No abstract

We evaluated the efficacy and safety of loading phase treatment with intravitreal brolucizumab for neovascular age-related macular degeneration (nAMD) with type 1 choroidal neovascularization (CNV). We analyzed consecutive 42 eyes of 40 patients with treatment-naïve nAMD associated with type 1 CNV. Three monthly injections of brolucizumab were completed in 36 eyes (85.7%). In those cases, best-corrected visual acuity (BCVA) was 0.24 ± 0.27 at baseline and improved significantly to 0.12 ± 0.23 after 3 months (P < 0.001). Central macular thickness was 301 ± 110 µm at baseline and decreased significantly to 160 ± 49 µm after 3 months (P < 0.001). Dry macula was achieved in 34 eyes (94.4%) after the loading phase. Central choroidal thickness was 264 ± 89 µm at baseline and decreased significantly to 223 ± 81 µm after 3 months (P < 0.001). Indocyanine green angiography after the loading phase revealed complete regression of polypoidal lesions in 15 of the 19 eyes (78.9%) with polypoidal lesions. Non-infectious intraocular inflammation (IOI) was observed in 8 of 42 eyes (19.0%) during the loading phase, while showing amelioration in response to combination therapy with topical and subtenon injection of steroids. In these eyes, BCVA after 3 months had not deteriorated as compared to that at baseline. These results indicate that loading phase treatment with intravitreal brolucizumab might be effective for improving visual acuity and reducing exudative changes in eyes with nAMD associated with type 1 CNV. Moreover, polypoidal lesions appear to frequently regress after this treatment. However, we must monitor patients carefully for brolucizumab-related IOI, and administer steroid therapy promptly.

We evaluated 1-year outcomes of loading phase treatment followed by maintenance treatment using a treat-and-extend (TAE) regimen with intravitreal brolucizumab for neovascular age-related macular degeneration (nAMD) associated with type 1 macular neovascularization (MNV). We analyzed 68 eyes of 65 consecutive patients with treatment-naïve nAMD associated with type 1 MNV. Forty-five eyes (66.2%) completed the 1-year treatment with intravitreal brolucizumab. In those cases, best-corrected visual acuity (BCVA) showed significant improvement, while there were significant reductions in foveal thickness and central choroidal thickness, after the initial brolucizumab injection, which were maintained until the last visit. The average total number of injections over 1 year was 6.4 ± 0.6. The average intended injection interval at the last visit was 14.0 ± 2.9 weeks. Moreover, 17of 23 eyes (73.9%) with polypoidal lesions showed complete regression of these lesions after the loading phase treatment. Although intraocular inflammation (IOI) was observed in 15 of 68 eyes (22.1%) within 1 year, amelioration in response to combination therapy with topical and subtenon injection of steroids, without visual decline, was obtained. These results indicate that loading phase treatment followed by the TAE regimen with intravitreal brolucizumab might improve BCVA and ameliorate exudative changes in eyes with treatment-naïve nAMD associated with type 1 MNV. Moreover, intravitreal brolucizumab can potentially reduce the treatment burden of nAMD. Prompt steroid therapy might be efficacious for ameliorating brolucizumab-related IOI without visual decline.

Pachychoroid spectrum diseases have attracted increasing attention, though their pathophysiology has yet to be fully elucidated. In this study, we assessed the vascular diameters of vortex veins in pachychoroid spectrum diseases such as central serous chorioretinopathy (CSC), pachychoroid neovasculopathy without polypoidal lesions (PNV), and pachychoroid neovasculopathy with polypoidal lesions (polypoidal choroidal vasculopathy: PCV). In a retrospective case series of 94 eyes with CSC, 60 eyes with PNV and 57 with PCV, we binarized en face optical coherence tomography (OCT) images of choroidal vortex veins and analyzed the mean diameter of vortex veins. The presence of anastomosis between the superior and inferior vortex veins and central choroidal thickness (CCT) were also evaluated using OCT images. CSC showed significantly larger mean diameter of vortex veins than PCV (P < 0.05). Anastomosis between superior and inferior vortex veins was observed in over 90% of eyes with each pachychoroid spectrum disease. The patients with CSC were the youngest, followed by PNV patients, and then patients with PCV. The largest CCT values were observed in CSC eyes, followed by PNV eyes, and then PCV eyes. CCT correlated with the mean diameter of vortex veins (rs = 0.51, P < 0.01). These findings suggest that congestion of vortex veins might show gradual amelioration corresponding to the development of anastomosis between the superior and inferior vortex veins during the course of progression of pachychoroid spectrum diseases. Moreover, the mean diameter of vortex veins can be used as a parameter indicating choroidal congestion.

We evaluated choroidal congestion using multimodal imaging in pachychoroid neovasculopathy (PNV). In a retrospective case series of 100 eyes of 99 treatment-naïve PNV patients, their clinical records were reviewed and the corresponding multimodal imaging studies were analyzed. We assessed areas of choriocapillaris filling delay which overlapped with dilated outer choroidal vessels, choroidal neovascularization (CNV), and retinal pigment epithelium (RPE) atrophy. The study subjects were 78 men (78.8%) and 21 women (21.2%). The mean patient age was 67.5 ± 10.5 years. On indocyanine green angiography, all eyes showed choriocapillaris filling delay in the early phase. Dilated outer choroidal vessels were demonstrated in all eyes by en face optical coherence tomography. The areas of choriocapillaris filling delay overlapped extensively with that of dilated outer choroidal vessels. All eyes showed CNV localized within the sites of choriocapillaris filling delay. RPE atrophy was noted in 71 eyes (71.0%), and 68 of these (95.8%) had RPE atrophy within the areas showing choriocapillaris filling delay. These findings indicate that chronic choriocapillaris ischemia secondary to vortex vein congestion may lead to CNV development as well as RPE atrophy in eyes with PNV.