Thrombosis pathogenesis is closely linked to dysregulated lipid metabolism and inflammatory processes. However, the direct regulatory role of mevalonate pathway within the coagulation cascade is still not well understood. This study aimed to elucidate the regulatory effects of mevalonic acid (MVA) on the coagulation system. The effects of MVA on coagulation were measured by recalcification. Enzymatic kinetic analysis and natural substrate hydrolysis assays were performed to identify the coagulation target of MVA. Mice bleeding and thrombosis models were applied to evaluate the effects of MVA administration on hemostasis and thrombosis. Our current study reveals that MVA significantly accelerates plasma coagulation through potentiating the procoagulant activity of FXa, without influencing the platelet aggregation. Studies showed that MVA administration substantially shortened activated partial thromboplastin time, prothrombin time, and reduced bleeding time in both tail bleeding and saphenous vein injury models. Furthermore, using ferric chloride-induced thrombosis, deep vein thrombosis and cerebral infarction models, we observed that MVA markedly potentiated thrombus formation and stroke. Our findings establish for the first time that MVA directly regulates FXa procoagulant activity, while also suggesting potential crosstalk between lipid metabolic pathways and inflammatory signaling in coagulation modulation. These results provide novel mechanistic insights into coagulation abnormalities associated with metabolic disorders such as atherosclerosis and diabetes, highlighting the mevalonate pathway as a potential therapeutic target for thrombotic complications.

The complex interplay between inflammation and coagulation drives thromboinflammatory disorders. While previous studies have shown that interleukin-1β (IL-1β) can induce a hypercoagulable state in response to tissue hypoxia and inflammation, the specific mechanisms of its action on the coagulation cascade remain unclear. Here, we demonstrate that IL-1β directly potentiates key coagulation factors (FXIa, FXa, thrombin, and kallikrein) to accelerate thrombosis. Mechanistically, IL-1β enhances FXIa enzymatic activity through specific binding to its exosite domain. Additionally, we established an IL-1β-FXIa interaction model, based on which the inhibitory peptide QK10 was derived to specifically disrupt their interaction interface and effectively block IL-1β’s potentiation of FXIa. Critically, in multiple thrombosis models, QK10 exhibited significant antithrombotic efficacy at doses equal to low molecular weight heparin (LMWH). Notably, bleeding assays revealed a significantly lower bleeding risk with QK10 compared to LMWH. Notably, QK10 also demonstrated promising anti-stroke efficacy in ischemic stroke models. Taken together, these findings establish QK10 as a viable therapeutic candidate that targets the IL-1β-FXIa prothrombotic axis for disruption, features enhanced safety, and offers a new approach to treating thrombo-inflammatory conditions, including ischemic stroke.

Background: Inflammation is crucial in regulating coagulation and hemostasis. While prior research shows that apolipoprotein A-IV (ApoA-IV) has anti-inflammatory and antiplatelet effects, its specific impact on coagulation remains unclear. Objectives: To investigate the effects of ApoA-IV on the coagulation system, including its interactions with potential targets and the underlying mechanisms. Methods: Plasma ApoA-IV levels in deep vein thrombosis patients were tested by enzyme-linked immunosorbent assay. The effects of ApoA-IV on coagulation were assessed through thromboelastography. Potential interactions and mechanisms were analyzed using surface plasmon resonance and AlphaFold 3. Mice bleeding and stroke models were employed to evaluate the effects on hemostasis and thrombosis. Results: ApoA-IV levels were reduced in deep vein thrombosis patients and correlated with increased thrombotic risk. Thromboelastography showed that ApoA-IV treatment delayed clot reaction and kinetic times while decreasing thrombus generation angle and maximum amplitude, highlighting its crucial role in inhibiting coagulation and platelet aggregation. We identified ApoA-IV as a functional activator of activated protein C (APC), with critical interactions occurring at residues 144 to 148 within the exosite loop of the APC protease domain. In animal models, anti-ApoA-IV antibody administration shortened bleeding time but exacerbated ischemic stroke outcomes. Notably, inhibitory peptide HE5, which inhibits ApoA-IV-APC interaction, effectively counteracted the anticoagulant activity of ApoA-IV. Conclusion: These findings establish ApoA-IV as a pivotal regulator of coagulation and hemostasis, primarily through enhancing APC activity. This research advances our understanding of the interplay between inflammation, lipid metabolism, and thrombosis, offering insights for developing novel antithrombotic therapies.

