Frontiers in medicine · 2021
Choriocapillaris Ischemia at the Leakage Point of Patients With Acute Central Serous Chorioretinopathy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Zuofen, Xin Zhaoting, Yang Jun, Lu Huawen, Wang Haiying, Zhu Lin
Аннотация
Purpose: We aimed to determine ischemia of the choriocapillaris at the leakage point of patients with acute central serous chorioretinopathy (CSC) by optical coherence tomographic angiography (OCTA). Methods: A retrospective study of 38 eyes of 38 acute CSC patients with spontaneous complete resolution of subretinal fluid (SRF) was conducted and patients were followed for 3 months. Fundus fluorescein angiography (FFA) and indocyanine green angiography (ICGA) were performed at baseline. Best corrected visual acuity (BCVA) and OCTA were collected at baseline and at follow-up visits. An age- and refractive error-matched control group consisted of 40 eyes of 40 healthy people. Results: The BCVA of patients significantly improved at 1 and 3 months. At baseline, all eyes showed a decreased choriocapillaris vessel density. The mean vessel density of superficial choroid (VDSC) at the leakage point area was 44.18 ± 9.27, which increased to 54.31 ± 9.70 at 1 month (p < 0.001) and to 55.19 ± 6.46 at 3 months (p < 0.001). The mean vessel density ratio was 0.90 ± 0.16 at baseline, which increased to 0.96 ± 0.15 at 1 month (p = 0.037) and to 0.97 ± 0.08 at 3 months (p = 0.016). The highest VDSC of patients was lower than that of normal control (p < 0.001). Conclusions: The VDSC at the leakage point of acute CSC patients was significantly thinner and regularly increased with the recovery process, which suggested that ischemia might be one of the initiating factors in the pathogenesis of acute CSC.