AngioJet thrombectomy in the treatment of pulmonary embolism complicated with left subclavian artery embolism: a case report.

Coexistence of pulmonary embolism (PE) and arterial thrombosis in a single patient is rare. Management of such cases is challenging because there is no unified standard on how to treat this type of disease. We herein report a case involving a 73-year-old man who was admitted to the hospital because of a 2-day history of chest tightness. Pulmonary computed tomography angiography revealed a filling defect of the main pulmonary artery and bilateral branches as well as a left subclavian artery embolism. AngioJet mechanical thrombectomy (Boston Scientific, Marlborough, MA, USA) was used to treat the PE, and this was combined with left brachial artery incision and thrombectomy for treatment of the left subclavian artery embolism. The patient recovered well after the operation. The prognosis was good after 9 months of regular follow-up. AngioJet mechanical thrombectomy combined with left brachial artery incision thrombectomy may be a feasible treatment option for cases of PE combined with left subclavian artery embolism.

ADAMTS13 inhibits H2O2-induced human venous endothelial cell injury to attenuate deep-vein thrombosis by blocking the p38/ERK signaling pathway.

Deep vein thrombosis (DVT) is a common complication in hematologic malignancies and immunologic disorders. Endothelial cell injury and dysfunction comprise the critical contributor for the development of DVT. A disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS13), a plasma metalloprotease that cleaves von Willebrand factor, acts as a critical regulator in normal hemostasis. This study was aimed to explore the role of ADAMTS13 in endothelial cell injury during DVT and the possible mechanism. First, human umbilical vein endothelial cells (HUVECs) were exposed to hydrogen peroxide (H2O2). Then, the mRNA and protein expressions of ADAMTS13 were evaluated with the reverse transcription-quantitative polymerase chain reaction and western blot. After treatment with recombinant ADAMTS13 (rADAMTS13; rA13), the viability and apoptosis of H2O2-induced HUVECs were assessed by cell counting kit-8 assay and terminal-deoxynucleoitidyl transferase-mediated nick end labeling staining. In addition, the levels of prostaglandin F1-alpha, endothelin-1, and reactive oxygen species were detected using the enzyme-linked immunosorbent assay and dichloro-dihydro-fluorescein diacetate assay. The expressions of proteins related to p38/extracellular signal-regulated kinase (ERK) signaling pathway were estimated with the western blot. Then, p79350 (p38 agonist) was used to pretreat cells to analyze the regulatory effects of rA13 on p38/ERK signaling in H2O2-induced HUVEC injury. The results revealed that ADAMTS13 expression was significantly downregulated in H2O2-induced HUVECs. The reduced viability and increased apoptosis of HUVECs induced by H2O2 were revived by ADAMTS13. ADAMTS13 also suppressed the oxidative stress in HUVECs after H2O2 treatment. Besides, ADAMTS13 was found to block p38/ERK signaling pathway, and p79350 reversed the impacts of ADAMTS13 on the damage of HUVECs induced by H2O2. To sum up, ADAMTS13 could alleviate H2O2-induced HUVEC injury through the inhibition of p38/ERK signaling pathway.

Hydroxysafflor yellow A inhibits endothelial cell ferroptosis in diabetic atherosclerosis mice by regulating miR-429/SLC7A11.

CONTEXT: Ferroptosis may play an essential role in lipid peroxidation and endothelial dysfunction of aortic endothelial cells (ECs) in type 2 diabetes mellitus (T2DM) with atherosclerosis (AS). Hydroxysafflor yellow A (HSYA) has shown substantial antioxidant stress and anti-ferroptosis. OBJECTIVE: This study confirms whether HSYA improves symptoms in a mouse model of T2DM/AS and elucidates the underlying mechanisms. MATERIALS AND METHODS: ApoE-/- mice were fed with high fat combined with 30 mg/kg streptozotocin to establish a T2DM/AS model. Then mice were treated with intraperitoneal injections of 2.25 mg/kg HSYA for 12 weeks. Human Umbilical Vein Endothelial cells (HUVEC) induced by 33.3 mM d-glucose +100 µg/mL ox-LDL were used to construct a high lipid and high glucose cell model treated with 25 µM HSYA. The changes in oxidative stress- and ferroptosis-related markers were detected, and the regulatory effect of HSYA on the miR-429/SLC7A11 was also verified. Normal ApoE-/- mice or HUVEC cells were used as the control group. RESULTS: HSYA effectively reduced atherosclerotic plaque formation in the T2DM/AS mouse model and inhibited HUVEC ferroptosis, such as upregulating GSH-Px, SLC7A11 and GPX4, but inhibited ACSL4. Furthermore, HSYA also downregulated the expression of miR-429, which further regulated SLC7A11 expression. After miR-429 mimic or SLC7A11 siRNA transfection in the HUVEC, the antioxidative stress and anti-ferroptosis effects of HSYA were significantly abolished. CONCLUSIONS: HSYA is expected to become an important health drug to prevent the occurrence and development of T2DM/AS.

