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      Release of experimental retinal vein occlusions by direct intraluminal injection of ocriplasmin

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          Abstract

          Purpose

          Retinal vein occlusions (RVO) are a major cause of vision loss in people aged 50 years and older. Current therapeutic options limit the consequences of RVO but do not eliminate the cause. Cannulation of the involved vessel and removal of the clot may provide a more permanent solution with a less demanding follow-up. However, cannulation of smaller retinal veins remains challenging. This paper explores the use of ocriplasmin (recombinant plasmin without its kringles) to clear RVO, using a robotic micromanipulator.

          Methods

          Branch RVO were induced in a porcine model with rose bengal followed by 532 nm endolaser to the superior venous branch of the optic nerve. The vein was cannulated proximal to the occlusion or beyond the first branching vessel from the obstruction. The vein was infused with a physiologic citric acid buffer solution (CAM) or CAM/ocriplasmin. The time of cannulation, number of attempts, and the ability to release the thrombus were recorded.

          Results

          Cannulation and infusion was possible in all the cases. The use of a micromanipulator allowed for a consistent cannulation of the retinal vein and positional stability allowed the vein to remain cannulated for up to 20 min. In none of the attempts (5/5) with CAM did the thrombus dissolve, despite repeat infusion/relaxation cycles. In 7/7 injections of CAM/ocriplasmin near to the point of obstruction, the clot started to dissolve within a few minutes of injection. An infusion, attempted beyond the first venous branch point proximal to the clot, was unsuccessful in 2/3 attempts.

          Conclusions

          Ocriplasmin is effective in resolving RVO if injected close to the site of occlusion with the use of a micromanipulator.

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          Most cited references 14

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          Branch Retinal Vein Occlusion: Pathogenesis, Visual Prognosis, and Treatment Modalities

          In branch retinal vein occlusion (BRVO), abnormal arteriovenous crossing with vein compression, degenerative changes of the vessel wall and abnormal hematological factors constitute the primary mechanism of vessel occlusion. In general, BRVO has a good prognosis: 50–60% of eyes are reported to have a final visual acuity (VA) of 20/40 or better even without treatment. One important prognostic factor for final VA appears to be the initial VA. Grid laser photocoagulation is an established treatment for macular edema in a particular group of patients with BRVO, while promising results for this condition are shown by intravitreal application of steroids or new vascular endothelial growth factor inhibitors. Vitrectomy with or without arteriovenous sheathotomy combined with removal of the internal limiting membrane may improve vision in eyes with macular edema which are unresponsive to or ineligible for laser treatment.
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            Histopathologic study of nine branch retinal vein occlusions.

            Occlusions of nine branch retinal veins in eight eyes of seven patients were studied histopathologically by serial sections through the affected areas. Intravitreal neovascularization from the disc, retina, or both was noted in four eyes. Two additional eyes had intraretinal neovascularization (intraretinal microvascular abnormalities). Cystoid macular edema was present in five eyes. A fresh or recanalized thrombus was noted at the site of vein occlusion in all eyes. Inner ischemic atrophy of the retina was found distal to the area of occlusion in six of the nine affected quadrants of the eight eyes. Although the corresponding branch retinal arteries showed varying degrees of sclerosis (severe, three eyes; moderate, five eyes; and minimal, one eye), no definite thrombus was observed in any of them.
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              The plasmin-antiplasmin system: structural and functional aspects.

              The plasmin-antiplasmin system plays a key role in blood coagulation and fibrinolysis. Plasmin and α(2)-antiplasmin are primarily responsible for a controlled and regulated dissolution of the fibrin polymers into soluble fragments. However, besides plasmin(ogen) and α(2)-antiplasmin the system contains a series of specific activators and inhibitors. The main physiological activators of plasminogen are tissue-type plasminogen activator, which is mainly involved in the dissolution of the fibrin polymers by plasmin, and urokinase-type plasminogen activator, which is primarily responsible for the generation of plasmin activity in the intercellular space. Both activators are multidomain serine proteases. Besides the main physiological inhibitor α(2)-antiplasmin, the plasmin-antiplasmin system is also regulated by the general protease inhibitor α(2)-macroglobulin, a member of the protease inhibitor I39 family. The activity of the plasminogen activators is primarily regulated by the plasminogen activator inhibitors 1 and 2, members of the serine protease inhibitor superfamily.
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                Author and article information

                Journal
                Br J Ophthalmol
                Br J Ophthalmol
                bjophthalmol
                bjo
                The British Journal of Ophthalmology
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                0007-1161
                1468-2079
                December 2016
                28 September 2016
                : 100
                : 12
                : 1742-1746
                Affiliations
                [1 ]MicroInvasive Ocular Surgery Center (MIOS sa) , Lausanne, Switzerland
                [2 ]Preceyes nv , Eindhoven, The Netherlands
                [3 ]Crystapharm bvba , Lubbeek, Belgium
                [4 ]Thrombogenics nv , Leuven, Belgium
                Author notes
                [Correspondence to ] Professor Marc D de Smet, MicroInvasive Ocular Surgery Center (MIOS sa) , Av du Léman 32, Lausanne 1005, Switzerland; mddesmet1@ 123456mac.com
                Article
                bjophthalmol-2016-309190
                10.1136/bjophthalmol-2016-309190
                5256413
                27688592
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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