Blind killer of myopia — complete record of choroidal neovascularization

Abstract: the genetic denaturation hypothesis holds that myopic ametropia is determined by heredity, Studies have shown that single nucleotide polymorphisms of several genes (such as pigment epithelium derived factors) are related to the occurrence and progress of myopic CNV.

CNV is a killer and culprit complication of vision loss in myopic patients. The definitions of myopic CNV are diverse and often described as pathological myopia (PM) subretinal neovascularization, pmfuchs’ plaques or Forster Fuchs’ plaques or PM discoid degeneration. Although it was previously believed that myopic CNV occurred only in PM, it has been gradually recognized that myopic CNV can occur in any degree of myopia, even those without typical myopic fundus changes.

Therefore, in clinical practice, CNV can be attributed to myopia according to refractive status, and other CNV related diseases are excluded. A variety of effective treatment measures have been developed for myopic CNV, especially anti VEGF treatment. This review reviews the pathogenesis, epidemiological characteristics, natural course and treatment progress of myopic CNV.

pathogenesis of myopic CNV

there are many hypotheses about the pathogenesis of myopic CNV: the mechanical hypothesis is based on that the longer the ocular axis is, the greater the mechanical traction on the retina will lead to the imbalance of Pro angiogenic and anti angiogenic factors, and CNV will eventually appear; The appearance of paint crack is the inducement of myopic CNV, which supports the mechanical hypothesis. The genetic denaturation hypothesis of

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holds that myopic ametropia is determined by heredity, Studies have shown that single nucleotide polymorphisms of several genes (such as pigment epithelium derived factor) are related to the occurrence and progression of myopic CNV The hemodynamic hypothesis suggests that the occurrence of myopic CNV is related to the changes of choroidal circulation, such as choroidal filling delay, choroidal thinning and so on. However, myopic CNV can occur even if choroidal circulation is preserved and posterior scleral staphyloma is mild, which means that hemodynamics plays little role in the occurrence of myopic CNV.

diagnosis of myopic CNV

typical myopic CNV is small, flat and gray membrane under slit lamp. If it occurs chronically or repeatedly, pigmentation can be seen at the edge. The symptoms can be vision loss, central scotoma or visual distortion.

the standard examination for the diagnosis of myopic CNV includes fundus examination Fluorescence angiography (FA), optical coherence tomography (OCT). FA, Oct combined with fundus color photography and clinical physical examination are the basic examinations for the diagnosis of myopic CNV. FA can find the existence, type, area and activity of myopic CNV, and help to exclude other diseases. Most myopic CNV are typical CNV on FA, with clear outline hyperfluorescence in the early stage and fluorescein leakage in the late stage.

OCT is necessary for locating fovea, measuring retinal thickness, determining the presence of extracellular fluid and determining the baseline level of treatment. On Oct, Myopic CNV is a continuous hyperreflexive signal above the pigment epithelium (sometimes called type 2 CNV) with a small amount of subretinal effusion. Fundus autofluorescence can show the accumulation of lipofuscin in retinal pigment epithelial cells, which can be used as a part of the basic diagnostic measures and follow-up examination of myopic CNV, and help to evaluate and diagnose the progress of myopic CNV and associated map atrophy.