scholarly journals Multimodal Imaging of Microvascular Abnormalities in Retinal Vein Occlusion

2021 ◽  
Vol 10 (3) ◽  
pp. 405
Author(s):  
Yoshio Hirano ◽  
Norihiro Suzuki ◽  
Taneto Tomiyasu ◽  
Ryo Kurobe ◽  
Yusuke Yasuda ◽  
...  

The technologies of ocular imaging modalities such as optical coherence tomography (OCT) and OCT angiography (OCTA) have progressed remarkably. Of these in vivo imaging modalities, recently advanced OCT technology provides high-resolution images, e.g., histologic imaging, enabling anatomical analysis of each retinal layer, including the photoreceptor layers. Recently developed OCTA also visualizes the vascular networks three-dimensionally, which provides better understanding of the retinal deep capillary layer. In addition, ex vivo analysis using autologous aqueous or vitreous humor shows that inflammatory cytokine levels including vascular endothelial growth factor (VEGF) are elevated and correlated with the severity of macular edema (ME) in eyes with retinal vein occlusion (RVO). Furthermore, a combination of multiple modalities enables deeper understanding of the pathology. Regarding therapy, intravitreal injection of anti-VEGF drugs provides rapid resolution of ME and much better visual improvements than conventional treatments in eyes with RVO. Thus, the technologies of examination and treatment for managing eyes with RVO have progressed rapidly. In this paper, we review the multimodal imaging and therapeutic strategies for eyes with RVO with the hope that it provides better understanding of the pathology and leads to the development of new therapies.

2018 ◽  
Vol 3 (1) ◽  
pp. 45-48
Author(s):  
Omar Moinuddin ◽  
Matthew G. J. Trese ◽  
Cagri G. Besirli

Isolated retinal racemose hemangioma is a rare disorder that may lead to vision loss due to late complications, most commonly central retinal vein occlusion (CRVO). We describe the longitudinal clinical course using multimodal imaging of a 13-year-old girl diagnosed with CRVO and macular edema in the setting of isolated retinal racemose hemangioma treated with intravitreal antivascular endothelial growth factor.


Author(s):  
Teruyo Kida ◽  
Josef Flammer ◽  
Katarzyna Konieczka ◽  
Tsunehiko Ikeda

Abstract Purpose The pathomechanism leading to retinal vein occlusion (RVO) is unclear. Mechanical compression, thrombosis, and functional contractions of veins are discussed as the reasons for the increased resistance of venous outflow. We evaluated changes in the retinal venous pressure (RVP) following intravitreal injection of anti-vascular endothelial growth factor (VEGF) agent to determine the effect on RVO-related macular edema. Methods Twenty-six patients with RVO-related macular edema (16 branch RVOs [BRVOs] and 10 central RVOs [CRVOs], age 72.5 ± 8.8 years) who visited our hospital were included in this prospective study. Visual acuity (VA), intraocular pressure (IOP), central retinal thickness (CRT) determined by macular optical coherence tomography, and RVP measured using an ophthalmodynamometer were obtained before intravitreal injection of ranibizumab (IVR) and 1 month later. Results Comparison of the BRVOs and CRVOs showed that VA was significantly improved by a single injection in BRVOs (P < 0.0001; P = 0.1087 for CRVOs), but CRT and RVP were significantly decreased without significant difference in IOP after the treatment in both groups (P < 0.0001). Conclusion The anti-VEGF treatment resulted in a significant decrease in the RVP, but the RVP remained significantly higher than the IOP. An increased RVP plays a decisive role in the formation of macula edema, and reducing it is desirable.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Louisa Mezache ◽  
Heather Struckman ◽  
Anna Phillips ◽  
Stephen Baine ◽  
Amara Greer-short ◽  
...  

Atrial fibrillation (AF), the most common arrhythmia, is associated with inflammation and vascular dysfunction. AF patients have elevated levels of vascular endothelial growth factor (VEGF; 90-580 pg/ml), which promotes vascular leak and edema. We have previously identified edema-induced disruption of sodium channel (Na V 1.5) -rich intercalated disk (ID) nanodomains as a novel arrhythmia mechanism. We hypothesized that (i) elevated VEGF levels promote AF by disrupting ID nanodomains, and slowing atrial conduction, and (ii) protection of the vascular barrier can prevent these arrhythmias. Clinically-relevant VEGF levels (500 pg/ml, 60 minutes) increased FITC-dextran extravasation (99.3% vs. 24.3% in vehicle controls) in WT mouse hearts, consistent with increased vascular leak. Electron microscopy revealed ID nanodomain swelling, near both gap junctions (perinexi; 64±9nm vs 17±1nm) and mechanical junctions (63±4nm vs 27±2nm) in VEGF-treated hearts relative to controls. Super-resolution STORM microscopy revealed Na V 1.5 enrichment at perinexi (9±2 fold) and N-cadherin-rich sites (7±1 fold) relative to non-junctional ID sites in control hearts. VEGF reduced Na V 1.5 enrichment at both sites (6±1 and 4±1 fold, respectively), consistent with Na V 1.5 translocation from ID nanodomains. Atrial conduction, assessed by optical mapping, was slowed by VEGF (10±0.4 cm/s vs 21.3±1.3 cm/s at baseline). VEGF increased atrial arrhythmia burden both ex vivo (80% vs 0% in vehicle controls) and in vivo (70% vs 20% in vehicle controls). Next, we tested two strategies shown to prevent vascular barrier breakdown. Blocking connexin43 hemichannels (αCT11 peptide) decreased both incidence (40%) and duration (1.45±3.42s) of VEGF-induced arrhythmias. Likewise, blocking pannexin1 channels (Panx1-IL2 peptide) shortened VEGF-induced arrhythmias (2.48±0.83s). Mefloquine and spironolactone, which are small molecules that respectively inhibit Cx43 hemichannels and pannexin channels, were also found to effectively prevent VEGF-induced atrial arrhythmias. These results highlight VEGF-induced vascular leak as a novel mechanism for AF, and suggest vascular barrier protection as an anti-arrhythmic strategy.


