Suppressed endothelin-1 by anti-VEGF therapy is important for patients with BRVO-related macular edema to improve their vision.

Teruyo Kida,Katarzyna Konieczka,Hidehiro Oku,Tsunehiko Ikeda,Seita Morishita,Josef Flammer,Masanori Fukumoto,Hiroyuki Suzuki

doi:10.1186/s13167-016-0066-2

Teruyo Kida, Katarzyna Konieczka + Show 6 more

Open Access

https://doi.org/10.1186/s13167-016-0066-2

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Abstract

BackgroundBranch retinal vein occlusion (BRVO) commonly occurs at the arteriovenous crossing in the unilateral eye, and cardiovascular diseases can be risk factors of BRVO. However, the pathomechanism leading to BRVO is not yet clear. In addition to mechanical compression, the vein might locally constrict due to an altered biochemical environment, such as an increase in the concentration of endothelin-1 (ET-1). We evaluated changes in ET-1 following injection of intravitreal bevacizumab (IVB), which is the anti-vascular endothelial growth factor (VEGF) agent with the longest serum half-life, to determine the effect on BRVO-related macular edema.MethodsTwenty consecutive patients with BRVO-related macular edema (10 males, 10 females; age range 56–83 years) who visited our hospital were included in this prospective study. Visual acuity (VA); central retinal thickness (CRT), determined by macular optical coherence tomography (OCT); and plasma ET-1 levels were obtained before IVB treatment and 1 month later.ResultsPatients had hypertension (80 %), dyslipidemia (50 %), diabetes mellitus (35 %), or collagen disease (5 %). Mean CRT was significantly decreased from 673.0 ± 327.8 to 388.2 ± 155.0 μm (P = 0.0007), and mean VA was significantly improved after IVB (P = 0.0239). Mean plasma ET-1 was significantly decreased from 1.272 ± 0.451 to 1.095 ± 0.316 pg/mL (P = 0.0238); however, the plasma ET-1 level was increased in all five patients who did not show improved VA after IVB.ConclusionsIn patients with BRVO-related macular edema, anti-VEGF therapy leads to an expected reduction in ET-1 levels; however, the ET-1 level was found to increase in some patients; this is clearly related to less improvement of VA after anti-VEGF therapy.Trial registrationUniversity hospital Medical Information Network (UMIN) Center UMIN000013236. Registered 10 October, 2012.

Highlights

Branch retinal vein occlusion (BRVO) commonly occurs at the arteriovenous crossing in the unilateral eye, and cardiovascular diseases can be risk factors of BRVO
We investigated whether an anti-vascular endothelial growth factor (VEGF) therapy could influence the concentration of ET-1 which had never been measured before and after anti-VEGF therapy and, if so, whether changes in the ET-1 levels are somehow related to the recovery of Visual acuity (VA) in patients with BRVO-related macular edema
We indicated that ET-1 is possibly involved in the pathogenesis of BRVO, and some BRVO patients whose VA was not improved after intravitreal bevacizumab (IVB) showed increased plasma ET-1 levels even though intraocular VEGF was suppressed by anti-VEGF therapy

Summary

Introduction

Branch retinal vein occlusion (BRVO) commonly occurs at the arteriovenous crossing in the unilateral eye, and cardiovascular diseases can be risk factors of BRVO. In addition to mechanical compression, the vein might locally constrict due to an altered biochemical environment, such as an increase in the concentration of endothelin-1 (ET-1). It has been reported that the retinal vein seems to run deep under the artery at the crossing in eyes with arterial overcrossing, and the venous lumen often appears to be preserved, even at the arteriovenous crossing, as observed by thin sectioning with optical coherence tomography (OCT) in patients with acute BRVO [4]. The occlusions seem to be induced by an interaction between local and systemic factors; on the one hand, BRVOs generally occur unilaterally, while on the other hand, retinal venous pressure is simultaneously increased in the clinically unaffected contralateral eye [5, 6]

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