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According to angiographic features, the CNV can be divided into classic CNV and occult CNV. According to the composition and the location of lesions, the CNV was divided into subfoveal CNV, juxtafoveal CNV, and extrafoveal CNV. The present case series include 42 eyes of subfoveal CNV (7 eyes of classic type, 26 eyes of occult type, 9 eyes of disciform scars), 14 eyes of juxtafoveal CNV (2 eyes of classic type, 12 eyes of occult type), and 3 eyes of extrafoveal CNV (occult type). Visual acuity was severely impaired, less than LogMAR 1.0, including 13 eyes with atrophic AMD (28.9%) and 32 eyes with exudative AMD (71.1%) which include 30 eyes with subfoveal CNV.
DISCUSSION
Advanced AMD is the leading cause of irreversible central vision loss in people older than 50 years in the western world. The prevalence of early and advanced AMD increases with the age. The Beaver Dam Eye Study Group described that the incidence of AMD was 14.4% in people aged 55 to 64 years, 19.4% in those aged 65 to 74 years, and 36.8% in those older than 75 years. As the average age of the population in the western world increases, the prevalence of AMD is estimated to rise accordingly[5]. The average life expectancy of Chinese people is increasing and the prevalence of AMD will rise too[6].
AMD usually has two forms: atrophic (or dry), characterized by drusen and geographic atrophy(GA), and exudative (or wet), characterized by CNV, which eventually causes a disciform scar. Although CNV constitutes 10% of cases of AMD, it results in severe visual loss of 90% patients with AMD[7]. In our report, the atrophic AMD accounts for 60.4% and exudative AMD accounts for 39.6%. The rate of atrophic AMD was not as high as that in overseas report. Probably some patients with early stage AMD did not come to hospital for routine ophthalmological examinations until their vision was obviously affected, which leads to the low clinical number of atrophic AMD.
Early stage of AMD is featured by drusen and alteration of retinal pigment epithelium (RPE). Insoluble extracellular deposits are found beneath the basement membrane of RPE and between the inner collagenous layers of the Bruchs membrane, which is called drusen[8], composed of lipid, collagen and phospholipids. A few of hard drusens may be not related to AMD, but a great number of hard drusens are the independent risk factors of vision loss[9]. On the contrary, soft drusens are usually larger with blurry margin and have a tendency to become confluent, forming the retinal pigment epithelial detachments (RPED)[10]. In our report, 5 of the 37 eyes with drusens appeared hypofluorescence, and the rest 32 eyes were stained by fluorescence during FFA. The appearance of soft drusens during FFA depends on the decreasing number of RPE and the histochemical composition of drusen. Dye of fluorescence is attributed to the accumulation of phospholipids. Pauleikhoff et al[11] explained that deposits containing predominantly neutral lipids would be hydrophobic, resulting in hypofluorescence in fluorescein angiography, while the presence of polar phospholipids would be indicated clinically by hyperfluorescence because of its hydrophilic properties. In our report, 46 eyes appeared sheltered fluorescence or windowlike fluorescence during FFA for pigmentary abnormalities of the RPE, which is considered to be an early indication of risks of developing advanced AMD[12].
Late stage of AMD is characterized by presence of GA and formation of CNV. In our report, 7 eyes with GA appeared windowlike defects during FFA in the atrophic area. GA is the consequence of the degeneration and atrophy of photoreceptor cells and RPE cells[13]. So it is the cause for severe vision loss in GA patients.
Exudative AMD, named neovascular AMD, is characterized by abnormal growth of capillaries from the choroid and by subsequent exudation of fluid, lipid, and blood. CNV, which develops as new abnormal choroidal blood vessels proliferate through the outer layers of Bruchs membrane under the basement membrane of the RPE (subretinal pigment epithelial location), is named classic CNV on angiography [5]. Subretinal CNV induces the leakage because of the lack of structural integrity of the budding endothelium, and this, in turn, leads to subretinal clear fluid and hemorrhage. The loss of normal function of RPE cells may lead to the local tissue hypoxia, which triggers an upregulation of the growth of angiogenic factors. These factors, which include vascular endothelial growth factor (VEGF), may induce new vessels to bud off the choriocapillaries and pass through Bruchs membrane under the RPE, forming what have traditionally been described as occult neovascular membranes seen on angiography[14]. Therefore, CNV occurs in two forms: classic CNV and occult CNV. A classic CNV is a bright, often welldemarcated area with hyperfluorescence in the early phase of angiography, with progressive leakage of dye in the overlying subsensory retinal space during the late phase of angiography that obscures the margins. Occult CNV has indistinct and often poorly defined boundaries on FFA with less early leakage and irregular or punctate hyperfluorescence in late view of the angiogram[15].
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