2021 ◽  
Author(s):  
Emma L Brown ◽  
Thierry L Lefebvre ◽  
Paul W Sweeney ◽  
Bernadette Stolz ◽  
Janek Gröhl ◽  
...  

Mesoscopic photoacoustic imaging (PAI) enables non-invasive visualisation of tumour vasculature and has the potential to assess prognosis and therapeutic response. Currently, evaluating vasculature using mesoscopic PAI involves visual or semi-quantitative 2D measurements, which fail to capture 3D vessel network complexity, and lack robust ground truths for assessment of segmentation accuracy. Here, we developed an in silico, phantom, in vivo, and ex vivo-validated end-to-end framework to quantify 3D vascular networks captured using mesoscopic PAI. We applied our framework to evaluate the capacity of rule-based and machine learning-based segmentation methods, with or without vesselness image filtering, to preserve blood volume and network structure by employing topological data analysis. We first assessed segmentation performance against ground truth data of in silico synthetic vasculatures and a photoacoustic string phantom. Our results indicate that learning-based segmentation best preserves vessel diameter and blood volume at depth, while rule-based segmentation with vesselness image filtering accurately preserved network structure in superficial vessels. Next, we applied our framework to breast cancer patient-derived xenografts (PDXs), with corresponding ex vivo immunohistochemistry. We demonstrated that the above segmentation methods can reliably delineate the vasculature of 2 breast PDX models from mesoscopic PA images. Our results underscore the importance of evaluating the choice of segmentation method when applying mesoscopic PAI as a tool to evaluate vascular networks in vivo.


Macular edema secondary to retinal vein occlusions is a significant complication affecting the vision. Medical treatment of retinal vein occlusions first started with intraocular steroid injections and then enriched with intraocular Anti-VEGF (Vascular Endothelial Growth Factor) injections. But till now the length and frequency of therapy have not been defined clearly. In this review, the use of bevacizumab in the treatment of branch retinal vein occlusion and macular edema will be summarized in light of the current literature.


2013 ◽  
Vol 7 (1) ◽  
pp. 11-17 ◽  
Author(s):  
MJ Koss ◽  
M Pfister ◽  
F Rothweiler ◽  
R Rejdak ◽  
R Ribeiro ◽  
...  

Purpose: To correlate inflammatory and proangiogenic key cytokines from undiluted vitreous of treatment-naïve central retinal vein occlusion (CRVO) patients with SD-OCT parameters. Methods: Thirty-five patients (age 71.1 years, 24 phakic, 30 nonischemic) underwent intravitreal combination therapy, including a single-site 23-gauge core vitrectomy. Twenty-eight samples from patients with idiopathic, non-uveitis floaterectomy served as controls. Interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor (VEGF-A) levels were correlated with the visual acuity (logMar), category of CRVO (ischemic or nonischemic) and morphologic parameters, such as central macular thickness-CMT, thickness of neurosensory retina-TNeuro, extent of serous retinal detachment-SRT and disintegrity of the IS/OS and others. Results: The mean IL-6 was 64.7pg/ml (SD ± 115.8), MCP-1 1015.7 ( ± 970.1), and VEGF-A 278.4 ( ± 512.8), which was significantly higher than the control IL-6 6.2 ± 3.4pg/ml (P=0.06), MCP-1 253.2 ± 73.5 (P<0.0000001) and VEGF-A 7.0 ± 4.9 (P<0.0006). All cytokines correlated highly with one another (correlation coefficient r=0.82 for IL-6 and MCP-1; r=0.68 for Il-6 and VEGF-A; r=0.64 for MCP-1 and VEGF-A). IL-6 correlated significantly with CMT, TRT, SRT, dIS/OS, and dELM. MCP-1 correlated significantly with SRT, dIS/OS, and dELM. VEGF-A correlated not with changes in SD-OCT, while it had a trend to be higher in the ischemic versus the nonischemic CRVO group (P=0.09). Conclusions: The inflammatory cytokines were more often correlated with morphologic changes assessed by SD-OCT, whereas VEGF-A did not correlate with CRVO-associated changes in SD-OCT. VEGF inhibition alone may not be sufficient in decreasing the inflammatory response in CRVO therapy.


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