Effects on choroidal neovascularization after anti-VEGF upload using intravitreal ranibizumab, as determined by spectral domain-optical coherence tomography

Purpose. It is unclear whether anti-VEGF monotherapy in agerelated macular degeneration (AMD) achieves morphologic CNV regression or only stops further CNV growth. In this study, spectral domain-optical coherence tomography (SDOCT) was used to image CNV structure before and after anti- VEGF treatment. Methods. Out of 107 consecutive patients, a prospective CNV evaluation was possible in 78 of them. Newly diagnosed CNV (classic CNV: n = 16; occult CNV: n = 54; minimal classic CNV: n = 8) due to AMD was imaged before and 4 weeks after anti-VEGF upload in three intravitreal injections of ranibizumab. Qualitative (structural changes) and quantitative measurements (diameter and thickness) of the CNV were obtained from the OCT images. Results. Classic CNV components were observed above the RPE/photoreceptor complex, whereas occult CNVs stayed below. Of all postoperative OCTs, 59% revealed complete dry retinal structures, 27% showed reduced edema, and 14% showed edema remaining unchanged. Mean macular thickness decreased significantly from 427 to 303 μm (P = 0.000). Qualitatively, overall CNV architecture appeared to be unchanged in 78%, was reduced in thickness in 18%, and became larger in 4%. Quantitatively, in all CNV subtypes, the diameter of the CNV lesions (preoperative, 2813 μm; postoperative, 2804 μm) did not change after treatment (classic CNV: P = 0.390; occult CNV: P = 0.405, minimal classic CNV: P = 0.092) independent of postoperative retinal edema. The overall thickness of the lesion, however, was reduced from 205 to 175 μm (P = 0.000). Thickness reduction was significantly enhanced especially in CNV with classic components (n = 24; 252 to 197 μm; P = 0.000; reduction, 22%), whereas reduction was smaller but also significant in occult CNV (183 to 164 μm; P = 0.003; reduction, 10%). Conclusions. With SD-OCT, CNV size can be two-dimensionally determined and followed up after intravitreal anti-VEGF treatment. In only 4% of CNV was enlargement observed, whereas in 78%, CNV architecture appeared qualitatively unchanged, independent of retinal edema. Quantitative measurements underlined stable CNV diameters for all subtypes but revealed significant reduction of thickness especially for classic CNV components. In this series, ranibizumab monotherapy was able to morphologically stop further CNV growth but, in most patients, did not lead to a major regression of CNV, especially of its occult components.