Overview of the current knowledge on etiology, natural history and treatment of aortic dissection

Parve, Swapnil; Ziganshin, Bulat A.; Elefteriades, John A.

doi:10.23736/s0021-9509.17.09883-4

Cited by 25 publications

(14 citation statements)

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“…For all AD patients, rs13019803C is related to the sST2 level [beta(95% CI) = 0.106 (−0.006–0.219), p = 0.064]. Compared with type A AD, type B AD does not involve the ascending aorta and is less dangerous ( 22 ). We separately analyzed type A and type B patients.…”

Section: Resultsmentioning

confidence: 99%

“…There is a significantly positive correlation between rs13019803 and serum sST2 in type A AD; however, it showed no correlation in type B AD. Compared with type A AD, type B AD does not involve the ascending aorta and has less hemodynamic stress ( 22 ). This indicates that there may be differences for underlining pathophysiology between type A and type B.…”

Section: Discussionmentioning

confidence: 99%

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Association of IL1R1 Coding Variant With Plasma-Level Soluble ST2 and Risk of Aortic Dissection

Jiang

Wang

Gao

et al. 2021

Front. Cardiovasc. Med.

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Objective: Aortic dissection (AD) is characterized by an acute onset, rapid progress, and high mortality. Levels of soluble ST2 (sST2) on presentation are elevated in patients with acute AD, which can be used to discriminate AD patients from patients with chest pain. sST2 concentrations were found to be highly heritable in the general population. The aim of this study was to investigate the associations of variations in ST2-related gene expression with sST2 concentrations and AD risk.Methods: This case-control study involving a total of 2,277 participants were conducted, including 435 AD patients and age- and sex-matched 435 controls in the discovery stage, and 464 patients and 943 controls in the validation stage. Eight ST2-related genes were selected by systematic review. Tag single-nucleotide polymorphisms (SNPs) were screened out from the Chinese population of the 1,000 Genomes Database. Twenty-one ST2-related SNPs were genotyped, and plasma sST2 concentrations were measured.Results: In the discovery stage, rs13019803 located in IL1R1 was significantly associated with AD after Bonferroni correction (p = 0.0009) and was correlated with circulating sST2 levels in patients with type A AD(AAD) [log-sST2 per C allele increased by 0.180 (95%) CI: 0.002 – 0.357] but not in type B. Combining the two stages together, rs13019803C was associated with plasma sST2 level in AAD patients [log-sST2 increased by 0.141 (95% CI: 0.055–0.227) for per C allele]. Odds ratio of rs13019803 on the risk of AAD is 1.67 (95% CI: 1.33–2.09).Conclusions: The IL1R1 SNP rs13019803C is associated with higher sST2 levels and increased risk of AAD.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association of IL1R1 Coding Variant With Plasma-Level Soluble ST2 and Risk of Aortic Dissection

Jiang

Wang

Gao

et al. 2021

Front. Cardiovasc. Med.

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“…According to the Stanford classification, type A aortic dissections (TAAD) involve the presence of dissection proximal to the left subclavian artery, while type B aortic dissections are limited to the descending aorta without any proximal extension. The incidence of AD was approximately 3 to 6 per 100,000 people per year and was rising dramatically over the last decade [ 3 , 4 ]. Acute AD followed by aortic rupture results in a high mortality rate of up to 90% in the absence of prompt intervention.…”

Section: Introductionmentioning

confidence: 99%

Role of Necroptosis and Immune Infiltration in Human Stanford Type A Aortic Dissection: Novel Insights from Bioinformatics Analyses

Liu

Wei

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Stanford type A aortic dissection (TAAD) is one of the most life-threatening cardiovascular emergencies with high mortality and morbidity, and necroptosis is a newly identified type of programmed cell death and contributes to the pathogenesis of various cardiovascular diseases. However, the role of necroptosis in TAAD has not been elucidated. This study was aimed at determining the role of necroptosis in TAAD using bioinformatics analyses. Methods. The RNA sequencing dataset GSE153434 and the microarray dataset GSE52093 were obtained from Gene Expression Omnibus (GEO) database. Differentially expressed genes of necroptosis (NRDEGs) were identified based on differentially expressed genes (DEGs) and necroptosis gene set. Gene set enrichment analysis (GSEA) was applied to evaluate the gene enrichment signaling pathway in TAAD. The STRING database and Cytoscape software were used to establish and visualize protein-protein interaction (PPI) networks and identify the key functional modules of NRDEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of NRDEGs were also performed. Additionally, Spearman correlations were used to construct the necroptosis-related transcription factor-target genes regulatory network, immune infiltration patterns were analyzed using the ImmuCellAI algorithm, and the correlation between immune cell-type abundance and NRDEGs expression was investigated. The expression levels of NRDEGs and immune infiltration were additionally verified in the GSE52093 dataset. Results. We found that the necroptosis pathway was considerably enriched and activated in TAAD samples. Overall, 25 NRDEGs were identified including MLKL, RIPK1, and FADD, and among them, 18 were verified in the validation set. Moreover, GO and KEGG enrichment analyses found that NRDEGs were primarily involved in the tumor necrosis factor signaling pathway, nucleotide-binding oligomerization domain-like receptor signaling pathway, and interleukin-17 signaling pathway. The imbalance of Th17/Treg cells was identified in the TAAD samples. Furthermore, correlation analysis indicated that expression of NRDEGs was positively associated with proinflammatory immune-cell infiltrations and negatively associated with anti-inflammatory or regulatory immune-cell infiltrations. Conclusions. The present findings suggest that necroptosis phenomenon exists in TAAD and correlates with immune cell infiltration, which indicate necroptosis may promote the development of TAAD through activating immune infiltration and immune response. This study paves a new road to future investigation of the pathogenic mechanisms and therapeutic strategies for TAAD.