Retrospective Analysis of the Safety and Efficacy of AngioJet Rheolytic Thrombectomy for Acute Pulmonary Embolism: A Single-Center Study.

BACKGROUND: To investigate the efficacy, safety, and feasibility of AngioJet Rheolytic Thrombectomy (ART) in the treatment of acute pulmonary embolism (APE). METHODS: Twelve patients with intermediate- or high-risk APE received ART and were followed up for 6-32 months. The technical success rate, clinical success rate, mortality, complication, and ancillary and laboratory tests before and after operation were analyzed retrospectively. RESULTS: The technical and clinical success rates of ART were both 91.67% (11/12). Except for the patient who died of heart failure during the operation, the rest of patients had no serious complications. After operation, arterial oxygen partial pressure increased while hemoglobin and troponin decreased (P < 0.05). All patients were free of recurrence of APE after 6-32 months of follow-up. Pulmonary artery thrombosis significantly reduced or disappeared. CONCLUSIONS: ART is an effective treatment for intermediate- and high-risk APE. It quickly clears the main pulmonary artery thrombus, relieves pulmonary hypertension, and improves the long-term prognosis of patients.

MiR-296-5p ameliorates deep venous thrombosis by inactivating S100A4.

Deep venous thrombosis is one of the most common venous thromboembolic diseases and has a low cure rate and a high postoperative recurrence rate. Furthermore, emerging evidence indicates that microRNAs are involved in deep venous thrombosis. miR-296-5p is an important microRNA that plays a critical role in various cellular functions, and S100A4 is closely related to vascular function. miR-296-5p is downregulated in deep venous thrombosis patients, and its predicted target S100A4 is upregulated in deep venous thrombosis patients. Therefore, it was hypothesized that miR-296-5p may play a vital role in the development of deep venous thrombosis by targeting S100A4. An Ox-LDL-stimulated HUVEC and deep venous thrombosis mouse model was employed to detect the biological functions of miR-296-5p and S100A4. Dual luciferase reporter assays and pull-down assays were used to authenticate the interaction between miR-296-5p and S100A4. ELISA and Western blotting were employed to detect the protein levels of thrombosis-related factors and the endothelial-to-mesenchymal transition (EndMT)-related factors. The miR-296-5p levels were reduced, while the S100A4 levels were enhanced in deep venous thrombosis patients, and the miR-296-5p levels were negatively correlated with the S100A4 levels in deep venous thrombosis patients. miR-296-5p suppressed S100A4 expression by targeting the 3' UTR of S100A4. MiR-296-5p knockdown accelerated ox-LDL-induced HUVEC apoptosis, oxidative stress, thrombosis-related factor expression, and EndMT, while S100A4 knockdown antagonized these effects in ox-LDL-induced HUVECs. S100A4 knockdown reversed the effect induced by miR-296-5p knockdown. Moreover, the in vivo studies revealed that miR-296-5p knockdown in deep venous thrombosis mice exacerbated deep venous thrombosis formation, whereas S100A4 knockdown had the opposite effect. These results indicate that elevated miR-296-5p inhibits deep venous thrombosis formation by inhibiting S100A4 expression. Both miR-296-5p and S100A4 may be potential diagnostic markers and therapeutic targets for deep venous thrombosis.

Efficacy and safety of Buyang Huanwu decoction in the treatment of varicose veins of the lower extremities: A protocol of randomized controlled trial.

