Treatment of polypoidal choroidal vasculopathy in the real world and its underlying mechanisms

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Aims/Purpose: To evaluate the efficacy of combined therapy (verteporfin PDT plus anti‐VEGF) vs. anti‐VEGF monotherapy in symptomatic macular polypoidal choroidal vasculopathy (PCV) and its underlying therapeutic mechanisms.Methods: In this retrospective indocyanine green angiography (ICG)–proved PCV study, 21 Chinese (mean age: 67.50 ± 2.22 years; 17 males; 4 females; 11 left eyes) were treated randomized to mainly verteporfin PDT (standard fluence) + anti‐VEGF, or anti‐VEGF monotherapy. Patients were followed monthly by 3D OCT and re‐treated if signs/symptoms (e.g. cystoid macular edema/deteriorated best corrected vision, BCVA) recurred or persisted. Patients were evaluated with ICG to observe the regression of polyps. Change in BCVA/central retinal thickness, CRT, and safety were also included.Results: The mean follow‐up period (37.04 ± 7.74 months) showed that verteporfin PDT combined with antibodies (bevacizumab, ranibizumab or aflibercept) was compared to anti‐VEGF monotherapy in reducing the CRT (151.75 ± 40.37μm vs. 151.00 ± 58.83); BCVA changes (LogMAR) were ‐0.01 ± 0.21 (verteporfin PDT+antibodies) vs. 0.08 ± 0.09 (anti‐VEGF monotherapy). The mean injection numbers are 1.1# PDT+2# anti‐VEGF agents for combined therapy; 4.6 ± 1.2 anti‐VEGF agents for monotherapy. Three patients of PCV (30%) were recurrent and averaged 18.50 ± 9.26 months. Incomplete remission of polyps/BVN were observed in all eyes. There were no new safety issues with defined therapies. The PCV/nvAMD (control) levels of PLGF, VEGF, HIF1α and Wnt were 3.60 ± 1.48 (n = 8)/32.45 ± 10.53 (n = 28), 105.52 ± 16.15 (n = 8)/235.38 ± 42.13 (n = 27), 2.78 ± 1.40 (n = 3)/2.27 ± 0.43 (n = 63) and 2.13 ± 1.22 (n = 5)/2.40 ± 0.34 (n = 20). As compared to nvAMD, those concentrations of PLGF and VEGF in PCV were much lower.Conclusions: Verteporfin PDT plus antibodies was compared to anti‐VEGF monotherapy in achieving less number of visits/injections in this study in symptomatic macular PCV. However, BCVA was only stable (‐0.01 ± 0.21) but not improved, which was not correlating to the anatomic improvement. All treatments were well tolerated over the around 2‐year follow‐up period. As shown by various biomarkers, PCV should be a variant of nvAMD. It might therefore explain dissimilarity in response to anti‐VEGF and/or PDT treatment.