thoracic aortic dissection
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2021 ◽  
Vol 8 ◽  
Author(s):  
Guangwei Pan ◽  
Mengyang Liao ◽  
Yong Dai ◽  
Yang Li ◽  
Xiaole Yan ◽  
...  

Background: Numerous pieces of evidence have indicated that thoracic aortic dissection (TAD) is an inflammatory disease. Sphingosine-1-phosphate receptor 2 (S1PR2) signaling is a driver in multiple inflammatory diseases. Here, we examined the S1PR2 expression in TAD lesions and explored the effect of interfering with S1PR2 on TAD formation and progression.Methods: Aorta specimens and blood samples were collected from patients with TAD and matched controls. The expression of S1PR1, S1PR2, and S1PR3 was examined. The effect of inhibiting S1PR2 on TAD was evaluated in a TAD mouse model induced by β-aminopropionitrile fumarate (BAPN) and AngII. The presence of sphingosine kinase 1 (SPHK1), S1P, and neutrophil extracellular traps (NETs) was investigated. Further, the possible association between S1PR2 signaling and NETs in TAD was analyzed.Results: In the aortic tissues of patients with TAD and a mouse model, the S1PR2 expression was significantly up-regulated. In the TAD mouse model, JTE013, a specific S1PR2 antagonist, not only blunted the TAD formation and aortic rupture, but also preserved the elastic fiber architecture, reduced the smooth muscle cells apoptosis level, and mitigated the aortic wall inflammation. Augmented tissue protein expression of SPHK1, citrullinated histone H3 (CitH3, a specific marker of NETs), and serum S1P, CitH3 were detected in TAD patients. Surgical repair normalized the serum S1P and CitH3 levels. Immunofluorescence staining revealed that S1PR2 colocalized with NETs. The protein expression levels of SPHK1 and serum S1P levels positively correlated with the protein expression and serum levels of CitH3, separately. Furthermore, JTE013 treatment reduced NETs accumulation.Conclusion: Inhibiting S1PR2 attenuates TAD formation and prevents aortic rupture. Targeting S1PR2 may provide a promising treatment strategy against TAD.


2021 ◽  
pp. 101-108
Author(s):  
Leonard M Shapiro ◽  
Antoinette Kenny

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Fang Huang ◽  
Hong Wu ◽  
Qing-Quan Lai ◽  
Xiao-Ting Ke

Abstract Objective To investigate the application value of dual-source computed tomography (DSCT) in preoperative assessment the rupture site of an thoracic aortic dissection (TAD). Methods A retrospective analysis of preoperative DSCT, multislice computed tomography (MSCT), and transthoracic echocardiography (TTE) results of 150 patients with suspected TAD in our hospital was conducted, and the intraoperative findings or interventional treatment results were used as the diagnostic gold standard. Results Of all 150 suspected TAD patients, 123 patients were confirmed to have TAD. The rupture site of TAD was in the ascending aorta in 46 patients, in the aortic arch in 13 patients, and in the descending aorta in 64 patients. The sensitivity of DSCT, MSCT, and TTE for locating the rupture site of the TAD was 100%, 93.5%, and 89.5%, respectively, and the specificity was 100%, 88.9%, and 81.5%. The differences were statistically significant. The distance between the actual rupture site and the one diagnosed by DSCT, MSCT, and TTE was 1.9 ± 1.2 mm, 5.1 ± 2.7 mm, and 7.8 ± 3.5 mm, respectively; the latter two were significantly worse than DSCT. The size of the rupture site diagnosed by DSCT, MSCT, and TTE was 1.5 ± 0.8 cm, 1.7 ± 0.9 cm, and 1.9 ± 1.0 cm, respectively. The size of the rupture site diagnosed by DSCT was not significantly different from the actual size of 1.4 ± 0.7 cm, while those by MSCT and TTE were. Conclusion DSCT has high sensitivity and specificity in diagnosing the rupture site of TAD and can clearly locate the rupture site. It can be a preferred imaging method for TAD.


2021 ◽  
pp. 20210043
Author(s):  
Priyesh Karia ◽  
Ayyaz Quddus ◽  
Kesavan Nayagam ◽  
Olga Lazoura

Rupture of ascending thoracic aortic dissection mimicking pulmonary thromboembolism due to pulmonary artery occlusion is rare and should be considered in hypoxic patients with aortic dissection.


2021 ◽  
pp. 58-63
Author(s):  
Eugene Sharma Henry

Acute myocarditis usually presents with a broad spectrum of symptoms and has variable clinical outcomes. A proportion of acute myocarditides may develop into fulminant myocarditis resulting in significant mortality if left untreated. This case report describes an unusual presentation of fatal lymphocytic myocarditis mimicking a thoracic aortic dissection in a previously healthy 45-year-old male. Fulminant myocarditis should be considered as part of the differential diagnosis in an acutely unwell young adult presenting to the Emergency Department with non-specific symptoms.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Peiru Liu ◽  
Jing Zhang ◽  
Duo Du ◽  
Dandan Zhang ◽  
Zelin Jin ◽  
...  

Abstract Background Thoracic aortic dissection (TAD) is a severe disease with limited understandings in its pathogenesis. Altered DNA methylation has been revealed to be involved in many diseases etiology. Few studies have examined the role of DNA methylation in the development of TAD. This study explored alterations of the DNA methylation landscape in TAD and examined the potential role of cell-free DNA (cfDNA) methylation as a biomarker in TAD diagnosis. Results Ascending aortic tissues from TAD patients (Stanford type A; n = 6) and healthy controls (n = 6) were first examined via whole-genome bisulfite sequencing (WGBS). While no obvious global methylation shift was observed, numerous differentially methylated regions (DMRs) were identified, with associated genes enriched in the areas of vasculature and heart development. We further confirmed the methylation and expression changes in homeobox (Hox) clusters with 10 independent samples using bisulfite pyrosequencing and quantitative real-time PCR (qPCR). Among these, HOXA5, HOXB6 and HOXC6 were significantly down-regulated in TAD samples relative to controls. To evaluate cfDNA methylation pattern as a biomarker in TAD diagnosis, cfDNA from TAD patients (Stanford type A; n = 7) and healthy controls (n = 4) were examined by WGBS. A prediction model was built using DMRs identified previously from aortic tissues on methylation data from cfDNA. Both high sensitivity (86%) and specificity (75%) were achieved in patient classification (AUC = 0.96). Conclusions These findings showed an altered epigenetic regulation in TAD patients. This altered epigenetic regulation and subsequent altered expression of genes associated with vasculature and heart development, such as Hox family genes, may contribute to the loss of aortic integrity and TAD pathogenesis. Additionally, the cfDNA methylation in TAD was highly disease specific, which can be used as a non-invasive biomarker for disease prediction.


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