Choroidal neovascularization

From Wikipedia, the free encyclopedia

Choroidal neovascularization (CNV) is the creation of new blood vessels in the choroid layer of the eye. This is a common symptom of the degenerative maculopathy wet AMD (age-related macular degeneration).[1]

Causes

CNV can occur rapidly in individuals with defects in Bruch's membrane, the innermost layer of the choroid. It is also associated with excessive amounts of Vascular endothelial growth factor (VEGF). As well as in wet AMD, CNV can also occur frequently with the rare genetic disease pseudoxanthoma elasticum and rarely with the more common optic disc drusen. CNV has also been associated with extreme myopia or malignant myopic degeneration, where in choroidal neovascularization occurs primarily in the presence of cracks within the retinal (specifically) macular tissue known as lacquer cracks.

Symptoms

CNV can create a sudden deterioration of central vision, noticeable within a few weeks. Other symptoms which can occur include metamorphopsia, and colour disturbances. Hemorrhaging of the new blood vessels can accelerate the onset of symptoms of CNV.

Signs

CNV can be detected by using a type of perimetry called preferential hyperacuity perimetry.[2] On the basis of fluorescein angiography, CNV may be described as classic or occult.

Treatment

Standard of care in retinology today are intravitreal injections of anti-VEGF drugs to control neovascularization and reduce the area of fluid below the retinal pigment epithelium. These drugs are commonly known as Avastin and Lucentis, and although their effectiveness has been shown to significantly improve visual prognosis with CNV, the recurrence rate for these neovascular areas remains high. Individuals with CNV should be aware that they are at a much greater risk (25%) of developing CNV in fellow eye, this according to the American Academy of Ophthalmology and further supported by clinical reports.

  • In 'wet' (also known as 'neovascular') Age-Related Macular Degeneration, CNV is treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin. The drug is given intravenously. It is then activated in the eye by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi.[3]
  • Anti-VEGF drugs, such as pegaptanib and ranibizumab, are also used to treat CNV. Anti-VEGFs bind to and inactivate Vascular endothelial growth factor.[4]

See also

  • Macula
  • Age-Related Macular Degeneration

References

  1. Spalton DJ, Hitchings RA, Hunter PA (2005). Atlas of Clinical Ophthalmology (3rd Edition ed.). 
  2. "Elsevier". Ophsource.org. Retrieved 2012-12-14. 
  3. Donati, Guy (2007). "Emerging Therapies for Neovascular Age-Related Macular Degeneration: State of the Art". Ophthalmologica 221 (6): 366–377. doi:10.1159/000107495. PMID 17947822. 
  4. Takeda, AL; Colquitt, J; Clegg, AJ; Jones, J (Sep 2007). "Pegaptanib and ranibizumab for neovascular age-related macular degeneration: a systematic review.". The British journal of ophthalmology 91 (9): 1177–82. doi:10.1136/bjo.2007.118562. PMC 1954893. PMID 17475698. Retrieved 15 December 2012. 
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