Treatment of inadvertent cervical arterial catheterization: Single-center experience.

OBJECTIVES: Inadvertent arterial catheterization can occur during transjugular central venous catheter insertion and should be promptly treated to prevent serious consequences. Although many treatment modalities are available, no exist guidelines regarding the selection of treatment. We aimed to describe our experience with the treatment of 11 patients who underwent inadvertent cervical arterial catheterization and propose an algorithm for the selection of treatment methods. METHODS: We retrospectively identified all patients who were treated for inadvertent arterial catheterization at our center between January 2016 and March 2021. We reviewed patient profiles, images, treatment methods, and follow-up data. RESULTS: Eleven patients were included (eight men and three women, age: 36-73 years). Ten catheter misplacements were in the right common carotid artery. The remaining catheter was inserted into the right subclavian artery after penetrating the right common carotid artery. Two catheters were 5-Fr and nine catheters were 11.5-Fr. Two patients underwent manual compressions, three underwent open surgery, three underwent stent-graft repairs, and four underwent Perclose Proglide closure. Clinical success was achieved in all 11 patients. Primary technical success was achieved in 10 patients. In one patient, unsuccessful manual compression was followed by successful stent-graft repair; the manual compression failed to prevent bleeding, possibly because of the long-term oral administration of aspirin for coronary heart disease. The mean follow-up was 5.4 months (range, 1-12 months). The overall mortality rate was zero, and no vascular or neurological events occurred. CONCLUSIONS: The existing data show that the current protocol for the treatment of inadvertent cervical arterial catheterization at our center is safe and effective. However, the data are insufficient and require further clinical validation.

LncRNA FGF7-5 and lncRNA GLRX3 together inhibits the formation of carotid plaque via regulating the miR-2681-5p/ERCC4 axis in atherosclerosis.

Atherosclerotic plaques belong to the common vascular disease in the aged, which rupture will lead to acute thromboembolic diseases, the leading cause of fatal cardiovascular events. Accumulating evidence indicates that the lncRNAs-miRNAs-mRNA regulatory network plays a critical role in atherosclerosis. Based on RNA sequencing (GSE207252), we constructed expression profiles of lncRNAs, microRNAs, and mRNA in the carotid plaque of atherosclerosis patients and analyzed differentially expressed genes (DEGs). We identified three candidate lncRNAs using two algorithms (LASSO and SVM-RFE): lnc_GLRX3, lnc_FGF7-5, and DISC1FP1). LNCipedia, TargetScan, and miRDB databases were used to predict target miRNAs of lncRNAs and target genes of miRNAs. Gene ontology (GO) functional annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and Gene Set Enrichment Analysis (GSEA) analysis of DEGs was carried out using the R package clusterProfiler. A PPI network was constructed using the STRING website and visualized by Cytoscape. According to the "MCC" method of the plug-in cytoHubba in Cytoscape, ERCC4 was the top hub gene of the PPI network. We constructed a lncRNA_FGF7-5/lncRNA_GLRX3-miR-2681-5p-ERCC4 regulatory network for carotid plaque using lncRNA-miRNA and miRNA-mRNA pairs. Next, lncRNA_FGF7-5 and lncRNA_GLRX3 targeted miR-2681-5p directly to upregulate ERCC4 expression. Silencing of lncRNA_FGF7-5 and lncRNA_GLRX3 promoted apoptosis and TP53 expression in HUVECs treated with ox-LDL; however, these effects were reversed by ERCC4-overexpression. Taken together, these findings indicated that lncRNA_FGF7-5 and lncRNA_GLRX3 together reduced atherosclerosis-induced apoptosis of HUVECs via targeting miR-2681-5p to increase ERCC4 expression, thereby preventing the formation of carotid plaque and finally inhibiting atherosclerosis progression.

Long-segment common carotid occlusion presenting with limb-shaking transient ischemic attack: Case report.

Background: Limb-shaking transient ischemic attack (LS-TIA) is a rare manifestation of carotid artery occlusion. Common carotid artery occlusion (CCAO) is a relatively rare condition, and both its natural history and recommendations for treatment are still unclear. Case description: A 67-year-old female suffered from transient episodes of unilateral limb shaking. Computer tomographic angiography (CTA) showed long-segment occlusion of the right common carotid artery. Computer tomographic perfusion (CTP) demonstrated hypoperfusion of the corpus striatum, which suggests that hemodynamic failure is a potential mechanism underlying the LS-TIA secondary to common carotid artery occlusion. The occlusion was successfully recanalized by retrograde common carotid endarterectomy, and the episodes of left limb shaking disappeared after surgery. Conclusions: The occlusion was successfully recanalized by retrograde common carotid endarterectomy, and the episodes of left limb shaking disappeared after surgery. Hypoperfusion of the corpus striatum might be a potential mechanism underlying the LS-TIA secondary to common carotid occlusion.

Biphasic effects of autophagy on decompression bubble-induced endothelial injury.

Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble-induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3-methyladenine (3-MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3-II/I ratio and Beclin-1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase-3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3-II/I ratio and partially reversed by 3-MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre-conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre-conditioning, and 30-minutes pre-conditioning induced opposing changes, all of which were inhibited by 3-MA. In conclusion, autophagy was involved and played a biphasic role in bubble-induced endothelial injury.