to Age-related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6299.
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To compare the subfoveal choroidal thickness (SCT) in eyes with geographic atrophy (GA) secondary to age-related macular degeneration (AMD) with normal eyes using enhanced depth imaging optical coherence tomography (EDI-OCT).
A total of 42 eyes (42 patients, mean age: 77.4 ± 7.5 years) with GA and 40 eyes of 40 healthy subjects (mean age 74.6 ± 5.9 years) were examined by confocal scanning laser ophthalmoscopy (cSLO) and EDI-OCT (Spectralis HRA+OCT, Heidelberg Engineering, Germany). Two independent readers measured the SCT. Analysis included Bland-Altman statistics and correlation of SCT with age, gender and refractive error (RE, eyes with RE > -3 D have been excluded from the analysis), respectively. In the GA group, SCT was also correlated with both uni-/multifocality and the total size of the atrophic area measured by semi-automated image analysis software (RegionFinder, Heidelberg Engineering).
Mean SCT was significantly thinner in the GA group (154.2 ± 70.8 µm) compared to the control group (231.9 ± 60.3 µm) (p=0.001). Mean interobserver agreement for SCT measurements was 20.0 µm (95% confidence interval (CI) [-3.3; 1.1]). In both groups, there was a significantly negative correlation between SCT and age (p=0.004) while gender and RE (range -1.75 to +3.36 D) were not significantly correlated with SCT (p=0.95 and p=0.72) respectively. In the GA group, there was no significant correlation between SCT and neither total size of atrophy (mean 8.98 ± 7.48 mm2, p=0.46) nor uni-/multifocality (p=0.98).
The results indicate that advanced dry AMD is associated with thinner choroid compared to normal eyes. This may possibly implicate alterations in choroidal perfusion and supply to outer retinal layers as a pathophysiologic factor in the development and progression of GA.
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