May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Microvascular Dysregulation in Central Serous Chorioretinopathy
Author Affiliations & Notes
  • C. Pruente
    Eye Clinic, University of Basel, Basel, Switzerland
  • T. Haufschild
    Eye Clinic, University of Basel, Basel, Switzerland
  • B. Schroeder
    Eye Clinic, University of Basel, Basel, Switzerland
  • J. Flammer
    Eye Clinic, University of Basel, Basel, Switzerland
  • Footnotes
    Commercial Relationships  C. Pruente, None; T. Haufschild, None; B. Schroeder, None; J. Flammer, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4308. doi:
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      C. Pruente, T. Haufschild, B. Schroeder, J. Flammer; Microvascular Dysregulation in Central Serous Chorioretinopathy . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4308.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Abnormalities in choroidal perfusion have been hypothesized to be causative factors in central serous chorioretinopathy (CSC). Recent results suggest that capillary and venous congestion in one or more choroidal lobules, probably caused by microvascular dysregulation, might be the reason for the choroidal hyperpermeability found in eyes with CSC. The aim of this study was to investigate whether CSC-patients have pathologic Endothelin-1 (ET-1) plasma levels which could explain some of the changes in the choroidal microcirculation in these patients. Methods: In 14 consecutive patients with acute CSC (mean age 42.0±1.9 yrs) and 14 age- and sexmatched normals (mean age 42.2±1.8 yrs) ET-1 plasma levels were determined by specific radioimmunoassay after a 30 minutes rest in lying position and microscopic capillaroscopy was performed at the nailfold. All CSC-patients had acute visual disturbances, localized neurosensory detachment and typical angiographic changes at the time of first ET-1 determination. In all patients the examinations were repeated after recovery 3 to 6 month later. All values are expressed as mean ± SEM, statistical evaluation was done with a independent sample t-test (2-tailed). Results: Plasma ET-1 levels were markedly and significantly (p<0.001) elevated in patients with CSC (2.76±0.17; min: 1.94, max: 4.37) compared to the normal group (1.50±0.10; min: 0.68, max: 2.13). A flow-stop after cold provocation in the nailfold capillaries was found in 93% of the CSC patients and 35% of controls. After recovery ET-1 levels in patients were still increased (2.08±0.16; min: 1.68, max: 2.64) with a flow-stop in nailfold capillaries in 71% of the patients. Conclusions: These findings show that plasma ET-1 levels are significantly increased in patients with CSC. Since ET-1 is a potent vasoactive substance in the arterial and venous parts of the microcirculation these results could explain the changes in the choroidal lobular blood-flow demonstrated in CSC, providing a further hint for the possible involvement of microvascular dysregulation in the pathogenesis of CSC. Furthermore, microvasculatory dysregulation in CSC probably is not limited to the choroid, but also involves systemic circulation.

Keywords: choroid • blood supply • retinal pigment epithelium 

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