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Peripheral Vascular Endothelial Dysfunction in Central Serous Chorioretinopathy.
Nan-Kai Wang1,2, Yun Fu2,3, Jung-Pan Wang4,5
1Department of Ophthalmology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan, Taiwan.
Investigative Ophthalmology & Visual Science
|September 7, 2017
Summary
Patients with central serous chorioretinopathy (CSC) exhibit impaired flow-mediated vasodilation (FMD), indicating peripheral endothelial dysfunction. This finding suggests a systemic vascular component in CSC pathophysiology.
Area of Science:
- Ophthalmology
- Vascular Biology
- Endocrinology
Background:
- Central serous chorioretinopathy (CSC) is a condition affecting vision, primarily in middle-aged men.
- The underlying pathophysiology of CSC is not fully understood, with potential links to vascular and systemic factors.
- Previous research has not extensively investigated peripheral vascular endothelial function in CSC patients.
Purpose of the Study:
- To investigate the pathophysiology of central serous chorioretinopathy (CSC).
- To compare peripheral vascular endothelium function between patients with CSC and healthy control subjects.
- To determine if endothelial dysfunction is associated with CSC.
Main Methods:
- The study included 34 patients with CSC and 34 age- and sex-matched healthy controls.
- Endothelium-dependent flow-mediated vasodilation (FMD) and endothelium-independent nitroglycerine-mediated vasodilation (NMD) were measured using brachial artery ultrasonography.
- Serum biochemical markers including glucose, lipids, and hs-CRP were analyzed.
Main Results:
- No significant differences were found in age or serum biochemical data between CSC patients and controls.
- Flow-mediated vasodilation (FMD) was significantly impaired in patients with CSC compared to controls (P < 0.001).
- Nitroglycerine-mediated vasodilation (NMD) showed no significant difference between the groups (P = 0.950).
Conclusions:
- This study provides evidence of peripheral endothelial dysfunction in patients with CSC.
- Impaired FMD suggests a compromised endothelium-dependent vascular response in individuals with CSC.
- The findings highlight a potential systemic vascular contribution to the pathophysiology of CSC.

