Choroidal vascularity changes in idiopathic central serous chorioretinopathy after half-fluence photodynamic therapy

This study evaluated changes in choroidal vascularity after half-fluence photodynamic therapy (HF-PDT) in patients with central serous chorioretinopathy (CSC) using swept-source optical coherence tomography (SS-OCT) en face imaging.

This retrospective comparative case series included 50 eyes of 25 patients with unilateral CSC who underwent HF-PDT and 50 age-and sex-matched normal healthy control eyes. En face SS-OCT images of the choriocapillaris, Sattler's layer, and Haller's layer were converted into binary images. The vascular proportions were defined as the percentage of the area of vascular lumen against the area of the 3.0-mm-diameter circular area. The main outcome measures were the vascular proportions before HF-PDT and at 6 weeks, 6 months, and 12 months after HF-PDT.

At baseline, the vascular proportions in the CSC eyes were significantly greater than those in the control eyes in all layers (choriocapillaris: 51.8% ± 15.5% vs. 41.3 ± 18.7%, P = 0.018; Sattler's: 58.6% ± 13.4% vs. 49.7% ± 15.7%, P = 0.017; Haller's: 65.3% ± 15.3% vs. 53.0% ± 13.4%, P = 0.001). In the CSC eyes, the vascular proportion in the choriocapillaris significantly decreased at 6 weeks (36.6% ± 16.9%, P < 0.001), 6 months (34.0% ± 12.3%, P < 0.001), and 12 months (34.8% ± 17.6%, P < 0.001) after HF-PDT compared with baseline. The vascular proportions in Sattler's and Haller's layers did not show a significant decrease at 6 weeks (Sattler's: 49.7% ± 17.3%, P = 0.052 and Haller's: 58.3% ± 12.9%, P = 0.558) but decreased significantly at 6 months (Sattler's: 48.9% ± 12.4%, P < 0.001 and Haller's: 57.7% ± 15.7%, P = 0.027) and 12 months after HF-PDT from the baseline values (Sattler's: 45.8% ± 10.4%, P < 0.001 and Haller's: 56.8% ± 15.7%, P < 0.001).

After HF-PDT, the choriocapillaris showed the earliest decrease in vascular proportion of en face images, Sattler's and Haller's layers showed later decreases. The temporal differences in the response of each layer may reflect the pathophysiology of CSC and the therapeutic mechanism of HF-PDT.