Enzehua Xie

Background: Succinate has emerged as an immunometabolic mediator of cardiovascular diseases. However, the enzymatic mechanisms linking macrophage succinate metabolism to aortic dissection remain incompletely understood. This study investigated whether Suclg2, which encodes the GDP-forming β-subunit of succinyl-CoA ligase, regulates succinate-associated macrophage remodelling and aortic dissection progression. Methods: Suclg2 expression was examined in BAPN-induced AD and human acute type A aortic dissection tissues by Western Blot and immunofluorescence. Myeloid- and smooth muscle cell-specific Suclg2 conditional knockout mice were subjected to BAPN treatment to evaluate survival, aortic outcomes, histological injury and aortic morphology. Aortic RNA-seq was used to discover transcriptional changes. Bone marrow-derived macrophages were analysed under basal, M1-like and M2-like conditions to assess macrophage-intrinsic transcriptional responses. Plasma succinate levels and untargeted metabolomic profiles were further examined. Results: Suclg2 was increased in murine and human dissected aortas and partially localized to CD68+ cells. Myeloid Suclg2 deletion markedly reduced BAPN-induced aortic rupture and dissection, whereas smooth muscle cell Suclg2 deletion did not confer comparable protection. Aortic transcriptomic analysis showed that myeloid Suclg2 deficiency attenuated inflammatory adhesion and matrix-destructive programmes. In macrophages, Suclg2 deletion did not induce a simple M1/M2 polarization shift; instead, it remodelled lipid-handling, phagolysosomal, adhesive and matrix-remodelling pathways across stimulation states. Metabolic profiling showed reduced circulating succinate and broader changes in central carbon, lipid-associated, nucleotide and redox-related metabolites after myeloid Suclg2 deletion. Conclusions: Myeloid Suclg2 is a succinate-associated immunometabolic regulator of aortic dissection. Its deficiency protects against aortic dissection by reshaping macrophage inflammatory-remodelling programmes and the systemic metabolic environment.

Background: Cerebrospinal fluid drainage (CSFD) is commonly used to manage spinal cord injury (SCI) after aortic surgery. However, there is still limited evidence regarding its effectiveness in patients with type A aortic dissection undergoing total arch replacement plus frozen elephant trunk procedure. Methods: A total of 1931 patients were retrospectively enrolled between 2010 and 2023. Patients with high‐risk postoperative SCI (N=445) were divided into 2 groups: with or without prophylactic CSFD to evaluate the protective effect of prophylactic CSFD. Patients with postoperative SCI (N=119) were divided into 3 groups, without CSFD, therapeutic CSFD, and prophylactic CSFD, and analyzed to compare the treatment effect of different CSFD strategies. Results: Prophylactic CSFD significantly reduced the incidence of postoperative SCI in high‐risk patients (26.9% versus 17.7%, P =0.029), further supported by matching weights analysis of propensity score and conditional logistic regression. Analyses of the SCI population revealed less severe SCI symptoms in patients with prophylactic CSFD, as assessed by the American Spinal Injury Association Impairment Scale (adjusted P P =0.003) but not therapeutic CSFD ( P =0.981) was beneficial to the in‐hospital recovery of postoperative SCI. Long‐term SCI outcomes did not differ among groups. Conclusions: A prominent protective effect on SCI occurrence and recovery after the total arch replacement plus the frozen elephant trunk procedure was observed with prophylactic CSFD use in patients with type A aortic dissection. However, the effectiveness of therapeutic CSFD fell short of significance.

Microplastics have been detected in human stool, lungs, and placentas, which have direct exposure to the external environment through various body cavities, including the oral/anal cavity and uterine/vaginal cavity. Crucial data on microplastic exposure in completely enclosed human organs are still lacking. Herein, we used a laser direct infrared chemical imaging system and scanning electron microscopy to investigate whether microplastics exist in the human heart and its surrounding tissues. Microplastic specimens were collected from 15 cardiac surgery patients, including 6 pericardia, 6 epicardial adipose tissues, 11 pericardial adipose tissues, 3 myocardia, 5 left atrial appendages, and 7 pairs of pre- and postoperative venous blood samples. Microplastics were not universally present in all tissue samples, but nine types were found across five types of tissue with the largest measuring 469 μm in diameter. Nine types of microplastics were also detected in pre- and postoperative blood samples with a maximum diameter of 184 μm, and the type and diameter distribution of microplastics in the blood showed alterations following the surgical procedure. Moreover, the presence of poly(methyl methacrylate) in the left atrial appendage, epicardial adipose tissue, and pericardial adipose tissue cannot be attributed to accidental exposure during surgery, providing direct evidence of microplastics in patients undergoing cardiac surgery. Further research is needed to examine the impact of surgery on microplastic introduction and the potential effects of microplastics in internal organs on human health.