BACKGROUND: Varicose veins of the lower extremities are common chronic venous diseases in the clinic. Although Western medicine has various surgical methods to treat varicose veins in the lower extremities, there are still a variety of complications. Some studies have shown that Buyang Huanwu decoction treatment of varicose veins of the lower extremities has a certain effect, and can reduce the occurrence of postoperative complications, but there is no evidence of evidence-based medicine. The research carried out in this scheme is to systematically evaluate the efficacy and safety of Buyang Huanwu decoction in the treatment of varicose veins in the lower extremities, and to provide reliable evidence for guiding clinical practice. METHODS: This is a randomized, double-blind, placebo-controlled, parallel-group clinical trial, which studies the effectiveness and safety of Buyang Huanwu decoction in the treatment of varicose veins of the lower extremities. The patients are randomly and evenly divided into treatment group and control group, the former one is given Buyang Huanwu decoction and the latter one is given placebo. The study will last 49 days, including a 7-day washout period, 14-day intervention and 28-day follow-up, focusing on its efficacy and safety indicators. Observation indicators include: TCM syndrome score, Venous Clinical Severity Score (VCSS), Venous Disability Scote (VDS), Aberdeen Varicose Vein Questionnaire (AVVQ), Hemorheology Indicators, Adverse Reactions, etc. Data analysis is performed using SPSS 25.0 software. DISCUSSION: This study will evaluate the effectiveness and safety of Buyang Huanwu decoction and provide clinical evidence for the treatment of varicose veins of the lower extremities. TRIAL REGISTRATION: OSF Registration number: DOI 10.17605/OSF.IO/WGJXT.

microRNA-331-3p maintains the contractile type of vascular smooth muscle cells by regulating TNF-α and CD14 in intracranial aneurysm.

Dysfunction of vascular smooth muscle cells (VSMCs) may be linked to intracranial aneurysm (IA) formation. VSMCs possess a phenotypic plasticity, capable of changing from a mature, contractile to a less differentiated, synthetic phenotype. In this study, we identify a microRNA candidate miR-331-3p that participates in regulating differentiation properties of VSMCs. The expression of TNF-α and CD14 was quantified in IA wall tissues obtained from 96 IA patients and their associations with clinicopathological features of IA were assessed. Then the interactions between miR-331-3p, TNF-α and CD14 were evaluated by determination of luciferase activity. Differentiated properties of VSMCs were assessed from phenotypic markers of contractile VSMCs, a-SMA and E-cadherin, and of synthetic VSMCs, ICAM-1, MCP-1, IL-6, MMP-2 and MMP-9. Rat IA models by ligation of left carotid artery and left renal artery and histological analysis of induced IAs were performed. The TNF-α and CD14 was highly expressed in IA wall tissues and associated with the type and diameter of aneurysm. Depletion of TNF-α or CD14 retarded VSMC apoptosis and transformation to the synthetic type but facilitated cell proliferation. Elevations in miR-331-3p, a direct negative regulator of both TNF-α and CD14, also reduced VSMC apoptosis and prevented VSMCs from synthetic type and increase their proliferation. Furthermore, miR-331-3p was demonstrated to inhibit the formation of IA by down-regulating TNF-α and CD14 in vivo. In conclusion, miR-331-3p maintains the contractile type of VSMCs, thus possibly inhibiting the progression of IA. These findings provide potential new strategies for the clinical treatment of IA.

Thoracic endovascular aortic repair in penetrating aortic ulcer combined with isolated left vertebral artery: A case report.

RATIONALE: Penetrating aorta ulcer (PAU) with isolated left vertebral artery (ILVA) is a rare condition, accounting for no more than 1% of all kinds of aorta diseases. And traditional treatment was open surgery with total arch replacement by elephant trunk. Here, we report a case of PAU combined with ILVA managed by thoracic endovascular aortic repair (TEVAR) technique. PATIENT CONCERNS: A 65-year-old male with chronic hypertension and Nicotine abuse underwent intermittent back pain for 2 years and aggravated a bit for 1 week. DIAGNOSES: Preoperative computed tomography angiogram (CTA) indicated PAU combined with ILVA. INTERVENTIONS: TEVAR was performed for PAU following with retrograde in situ fenestration and chimney technique for revascularization of ILVA and left subclavian artery (LSA), respectively. OUTCOMES: The operation was successfully and the patient was discharged from hospital after 1 week of treatment. Postoperatively, the images of CTA illustrated the patency of aorta, ILVA, and LSA without obvious endoleak. Besides, no ischemia attack or other relative syndromes were detected at 6-months follow-up. LESSONS: This case demonstrates that TEVAR is an alternative to elephant trunk especially for PAU with ILVA. And it also showed the precise exposure of ILVA and necessity to reconstruct ILVA during TEVAR operation in order to reduce the occurrence of ischemia attack.