# Choroidal Vascularity Index in Adult-Onset Foveomacular Vitelliform Dystrophy: A Pilot Study
## 4 Discussion
To our knowledge, there are no previous studies in the literature that evaluate CVI in patients with AOFVD; therefore, we cannot compare our results with previous data. More importantly, our cohort of patients exclusively had AOFVD in the vitelliform stage. We found that eyes with AOFVD in comparison with control eyes exhibited a greater CVI due to a larger luminal area, indicating possible compensatory choroidal response mechanisms reflected in vessel dilatation. Indeed, it is well known that the choroid is prevalently vascular tissue that exhibits significant physiological modifications in thickness based on circadian rhythms, use of caffeine, and excessive liquid ingestion [23,24, 25]. Retinal and choroidal disease mechanisms are probably not an exception in CT modifications. Eyes with AOFVD presented a higher CVI than eyes with CD in our study. This could indicate CVI as a possible early biomarker heralding evolution to more advanced stages. We may speculate that choroidal vessels enlarge in an effort to clear vitelliform material. This could affect the normal equilibrium between the three vessel layers of the choroid, thus leading to a secondary CC impairment shown by OCTA reports of reduced CC vessel density [10,18,19]. Choroidal and outer retina alterations are shown even in later stages of AOFVD. [PERSON] et al. found discontinuity and the appearance of bumps in the RPE in pseudohypopyon and vitelliruptive stages [8]. It is known that vitelliform material, located between the RPE and outer segments of the photoreceptors, consists of photoreceptor outer segment debris, macrophages loaded with melanin/lipofuscin, and RPE cells [26,27]. In clinicopathological studies, the RPE at the base of the lesion was reported to be initially hypertrophic [26,27]. These could be compensatory attempts to remove metabolic waste products and restore retinal integrity. The choroid could manifest tentative repair mechanisms and the increased luminal area could reflect choroidal vasodilation in a compensatory attempt to overcome the damage inflicted due to a mechanical effect of vitelliform material on blood vessels, as postulated by [PERSON] et al. [19]. The present study had some limitations: it was retrospective in nature; manual segmentation was used for CT measurement; image binarization is not corroborated by histopathological studies, and the analysis is based on the dark-pixel and light-pixel regions of the choroid that represent vasculature and stromal areas; calculations of CVI were performed on a single subfoveal B-scan owing to software limits; the sample size and standard deviation were small, but we included only patients in the vitelliform stage of the disease. Finally, this was a pilot investigation, so we could not directly compare our results with the existing literature. Despite these drawbacks, our results revealed a greater CVI in AOFVD than in eyes with CD and in healthy eyes. This alteration was associated with preferential vasodilitation of the luminal component already evident in the vitelliform stage of AOFVD, indicating a possible role of choroidal vasculature in this condition. Moreover, CVI may represent a sensitive index that may have implications in predicting disease progression. Further prospective studies with larger patient populations and division in stages of vitelliform deposit progression are warranted to corroborate our findings. Conceptualization, S.A. and S.F. ; methodology, S.F. ; software, C.C. ; validation, S.A., M.D.P. and G.S. ; formal analysis, S.F. ; investigation, S.F. ; resources, S.A.; data curation, C.C. ; writing--original draft preparation, S.F. ; writing--review and editing, S.A.; visualization, S.A.;supervision, S.A.; project administration, G.S. ; funding acquisition, S.A. All authors have read and agreed to the published version of the manuscript. This research received no external funding.