Optical Coherence Tomography Angiography Signs of Vascular Abnormalization With Antiangiogenic Therapy for Choroidal Neovascularization

• Published in: American journal of ophthalmology Vol. 160; no. 1; pp. 6 - 16
• Main Author: Spaide, Richard F
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2015; Elsevier Limited
• Subjects: Aged; Aged, 80 and over; Angiogenesis; Angiogenesis Inhibitors - therapeutic use; Capillary Permeability; Choroid - blood supply; Choroidal Neovascularization - diagnosis; Choroidal Neovascularization - drug therapy; Choroidal Neovascularization - etiology; Disclosure; Disease; Extracellular matrix; Female; Fluids; Fluorescein Angiography; Humans; Intravitreal Injections; Macular degeneration; Macular Degeneration - complications; Male; Medical imaging; Morphology; Ophthalmology; Physiology; Prospective Studies; Retrospective Studies; Tomography, Optical Coherence; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - antagonists & inhibitors
• ISSN: 0002-9394; 1879-1891
• DOI: 10.1016/j.ajo.2015.04.012

Purpose To investigate the vascular appearance of choroidal neovascularization (CNV) treated with recurrent intravitreous anti–vascular endothelial growth factor (VEGF) injections, which have been proposed to cause transient vascular normalization along with decreased vascularity and leakage. Design Retrospective case series with perspective on the topic. Methods Patients with treated CNV secondary to age-related macular degeneration from a community-based retinal referral practice were evaluated with optical coherence tomography angiography employing split-spectrum amplitude decorrelation. The choroidal neovascular morphology of the 17 eyes of 14 consecutive patients was described. Results The mean age of the patients, 8 men and 6 women, was 78.4 (standard deviation ± 9.3) years. The mean greatest linear dimension of the lesion was 3600 μm. The mean number of anti-VEGF injections was 47 (±21). The vascular diameter of the vessels in the CNV appeared large even in small lesions, with feeder vessels approaching the size of the major arcade vessels of the retina. The vessels had few branch points and many vascular anastomotic connections among larger vessels. There was a paucity of capillaries visualized within the lesions. Conclusions The findings of this study do not support the hypothesis of vascular normalization in eyes receiving recurrent periodic antiangiogenic treatment. The observed “abnormalization” of the vessels may be explained by periodic pruning of angiogenic vascular sprouts by VEGF withdrawal in the face of unimpeded arteriogenesis. As the eye is a readily accessible VEGF laboratory, features expressed therein may also apply to neovascularization elsewhere in the body, such as in tumors.