ABSTRACT
Background: Stanford type A aortic dissection (ATAAD) is a common life-threatening event in the aorta. Recently, immune disorder has been linked to the risk factors that cause ATAAD at the molecular level. However, the specific immune-related gene signature during the progression is unclear. Methods: The GSE52093 and GSE98770 datasets related to ATAAD from the Gene Expression Omnibus (GEO) database were acquired. The immune gene expression levels were analyzed by single sample gene set enrichment analysis (ssGSEA). The correlations between gene networks and immune scores were determined by weighted gene correlation network analysis (WGCNA). The different immune subgroups were finally divided by consensus clustering. The differentially expressed genes (DEGs) were identified and subsequent functional enrichment analyses were conducted. The hub genes were identified by protein-protein interaction (PPI) network and functional similarities analyses. The immune cell infiltration proportion was determined by the CIBERSORT algorithm. Results: According to the ssGSEA results, the 13 ATAAD samples from the GEO database were divided into high- and low-immune subgroups according to the ssGSEA, WGCNA, and consensus clustering analysis results. Sixty-eight immune-related DEGs (IRDEGs) between the two subgroups were enriched in inflammatory-immune response biological processes, including leukocyte cell-cell adhesion, mononuclear cell migration, and myeloid leukocyte migration. Among these IRDEGs, 8 genes (CXCR4, LYN, CCL19, CCL3L3, SELL, F11R, DPP4, and VAV3) were identified as hub genes that represented immune-related signatures in ATAAD after the PPI and functional similarities analyses. The proportions of infiltrating CD8 T cells and M1 macrophages were significantly higher in ATAAD patients in the immune-high group than the immune-low group. Conclusion: Eight immune-related genes were identified as hub genes representing potential biomarkers and therapeutic targets linked to the immune response in ATAAD patients.
ABSTRACT
BACKGROUND: Newly developed graft failure negatively affects the short- and long-term outcomes of patients who experience coronary artery bypass grafting (CABG) surgery. This study explored the value of transit time flow measurement (TTFM) parameters for predicting the risk of newly developed graft failure that occurs within 1 year after CABG, as well as investigated the relationship between newly developed graft failure and adverse cardiovascular events. METHODS: A total of 134 patients who underwent CABG and had CT angiography (CTA) data (1 year post-operatively) were divided into two groups: the patient group, in which patients did not have newly developed graft failure, and the occluded group, in which patients developed newly developed graft failure between 1 and 12 months after CABG. The patency rate of grafts in different targets was analyzed. The correlations between graft failure and TTFM parameters and between graft failure and the occurrence of adverse cardiovascular events were investigated. RESULTS: The overall rate of newly developed graft failure was 7.2%, the venous graft failure was 10.8%, and the arterial graft failure was 0.7%. The occluded group had a higher pulse index (PI) (2.9 vs. 2.4, P = 0.007), a lower mean graft flow (MGF) (20 vs. 25 ml/min, P = 0.028), and a lower diastolic flow fraction (DF) (63.5 vs. 70%, P = 0.019) than the patent group. The cut-off value for predicting newly developed graft failure was PI > 2.75 (P = 0.007), MGF < 23.5 ml/min (P = 0.03), and DF < 65.5% (P = 0.019). Compared with the patent group, the newly developed graft failure group had higher rates of recurrent angina (13.6 vs. 0.9%, P = 0.0014) and revascularization intervention (9.1 vs. 0% P = 0.026). However, there were no differences in death, cardiac death, myocardial infarction, and cerebral infarction after CABG operation between these two groups (P > 0.05). CONCLUSIONS: A high PI and low MGF and DF are risk factors for newly developed graft failure. The patients with newly developed graft failure had higher rates of recurrent angina and revascularization intervention. TTFM parameters may be used to predict the occurrence of newly developed graft failure in patients after CABG surgery.
ABSTRACT
@#Objective To explore the relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and aortic dissection (AD). Methods Fifty three patients with AD diagnosed by CTA in our hospital from January 2016 to January 2018 were selected. All the patients with AD were scored by the STOP-BANG questionnaire. The patients who scored more than or equal to 3 received polysomnography (PSG) after surgical or conservative treatment, and according to whether the sleep apnea-hypopnea index was higher than or equal to 5. Fifty-three patients were divided into an OSAHS group and a non OSAHS group. Results There were 18 patients with 17 males and 1 female at average age of 43.3±8.4 years in the OSAHS group, and 35 patients with 23 males and 12 females at average age of 56.6±12.9 years in the non OSAHS group. There was no statistical difference between the two groups in the Stanford classification of aortic dissection, the time of onset, personal history, the history of diabetes, coronary heart disease and hyperlipidemia, or post-treatment systolic/diastolic blood pressure before sleep (P>0.05). The age of patients in the OSAHS group was significantly less than that in the non OSAHS group (P<0.01), the proportion of men/women (P=0.021), weight (P<0.01), height (P=0.028), body mass index (P<0.01), and post-treatment systolic/diastolic blood pressure after waking up (P=0.028,P=0.044) in the OSAHS group were significantly higher than those in the non OSAHS group. In the OSAHS group, the proportion of previous hypertension was significantly higher than that in the non OSAHS group (P=0.042). Conclusion AD patients combined with OSAHS are mostly male patients. The number of young and high-fat people is significantly more than that in the non OSAHS group. OSAHS may be one of the risk factors for young, high-fat men with AD.
ABSTRACT
Acute aortic dissection (AAD) faces great challenges in early diagnosis and effective drug treatment. Recent developments in systems biology approaches allow high-throughput screening of novel diagnostic biomarkers and potential therapeutic targets. In this review, we summarize the currently available AAD biomarkers identified in the context of genomic, transcriptomic, proteomic, and metabolic profiles, and highlight the benefits of using a combination of these findings for a better understanding of the molecular nature of this life-threatening disease. This review also provides a reference for future studies that employ a comprehensive, multiple-level approach at the single-cell level to decipher the underlying molecular pathophysiology of AAD.
