Indocyanine green angiographic findings in idiopathic choroidal neovascularization

Department of Ophthalmology, University of Ancona, Italy.
International Ophthalmology (Impact Factor: 0.55). 06/1996; 20(4):171-9. DOI: 10.1007/BF00175256
Source: PubMed


Evaluation of choroidal alterations associated with idiopathic choroidal neovascularization (ICNV) and the possible relation between this affection and Multifocal Choroidopathies (MC).
The authors analysed, using high definition videoangiography, the choroidal findings in 21 consecutive patients affected by ICNV (7 males and 14 females; 19-46 years; mean age: 31.8 years); with a follow-up at 5-30 months (mean 13 months). Moreover, a retrospective study of 20 cases of ICNV (11 males and 9 females; age: 17-39 years; mean age: 29.3 years) with a follow-up at 6-11 years (mean 8.9), was performed.
In 7 eyes, the indocyanine green angiography (ICGA) showed choroidal hypofluorescent spots similar to those observed in MC (in 3 cases even in the fellow unaffected eye), in 2 of them the regression of the spots was observed after steroid therapy. In 2 eyes, the ICGA revealed hyperfluorescent spots; in one of them the complete regression of the spots after oral cyprofloxacine was observed. In 6 patients (10 eyes), choroidal permeability alterations could be visualized (in 4 cases even in the unaffected eye).
The indocyanine green angiographic findings (hypo and hyperfluorescent spots, choroidal permeability alterations) could support the theory of Gass which considers that ICNV is not idiopathic but secondary to a widespread choroidal inflammatory disease. The similarity of the ICGA alterations in ICNV and MC, the observation that cases of ICNV would become MC in the follow-up, could allow the hypothesis of a close connection between these two affections.

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    • "ICNV that occurs in patients under 50 of age usually has an underlying inflammatory cause. Giovannini et al. suggested a link between ICNV and inflammatory choroidopathies based on common ICGA findings in both conditions consisting mostly of hypofluorescent areas and alterations in choroidal permeability.6 These authors further indicated that some cases of ICNV could evolve into inflammatory chorioretinopathies.6 Callanan and Gass also suggested that ICNV was likely secondary to choroidal inflammation.7 "
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    ABSTRACT: We report a case of multiple evanescent white dot syndrome (MEWDS) that presented with putative idiopathic choroidal neovascularisation (ICNV) before showing angiographic signs typical of MEWDS. A 16-year-old male presented with unilateral metamorphopsias and visual loss in his left eye. ICNV with subretinal hemorrhage was diagnosed and treated with intravitreal Avastin(®). Fifteen days later, regression of choriodal neovascularization (CNV) was documented together with the appearance of fluorescein angiography (FA) and indocyanine green angiography (ICGA) signs typical for MEWDS, that included faint mottled FA hyperfluorescence in the mid-peripheral fundus, irregularly shaped mid-peripheral ICGA dark areas in the intermediate angiographic phase that were clearly delineated in the late phase as well as peripapillary hypofluorescence. Fundus examination appeared completely normal during the follow-up except for the CNV hemorrhage noted at the initial visit. This case demonstrates the need to consider ICNV as a diagnosis of exclusion until inflammatory causes have been eliminated. In this case, the underlying occult inflammatory condition would have been missed without the ICGA data that clearly showed signs of MEWDS that was supported by FA findings.
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    ABSTRACT: The authors report the cases of two patients affected with idiopathic choroidal neovascularisation studied with combined fluorescein angiography and indocyanine green (ICG) angiography. In particular the presence of choroidal abnormalities at ICG angiography which could not be detected by fluorescein angiography was studied. Both patients underwent a complete systemic and ocular assessment. Fluorescein angiography and ICG angiography were performed in a routine fashion at the time of presentation in both cases and after 14 months in the second patient. Results of the systemic investigations were unremarkable. A distinct dark rim surrounding the choroidal neovascular net was evident until the late phases of ICG angiography despite the presence of subretinal blood. Dilated choroidal vessels were observed beneath the neovascular membrane in both cases. In the first patient a hyperfluorescent area beyond the primary lesion was detected in the affected eye and a distinct leaking subfoveal choroidal venous vessel was found in the fellow eye. The second patient never showed other angiographic alterations either in the affected or in the fellow eye. ICG angiography has proved to be useful, both to better define and follow up the true extent of the pigment halo (healing response) around the neovascular membrane when subretinal blood and dye leakage at fluorescein angiography prevent its full appreciation, and to rule out other causes of choroidal neovascularisation in young healthy adults associated with either choroidal inflammatory focal lesions or choroidal vascular dynamic or inflammatory alterations.
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