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Optical coherence tomography angiography of type 3 neovascularisation in age-related macular degeneration after antiangiogenic therapy
  1. Nopasak Phasukkijwatana1,2,
  2. Anna C S Tan3,4,5,
  3. Xuejing Chen1,
  4. K Bailey Freund3,4,
  5. David Sarraf1,6
  1. 1Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
  2. 2Department of Ophthalmology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
  3. 3Vitreous Retina Macula Consultants of New York, New York, New York, USA
  4. 4LuEsther T Mertz Retinal Research Center, Manhattan, Eye, Ear and Throat Hospital, New York, New York, USA
  5. 5Singapore National Eye Center/Singapore Eye Research Institute, Singapore
  6. 6Greater Los Angeles VA Healthcare Center, Los Angeles, California, USA
  1. Correspondence to Dr David Sarraf, Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; dsarraf{at}ucla.edu

Abstract

Background/aims To assess the microvascular response of type 3 neovascularisation secondary to age-related macular degeneration (AMD) after antivascular endothelial growth factor (anti-VEGF) therapy using optical coherence tomography angiography (OCTA).

Methods Consecutive patients diagnosed with AMD and type 3 neovascularisation based on clinical examination, structural optical coherence tomography and fluorescein angiography when available were retrospectively evaluated. En face OCTA imaging (3×3 mm scans) with quantitative microvascular analysis was performed at baseline and after a single anti-VEGF intravitreal injection.

Results 17 eyes of 14 patients underwent OCTA before and after anti-VEGF treatment. OCTA demonstrated significant regression of small calibre type 3 neovascular tufts in all eyes. Median lesion area was 0.061 mm2 (range 0.003–0.198 mm2) at baseline and 0.009 mm2 (range 0–0.085 mm2, p=0.0003) at follow-up. Cystoid macular oedema and/or subretinal fluid resolved in all cases after treatment. The type 3 lesions became undetectable with OCTA post-treatment in 5 of the 17 eyes. However, in 11 eyes, large feeder vessels were identified and remained unchanged after treatment.

Conclusions The microvascular morphology of type 3 neovascularisation secondary to AMD was assessed at baseline and follow-up and showed significant regression in response to anti-VEGF therapy by OCTA. Quantitative OCTA analysis was also performed and confirmed remarkable regression in response to a single intravitreal anti-VEGF injection.

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