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“…1,4 According to recent guidelines, thoracic endovascular aortic repair (TEVAR) is now considered the treatment of choice in thoracic aortic diseases, when compared with open surgical repair. [4][5][6] Nevertheless, DTAA derived from degenerative or atherosclerotic origin and other acute and AAS, such as dissections (including both long-term and acute) recognize different pathophysiological mechanisms and natural history, before and after TEVAR or others type of managements, [7][8][9][10][11] which may have different impacts on the long-term aortic modifications, to include both distal and proximal zones. 12,13 In this scenario, it is of paramount importance to describe and examine outcomes in patients treated for DTAA or AAS, to differentiate type and incidence of complications and establish a rigorous postoperative follow-up program depending on the type of each disease entity.…”

Section: Introductionmentioning

confidence: 99%

Differences in Mid-Term Outcomes Between Patients Undergoing Thoracic Endovascular Aortic Repair for Aneurysm or Acute Aortic Syndromes: Report From the Global Registry for Endovascular Aortic Treatment

et al. 2021

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Purpose: To analyze differences in baseline characteristics, overall mortality, device-related mortality, and re-intervention rates in patients who underwent thoracic endovascular aortic repair (TEVAR) for descending thoracic aortic aneurysm (DTAA) with atherosclerotic/degenerative cause or acute aortic syndrome (AAS), using the Global Registry For Endovascular Aortic Treatment (GREAT). Materials and Methods: Patients submitted to TEVAR for AAS or DTAA, included in GREAT, were eligible for this analysis. Primary outcome was 30-day all-cause mortality rate. Secondary outcomes were 30-day aorta-related mortality and re-intervention rate, 1-year and 3-year all-cause mortality, aorta-related mortality and re-intervention rate. Results: Five-hundred and seventy-five patients were analyzed (305 DTAA and 270 AAS). Thirty-day mortality rate was 1.3% and 1.8% for DTAA and AAS, respectively (p=0.741). One-year and 3-year mortality rates were 6.2% versus 9.3 and 17.3% versus 15.9% for DTAA and AAS, respectively (p=0.209 and p=0.655, respectively). Aorta-related mortality rates at 30 days, 1 year and 3 years were 1.3%, 1.3%, and 2.6% for DTAA, 1.8%, 4.2%, and 4.2% for AAS (p=ns). Re-intervention rates at 30 days, 1 year, and 3 years were 1.3%, 4.3%, and 7.5% for DTAA, 3.3%, 8.1%, and 10.7% for AAS (p=ns). Furthermore, a specific analysis with similar outcomes was performed dividing follow-up in 3 periods (1-30 days, 31-365 days, 366-1096 days) and describing mutual differences between 2 groups and temporal trends in each group. Conclusion Patients who underwent TEVAR for DTAA or AAS experienced different mortality and re-intervention rates among years during mid-term follow-up. Although all-cause related deaths within 30 days were TEVAR-related, aorta-related deaths were more common for AAS patients within 1 year. A greater re-intervention rate was described for AAS patients, although only 1 year after TEVAR.

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Overview of the current knowledge on etiology, natural history and treatment of aortic dissection

Cited by 25 publications

References 0 publications

Association of IL1R1 Coding Variant With Plasma-Level Soluble ST2 and Risk of Aortic Dissection

Association of IL1R1 Coding Variant With Plasma-Level Soluble ST2 and Risk of Aortic Dissection

Role of Necroptosis and Immune Infiltration in Human Stanford Type A Aortic Dissection: Novel Insights from Bioinformatics Analyses

Differences in Mid-Term Outcomes Between Patients Undergoing Thoracic Endovascular Aortic Repair for Aneurysm or Acute Aortic Syndromes: Report From the Global Registry for Endovascular Aortic Treatment

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