The Effect of a Single Intravitreal Anti-VEGF Therapy on Optic Nerve Head Perfusion
Status:
Terminated
Trial end date:
2011-11-01
Target enrollment:
Participant gender:
Summary
Age related macula degeneration is one of the most common sight threatening diseases of the
elderly. The so called wet form of AMD is caused by choroidal neovascularisation (CNV) of
pathological vessels, which lead to leakage, bleeding and macular edema. Several lines of
evidence suggest that vascular endothelial growth factor (VEGF) plays a key role in the
induction CNV. Recent evidence indicates that overexpression of VEGF in the retinal pigment
epithelium may lead to the development of CNV in experimental models, and intravitreal
injection of a VEGF blocker prevents the development of experimental CNV. This hypothesis is
also supported by the promising effects of anti-VEGF treatment in patients with choroidal
neovascularisation. The substances currently in clinical use include ranibizumab (Lucentis®),
bevacizumab (Avastin®) and pegaptanib (Macugen®).
However, from a physiological point of view, VEGF also serves as a survival factor for
existing vessels and for neuronal cells. Moreover, it has been reported that VEGF induces
vasodilatation, most probably by an increased production of nitric oxide. Accordingly one may
hypothesize that anti-VEGF treatment is associated with ocular vasoconstriction with unknown
long term results. Thus, in the current study, the investigators set out to investigate
whether the ocular perfusion is affected by a single intravitreal anti-VEGF.