To analyze the total choroidal thickness and thickness of the individual vascular layers of the choroid in eyes with geographic atrophy (GA), using spectral-domain optical coherence tomography.
A cross-sectional retrospective review identified 17 patients with GA (17 eyes) and 14 age-matched healthy subjects (14 eyes), who underwent high-definition raster scanning at New England Eye Center, Boston, MA. Patients were diagnosed with GA based on clinical examination and investigations. Two independent raters evaluated the thickness and vascular layers of the choroid.
Mean choroidal thickness was significantly lower in eyes with GA when compared with age-matched healthy eyes (P < 0.0001). Subfoveal choroidal thickness in eyes with GA was significantly less when compared with healthy eyes (158.1 ± 23.65 μm versus 267.5 ± 19.27 μm, P = 0.001). Subfoveal large choroidal vessel layer thickness and medium choroidal vessel layer/choriocapillaris layer thickness were significantly reduced in eyes with GA when compared with healthy eyes (P = 0.001 and P < 0.0001, respectively).
The choroid is significantly thinner in eyes with GA involving the fovea when compared with healthy eyes. Choroidal thinning in GA involves all its vascular layers. Further studies involving prospective correlation of choroidal vascular changes to the quantitative progression of GA is expected to provide further insight on the choroidal angiopathy associated with GA.
Using spectral-domain optical coherence tomography, this study demonstrates that the choroid is significantly thinner in eyes with geographic atrophy involving the fovea when compared with age-matched healthy eyes. Choroidal thinning in geographic atrophy involves all choroidal vascular layers. Choroidal vascular thinning has no correlation with retinal thinning in geographic atrophy.
*Department of Ophthalmology, New England Eye Center, Tufts Medical Center, Boston, Massachusetts; and
†UMDNJ - Robert Wood Johnson Medical School, Piscataway, New Jersey.
Reprint requests: Jay S. Duker, MD, New England Eye Center, Tufts Medical Center, 800 Washington Street, Boston, MA 02111; e-mail: Jduker@tuftsmedicalcenter.org
Supported in part by a Research to Prevent Blindness unrestricted grant to the New England Eye Center/Department of Ophthalmology, Tufts University School of Medicine and the Massachusetts Lions Eye Research Fund.
J. S. Duker receives research support from Carl Zeiss Meditech, Inc, and Optovue, Inc. The other authors have no conflicting interests to disclose.