scholarly journals COVID-19 as a new risk factor for the development of acute vascular diseases of the optic nerve and retina

2021 ◽  
Vol 14 (2) ◽  
pp. 105-115
Author(s):  
Vadim A. Turgel ◽  
Vladimir A. Antonov ◽  
Svetlana N. Tultseva ◽  
Fedor E. Shadrichev ◽  
Niurguyana N. Grigorieva

The new coronavirus disease (COVID-19) is a viral respiratory infection accompanied by systemic endotheliitis. COVID-19 patients usually encounter changes related to hypercoagulability, hypofibrinolysis, and increased intravascular platelet aggregation. There is also a vascular wall thromboresistance decrease and impaired vasomotor function, which significantly increase the risk of thromboembolic complications. Currently, pathogenic aspects of the relationship between COVID-19 and vascular and inflammatory conditions of the optic nerve and retina are actively investigated. One of the triggers of impaired blood flow in ocular vessels may be a perfusion pressure decrease, observed in the acute period of the infectious process. This is related to both COVID-19 clinical course features and to resuscitation specificity as well. Secondary autoimmune inflammation is being considered as a mechanism of damage to the vascular wall in the post-infectious period. In this publication, possible pathogenic links of these diseases are considered for the first time in a specific context of the example of ischemic optic neuropathy associated with coronavirus infection.

2020 ◽  
Vol 25 (6) ◽  
pp. 613-621
Author(s):  
Y. S. Astakhov ◽  
S. N. Tultseva ◽  
A. I. Titarenko ◽  
S. Y. Astakhov ◽  
V. A. Antonov ◽  
...  

Respiratory changes caused by obstructive sleep apnea (OSA) syndrome increase the risk of ocular vascular diseases. Hypoxia, hypercapnia, endothelial dysfunction associated with OSA syndrome, promote local impairment of fibrinolysis, cause hypercoagulation and vasospasm, creating conditions for retinal vein occlusions as well as for those of posterior ciliary arteries. 91,5 % patients with retinal vein occlusions and 75 % patients with nonarteritic anterior ischemic optic neuropathy have moderate-to-severe OSA. OSA timely diagnosis and treatment prevent acute vascular pathology of the retina and optic nerve.


2020 ◽  
Vol 78 (10) ◽  
pp. 642-650
Author(s):  
Felipe Torres PACHECO ◽  
Luiz Celso Hygino da CRUZ JUNIOR ◽  
Igor Gomes PADILHA ◽  
Renato Hoffmann NUNES ◽  
Antônio Carlos Martins MAIA JUNIOR ◽  
...  

ABSTRACT Intracranial vessel wall imaging plays an increasing role in diagnosing intracranial vascular diseases. With the growing demand and subsequent increased use of this technique in clinical practice, radiologists and neurologists should be aware of the choices in imaging parameters and how they affect image quality, clinical indications, methods of assessment, and limitations in the interpretation of these images. Due to the improvement of the MRI techniques, the possibility of accurate and direct evaluation of the abnormalities in the arterial vascular wall (vessel wall imaging) has evolved, adding substantial data to diagnosis when compared to the indirect evaluation based on conventional flow analyses. Herein, the authors proposed a comprehensive approach of this technique reinforcing appropriated clinical settings to better use intracranial vessel wall imaging.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Allison Herman ◽  
Ross England ◽  
Dale Haines ◽  
Sheri Kelemen ◽  
Mitali Ray ◽  
...  

Vascular smooth muscle cells (VSMC) play a critical role in the etiology and progression of many vascular diseases including atherosclerosis and restenosis. Our laboratory has found that one anti-inflammatory interleukin, IL-19, is atheroprotective and can decrease vascular inflammation by reduction in mRNA stability of inflammatory transcripts by reduction of activity of HuR, an mRNA stability protein. HuR translocates from the nucleus to the cytoplasm where it recognizes AU-rich elements present almost exclusively in the 3’UTR of pro-inflammatory genes. Proteins and pathways which limit HuR translocation are understudied, but may reduce inflammatory mRNA stability. Using MASS SPEC to identify HuR-interacting proteins under different inflammatory conditions, we identified one protein, Fragile X-related protein (FXR1), which interacts with HuR in inflammatory, but not basal conditions, a novel interaction. FXR1 mRNA expression is enhanced in muscle cells, but nothing has been reported on expression of FXR1 in VSMC or function for FXR1 in vascular disease. The FXR1 promoter contains multiple cholesterol-response elements, and in this study we demonstrate that FXR1 expression is increased in injured arteries and TNFα and oxLDL stimulated human VSMC, but also by IL-19. RNA EMSA demonstrates that FXR1 directly interacts with ARE in 3’UTR. SiRNA knock down of FXR1 in VSMC increases stability of inflammatory mRNA and protein abundance as well as VSMC proliferation, while overexpression of FXR1 reduces both their abundance and stability in addition to reducing proliferation. Since FXR1 appears to be a novel repressor of inflammatory proteins, and is also induced by IL-19, our overall hypothesis is that FXR1 expression and HuR interaction is an inflammation responsive, counter-regulatory mechanism to reduce abundance of pro-inflammatory proteins and therefore reduce inflammation.


2020 ◽  
Vol 17 (165) ◽  
pp. 20190732 ◽  
Author(s):  
John Tarbell ◽  
Marwa Mahmoud ◽  
Andrea Corti ◽  
Luis Cardoso ◽  
Colin Caro

Atherosclerosis and vascular disease of larger arteries are often associated with hypoxia within the layers of the vascular wall. In this review, we begin with a brief overview of the molecular changes in vascular cells associated with hypoxia and then emphasize the transport mechanisms that bring oxygen to cells within the vascular wall. We focus on fluid mechanical factors that control oxygen transport from lumenal blood flow to the intima and inner media layers of the artery, and solid mechanical factors that influence oxygen transport to the adventitia and outer media via the wall's microvascular system—the vasa vasorum (VV). Many cardiovascular risk factors are associated with VV compression that reduces VV perfusion and oxygenation. Dysfunctional VV neovascularization in response to hypoxia contributes to plaque inflammation and growth. Disturbed blood flow in vascular bifurcations and curvatures leads to reduced oxygen transport from blood to the inner layers of the wall and contributes to the development of atherosclerotic plaques in these regions. Recent studies have shown that hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor associated with hypoxia, is also activated in disturbed flow by a mechanism that is independent of hypoxia. A final section of the review emphasizes hypoxia in vascular stenting that is used to enlarge vessels occluded by plaques. Stenting can compress the VV leading to hypoxia and associated intimal hyperplasia. To enhance oxygen transport during stenting, new stent designs with helical centrelines have been developed to increase blood phase oxygen transport rates and reduce intimal hyperplasia. Further study of the mechanisms controlling hypoxia in the artery wall may contribute to the development of therapeutic strategies for vascular diseases.


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