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Macular choroidal blood flow velocity decreases with regression of acute central serous chorioretinopathy
  1. Michiyuki Saito1,
  2. Wataru Saito1,2,
  3. Yuki Hashimoto1,
  4. Chikako Yoshizawa1,
  5. Akio Fujiya1,
  6. Kousuke Noda1,2,
  7. Susumu Ishida1,2
  1. 1Department of Ophthalmology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  2. 2Department of Ocular Circulation and Metabolism, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  1. Correspondence to: Dr Wataru Saito, Department of Ocular Circulation and Metabolism, Hokkaido University Graduate School of Medicine, Nishi 7, Kita 15, Kita-ku, Sapporo 060-8638, Japan; wsaito{at}med.hokudai.ac.jp

Abstract

Aim To quantitatively evaluate the time course of macular choroidal blood flow velocity in acute central serous chorioretinopathy (CSC).

Methods This retrospective observational case series included 21 eyes of 20 patients (17 men, 3 women; mean age, 53.0 years) with treatment-naïve acute CSC. Laser speckle flowgraphy was performed to calculate macular mean blur rate (MBR), an indicator of relative blood flow velocity at the first visit, 3 and 6 months thereafter. Changes in average MBR values were compared with visual improvement at 6 months.

Results Subretinal fluid completely resolved in all eyes within 6 months, while best-corrected visual acuity (BCVA) significantly improved at 6 months compared to the initial BCVA. During the follow-up period, the average MBR significantly decreased to 92.8% and 82.3% at 3 and 6 months, respectively, against baseline (100%). Importantly, there was a negative correlation between the BCVA recovery and the MBR decrease, showing the possible association of MBR increase with poor visual prognosis. Multiple regression analysis demonstrated no significant correlation between MBR and ocular perfusion pressure.

Conclusions These results indicate that macular choroidal blood flow velocity decreases concurrently with regression of CSC, suggesting a validity of choroidal blood flow elevation in the pathogenesis of acute CSC.

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