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Monika Fleckenstein, Steffen Schmitz-Valckenberg, Moritz Lindner, Athanasios Bezatis, Eva Becker, Rolf Fimmers, Frank G. Holz; The “Diffuse-Trickling” Fundus Autofluorescence Phenotype in Geographic Atrophy. Invest. Ophthalmol. Vis. Sci. 2014;55(5):2911-2920. doi: https://doi.org/10.1167/iovs.13-13409.
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To further characterize a subgroup of patients exhibiting the fundus autofluorescence (FAF) “diffuse-trickling” phenotype associated with geographic atrophy (GA).
In the context of the Fundus Autofluorescence in Age-Related Macular Degeneration (FAM) Study, patients with diffuse-trickling GA were examined and characterized by FAF and spectral-domain optical coherence tomography imaging. Age, sex distribution, and medical history were compared with FAM study patients (n = 288, 60.1% female) with other GA phenotypes (non–diffuse-trickling). In a subset of patients, subfoveal choroidal thickness (SCT) was analyzed.
Patients with diffuse-trickling (n = 61), compared with patients with non–diffuse-trickling GA, had a significantly younger age at first presentation (68.2 ± 11.6 vs. 75.4 ± 8.1 years, P < 0.001), a shift in the proportion of men from 55% in the age group younger than 65 to 19% in the age group older than or equal to 65, and a significantly higher rate of myocardial infarction (MI) in the age group younger than 65 (24% vs. 0%, P = 0.011); all but one patient with MI were male. Further evaluation revealed that in the age group younger than 65, 54% of patients with diffuse-trickling had been hospitalized due to cardiovascular diseases including hypertensive crisis, angina, and MI. Analysis of choroidal thickness revealed a significantly thinner SCT in diffuse-trickling compared with non–diffuse-trickling GA (135.2 ± 56.4 vs. 191.4 ± 77.8 μm, P < 0.001).
The results indicate an association of diffuse-trickling GA with systemic cardiovascular disorders in the younger study population. Together with the ocular morphologic characteristics including a lobular appearance and a thin choroid, a vascular insufficiency at the level of the choroid may play a pathogenetic role in this distinct GA phenotype. (ClinicalTrials.gov number, NCT00393692.)
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