Myopic choroidal neovascularization (mCNV) is the most common vision-threatening complication of pathologic myopia, developing in a meaningful proportion of highly myopic eyes over a lifetime.
It is a different disease from age-related macular degeneration in almost every respect that matters for prognosis and treatment planning: younger patients, smaller lesions, less exudation, and, importantly, a better overall response to a shorter course of treatment than typical neovascular AMD.
Pathogenesis
Pathologic myopia produces progressive axial elongation of the globe, which stretches and thins the choroid, retinal pigment epithelium, and Bruch’s membrane over time.
Breaks in Bruch’s membrane — visible clinically as lacquer cracks — create a pathway for choroidal new vessels to grow through into the subretinal space.
MCNV frequently arises at or near the site of one of these breaks, distinguishing its mechanism from the drusen-driven RPE dysfunction that underlies typical age-related neovascular disease.
Risk Factors
- High myopia, generally defined as greater than -6.00 diopters or axial length beyond 26 mm, with risk increasing further with more extreme myopia
- Presence of lacquer cracks on exam or imaging
- Posterior staphyloma
- Older age within the myopic population (though still generally younger rather than typical AMD patients)
- Fellow eye involvement — a history of mCNV in one eye significantly raises the risk of the second eye developing it as well
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From Choroida — the team behind this siteClinical Presentation
Patients report acute or subacute central vision loss, metamorphopsia, or a new central scotoma, developing against a background of longstanding high myopia and often against the additional visual limitation already present from myopic degenerative changes, which can make new symptoms harder for patients to characterize precisely.
Because the underlying myopic maculopathy already causes a degree of chronic visual limitation in many of these patients, a sudden change should be taken seriously rather than attributed to gradual progression of the underlying myopic degeneration.
Exam and Imaging Findings
- A small, grayish-green subretinal lesion, often with associated subretinal fluid or hemorrhage, typically smaller than the lesions seen in neovascular AMD
- Lacquer cracks — fine, yellowish, often branching lines in the posterior pole, representing breaks in Bruch’s membrane
- Background findings of myopic degeneration — posterior staphyloma, chorioretinal atrophy, tessellated fundus from visible choroidal vessels through a thinned RPE
- OCT showing a small, well-defined subretinal hyperreflective lesion, generally with less associated fluid than typical neovascular AMD
- OCT angiography and fluorescein angiography both useful for confirming the neovascular lesion and distinguishing it from other causes of subretinal change in a myopic eye
Differential Diagnosis
- Fuchs spot — an old, inactive, pigmented scar from prior mCNV, rather than an active lesion
- Simple subretinal hemorrhage without neovascularization, sometimes occurring after minor trauma or Valsalva in a highly myopic eye with fragile Bruch’s membrane
- Focal choroidal excavation or dome-shaped macula — structural myopic changes that can alter the macular contour without representing active neovascularization
- Age-related macular degeneration, in an older myopic patient where the two conditions can occasionally coexist
Management
Anti-VEGF therapy (ranibizumab, aflibercept, or bevacizumab) is first-line treatment and has transformed outcomes for mCNV, with many patients achieving good, durable visual results after a shorter treatment course than is typical for neovascular AMD.
A substantial proportion of eyes require only a few injections total, rather than the ongoing, often indefinite treatment schedule common in AMD, and this difference in expected treatment burden is worth explaining to patients up front, since it shapes expectations differently from what many patients may have heard about anti-VEGF therapy for AMD from family or friends.
Verteporfin photodynamic therapy was the standard treatment before anti-VEGF agents became available and is now used only rarely, generally reserved for cases where anti-VEGF therapy is not accessible or has not achieved adequate control.
Regular monitoring after apparent resolution remains important, since recurrence can occur, and the fellow eye should be monitored given the elevated risk of bilateral involvement over time.
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From Choroida — the team behind this siteReferences
- Wong TY, Ohno-Matsui K, Leveziel N, et al. Myopic choroidal neovascularisation: current concepts and update on clinical management. British Journal of Ophthalmology.
- Ikuno Y, Ohno-Matsui K, Wong TY, et al. Intravitreal aflibercept injection in patients with myopic choroidal neovascularization: the MYRROR study. Ophthalmology.
- Wolf S, Balciuniene VJ, Laganovska G, et al. RADIANCE: a randomized controlled study of ranibizumab in patients with choroidal neovascularization secondary to pathologic myopia. Ophthalmology.
- American Academy of Ophthalmology. Basic and Clinical Science Course, Section 12: Retina and Vitreous.
