Fibrinolytic therapy in retinal vessel occlusion

1998 ◽  
Vol 95 (8) ◽  
pp. 568-575 ◽  
Author(s):  
Lars-Olof Hattenbach
Keyword(s):  
Retinal Vessel ◽  
Fibrinolytic Therapy ◽  
Vessel Occlusion ◽  
Retinal Vessel Occlusion

scholarly journals Ocular Phenotype of Mice with Impaired Fibrillin-1 Function on Hypercholesterolemic Apolipoprotein E-Deficient Background

2018 ◽  
Vol 1 (1) ◽  
pp. 75-79
Author(s):  
Emmi Kokki ◽  
Tommi Karttunen ◽  
Sanna Kettunen ◽  
Kati Kinnunen ◽  
Guido R.Y. De Meyer ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Marfan Syndrome ◽  
High Fat Diet ◽  
Elastic Fiber ◽  
Retinal Vessel ◽  
High Fat ◽  
Vessel Occlusion ◽  
Collagen Formation ◽  
Fibrillin 1 ◽  
Retinal Vessel Occlusion

Aim: Transgenic mice with an elastic fiber mutation (C1039G+/-) in the fibrillin-1 gene and apolipoprotein E deficiency express vulnerable atherosclerotic plaque formation in the aorta and coronary and carotid arteries. The fibrillin-1 gene mutation alone leads to impaired fibrillin-1 function common to Marfan syndrome. The aim was to study for the first time the potential effects of atherosclerosis and vulnerable plaques in mouse eye and spontaneous retinal vessel occlusions in these mice.Methods: Apolipoprotein E-deficient and fibrillin-1 mutated mice (ApoE-/-/Fbn1C1039G+/-) were used for the study. ApoE-/- littermates served as controls. Optical coherence tomography and fluorescein angiography were used to study the retina and retinal vessels before and after the 12-week high-fat diet. Series of staining were performed to study morphology, apoptosis, glial fibrillary acidic protein activation, collagen formation, inflammatory cell infiltration and drusen formation.Results: No pathological changes were found in hypercholesterolemic ApoE-/-/Fbn1C1039G+/- mice in imaging studies nor in the histological stainings. There was neither abnormality in the retinal morphology nor any detectable biomarkers.Conclusion: ApoE-/-/Fbn1C1039G+/- mice did not present the ocular signs of Marfan syndrome.12-week high-fat diet is not sufficient to induce retinal vessel occlusion on 20 to 23 weeks old mice. This indicates that the mechanistic background of retinal vessel occlusion is more complex.

Prevalence of Atrial Fibrillation in Patients with Retinal Vessel Occlusion and Its Association: A Systematic Review and Meta-Analysis

2019 ◽  
Vol 44 (12) ◽  
pp. 1337-1344 ◽  
Author(s):  
Jakrin Kewcharoen ◽  
Elysse S. Tom ◽  
Chonlanan Wiboonchutikula ◽  
Angkawipa Trongtorsak ◽  
Chutikarn Wittayalikit ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Systematic Review ◽  
Meta Analysis ◽  
Retinal Vessel ◽  
Vessel Occlusion ◽  
Retinal Vessel Occlusion

scholarly journals Ischemia-induced spreading depolarization in the retina

2016 ◽  
Vol 36 (9) ◽  
pp. 1579-1591 ◽  
Author(s):  
Anja I Srienc ◽  
Kyle R Biesecker ◽  
Angela M Shimoda ◽  
Joanna Kur ◽  
Eric A Newman
Keyword(s):  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Vision Loss ◽  
Nmda Antagonist ◽  
Retinal Vessel ◽  
Vessel Occlusion ◽  
Spreading Depolarization ◽  
Vein Occlusion ◽  
Retinal Vessel Occlusion

Cortical spreading depolarization is a metabolically costly phenomenon that affects the brain in both health and disease. Following severe stroke, subarachnoid hemorrhage, or traumatic brain injury, cortical spreading depolarization exacerbates tissue damage and enlarges infarct volumes. It is not known, however, whether spreading depolarization also occurs in the retina in vivo. We report now that spreading depolarization episodes are generated in the in vivo rat retina following retinal vessel occlusion produced by photothrombosis. The properties of retinal spreading depolarization are similar to those of cortical spreading depolarization. Retinal spreading depolarization waves propagate at a velocity of 3.0 ± 0.1 mm/min and are associated with a negative shift in direct current potential, a transient cessation of neuronal spiking, arteriole constriction, and a decrease in tissue O2 tension. The frequency of retinal spreading depolarization generation in vivo is reduced by administration of the NMDA antagonist MK-801 and the 5-HT(1D) agonist sumatriptan. Branch retinal vein occlusion is a leading cause of vision loss from vascular disease. Our results suggest that retinal spreading depolarization could contribute to retinal damage in acute retinal ischemia and demonstrate that pharmacological agents can reduce retinal spreading depolarization frequency after retinal vessel occlusion. Blocking retinal spreading depolarization generation may represent a therapeutic strategy for preserving vision in branch retinal vein occlusion patients.

scholarly journals Optic Disc Vascular Density in Normal-Tension Glaucoma Eyes with or without Branch Retinal Vessel Occlusion

2021 ◽  
Vol 10 (12) ◽  
pp. 2574
Author(s):  
Jiwon Baek ◽  
Soo Ji Jeon ◽  
Jin Ho Kim ◽  
Chan Kee Park ◽  
Hae-Young Lopilly Park
Keyword(s):  
Optic Disc ◽  
Retinal Vessel ◽  
Normal Tension Glaucoma ◽  
Large Vessel ◽  
Vascular Density ◽  
Vessel Occlusion ◽  
Swept Source ◽  
Opposite Order ◽  
Retinal Vessel Occlusion ◽  
Fellow Eyes

We analyzed the vascular densities (VDs) of the optic disc areas in eyes with normal-tension glaucoma (NTG) according to their branch retinal vessel occlusion (BRVO) status. The VDs of the optic discs and peripapillary areas of 68 NTG patients with BRVO (BRVO group; BRVO eyes and fellow eyes) and 37 patients with NTG alone (control eyes) were measured on angiographic images obtained via swept-source optical coherence tomography angiography. VDs were compared among groups and correlations were assessed. The VD of the optic disc large vessel was the highest in BRVO eyes, followed by the fellow eyes and controls (all P < 0.05). Conversely, small and medium vessel VD was in the opposite order (all P < 0.05). Large vessel VD was negatively correlated with small and medium vessel VD (r = −0.697, P < 0.001). Peripapillary VD was lower in the BRVO eyes than in the control and fellow eyes (P < 0.001 and P = 0.861, respectively). In conclusion, significant changes in the distribution of VDs for optic disc larger vessel and small and medium vessels were observed in both eyes of NTG patients with BRVO, compared to NTG patients without BRVO.

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