Early response to the treatment of choroidal neovascularization complicating central serous chorioretinopathy: a OCT-angiography study

Abstract

Purpose To analyze the quantitative and qualitative early changes of choroidal neovascularization (CNV) associated with chronic central serous chorioretinopathy (CSC) after treatment using optical coherence tomography-angiography (OCT-A). Methods Charts of consecutive patients with diagnosis of chronic CSC complicated by CNV were retrospectively reviewed. Included patients were divided in photodynamic therapy (PDT) or aflibercept group on the basis of the treatment received (half-fluence PDT or aflibercept 2.0 mg/0.05 ml intravitreal injection). Main outcome measures included the changes between baseline and 1-month follow-up in CNV vessel density (VD) and area on OCT-A images after thresholding and binarization. Results A total of 30 eyes of 26 Caucasian patients were included: 17 eyes of 15 patients in PDT group (mean age 53 ± 11 years) and 13 eyes of 11 patients in aflibercept group (mean age 58 ± 8 years [p = 0.196]). In both PDT and aflibercept groups, best-corrected visual acuity improved at 1 month, and central macular thickness and subretinal fluid significantly decreased. VD did not change after the treatment in both groups (p = 0.502 and p = 0.086) although CNV area decreased significantly (from 0.586 ± 0.449 mm 2 to 0.553 ± 0.453 mm 2 [0.041]) in the PDT group, and nonsignificantly (from 0.767 ± 0.466 mm 2 to 0.733 ± 0.472 mm 2 [p = 0.095]) in the aflibercept group. The same results were confirmed in the subanalysis of the 18 treatment-naïve eyes. Conclusions We demonstrated that, despite all patients showed a favorable clinical response, VD of CNVs complicating chronic CSC did not change after treatment. These findings support the idea that arteriogenesis is the main driving force of CNV in pachychoroid-related macular disorders.

Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy

“…This may indicate an imbalance between the levels of VEGF and other growth factors, but such a hypothesis requires further research. Nonetheless, our results are in line with the study by Spaide (2015) and Sacconi et al (2019). They hypothesized that CNV in CSC is due to proliferation of new vessels during arteriogenesis, which is characterized by dilation of the existing vascular channels and is independent of VEGF (unlike angiogenesis, which is highly VEGF dependent) (Schierling et al 2009; Wu et al 2010).…”

“…Bousquet et al (2018) revealed the prevalence of CNV in 35.6% of patients with chronic CSC, with flat irregular pigment epithelial detachment. Sacconi et al (2019) considered arteriogenesis to be the central driving force of CNV development in the course of CSC, because despite noting some clinical response after anti‐VEGF therapy, the density of CNV vessels did not change on OCT angiography. Downregulated plasma VEGF levels in CSC observed in our study may explain the unsatisfactory effect of intravitreal anti‐VEGF treatment in patients with CSC, which was reported in meta‐analyses (Chung et al 2013; Ji et al 2017).…”

Imbalance in the Levels of Angiogenic Factors in Patients with Acute and Chronic Central Serous Chorioretinopathy

“…The fact that chronic CSC can be associated with the presence of CNV [ 16 , 17 ] does not contradict the results of our study, which revealed lower plasma VEGF levels in CSC patients compared with the controls. This is in line with the studies by Spaide et al [ 36 ] and Sacconi et al [ 43 ]. They hypothesized that CNV in CSC occurs as a result of proliferation of new vessels during arteriogenesis, which is characterized by dilation of the existing vascular channels and is independent of VEGF (unlike angiogenesis, which is highly VEGF dependent) [ 44 ].…”

Current diagnosis and management strategies in pachychoroid spectrum of diseases (Review)

“…However, the effect of anti-VEGF agents on persistent subretinal fluid and macular edema secondary to CSC was not clearly demonstrated in two large trials (41,42). Authors such as Schworm et al (43) and Sacconi et al (44) concluded that intravitreal anti-VEGF therapy is useful both in fluid resorption and visual acuity gain, but the vessel density in the neovascular membrane does not change after treatment, thus supporting the theory that arteriogenesis is the main pathogenic mechanism in pachychoroid related CNV.…”