Abstract Coagulation is related to inflammation, but the key pathway, especially innate immune system and coagulation regulation, is not well understood and need to be further explored. Here, we demonstrated that neutrophil gelatinase-associated lipocalin (NGAL), an innate immune inflammatory mediator, is upregulated in patients with thrombosis. Furthermore, it contributes to the initiation and amplification of coagulation, hemostasis, and thrombosis. This occurs by enhancing tissue factor expression on the cell surface, potentiating various clotting factors such as thrombin, kallikrein, factor XIa (FXIa), and FVIIa, promoting thrombin-induced platelet aggregation, and inhibiting antithrombin. NGAL knockout led to strikingly prolonged clot reaction time and kinetic time in thromboelastography analysis, along with reduced thrombus generation angle and lower thrombus maximum amplitude, which were in line with remarkably prolonged activated partial thromboplastin time and prothrombin time. In several mouse hemostasis and thrombosis models, NGAL overexpression or IV administration promoted coagulation and hemostasis and aggravated thrombosis, whereas NGAL knockout or treatment with anti-NGAL monoclonal antibody significantly prolonged bleeding time and alleviated thrombus formation. Notably, NGAL knockout prolonged mouse tail bleeding time or artery occlusion time to over 40 or 60 minutes, respectively, resembling uncontrollable bleeding and clotting disorder seen in hemophilic mice. Furthermore, anti-NGAL monoclonal antibody treatment markedly reduced the formation of blood clots in inflammation-induced thrombosis models. Collectively, these findings unveil a previously unidentified role of NGAL in the processes of coagulation, hemostasis, and thrombosis, as well as the cross talk between innate immunity, inflammation, and coagulation. Thus, modulating NGAL levels could potentially help balance thrombotic and hemorrhagic risks.

Succinate dehydrogenase (SDH)-deficient renal cell carcinoma (RCC) is a rare subtype of RCC classified as a molecularly defined RCC in the fifth edition of the WHO. Most gene alterations in patients with SDH-deficient RCC involve the SDHB subunit, with less involvement of the SDHC, SDHA, and SDHD subunits. Four cases of SDHA-deficient RCC have been reported in the literature, of which one case was associated with an NF2 gene mutation. Herein, we report six novel SDHA-deficient RCC cases, including two cases with NF2 gene mutations. In contrast to the typical morphology of SDH-deficient RCC, the six tumors mainly displayed glandular, sheet-like, or papillary growth patterns with prominent nucleoli (Grades 2-3), among which two cases with NF2 mutations had prominent nucleoli (Grade 3), large transparent vacuoles in the cytoplasm, and a large number of lymphocytes in the stroma. Six tumors showed negative immunohistochemical staining for SDHA and SDHB, and three cases presented with high expression of PD-L1. Second-generation sequencing revealed novel pathogenic somatic SDHA gene mutation and NF2 gene mutations in six and two tumors, respectively. Follow-up data were collected for the six patients with a follow-up time ranging from 7 to 268 months, and all six patients have survived to date. One patient received targeted therapy for tumor metastasis to the lungs after seven months, and another patient with an NF2 gene mutation received immunotherapy for lymph node metastasis revealed during surgery. SDHA-deficient RCCs with NF2 gene mutations have the ability to metastasize but might respond well to immunotherapy. For the first time, we report the largest number of SDHA-deficient RCC cases and comprehensively investigate their clinicopathological and molecular features to provide important guidance for diagnosis and clinical immunotherapy.

Coagulation is related to inflammation, but the key pathways, especially innate immunity inflammatory response-coagulation, hemostasis, and thrombosis regulation is poorly understood and need to be further explored. In the current study, we showed that innate immunity inflammatory mediator neutrophil gelatinase-associated apolipoprotein (NGAL) which was upregulated in plasma of deep vein thrombosis patients interacted with and potentiated thrombin, kallikrein, FXIa, and FVIIa and suppressed antithrombin to induce coagulation, hemostasis, and thrombosis. Furthermore, NGAL can augment thrombin-induced platelet aggregation. In multiple mice hemostasis and thrombosis models, NGAL overexpression or intravenous administration promoted coagulation and hemostasis and aggravated thrombus, whereas NGAL knockout or treatment with anti-NGAL monoclonal antibody significantly prolonged bleeding time and alleviated thrombus formation. Notably, NGAL knockout prolonged both mice tail bleeding time and artery occlusion time to over 40 min, resembling uncontrollable bleeding and clotting disorder seen in Hemophilia mice. Furthermore, anti-NGAL monoclonal antibody treatment markedly reduced the formation of blood clots in a mouse-tail thrombosis model induced by carrageenan, which is linked to inflammation. Collectively, these findings suggest NGAL is a crucial coagulation regulator and mediates the crosstalk between innate immunity inflammation and coagulation, hemostasis, and thrombus, and provide new target and strategy for the development of innovative antithrombotic drugs.### Competing Interest StatementThe authors have declared no competing interest.

1 临床资料 患者男,58 岁,突发腹痛伴双下肢截瘫10 h,来院急诊就诊.既往风湿性心脏病伴心房颤动病史30 年, 未抗凝治疗;2 d 前于当地医院行心脏超声检查示左心房内血栓,单纯给予口服华法林,未桥接其他抗凝药物治疗.

Abdominal aortic aneurysm (AAA) is a common and serious disease with a high mortality rate, but its genetic determinants have not been fully identified. In this feasibility study, we aimed to elucidate the transcriptome profile of AAA and further reveal its molecular mechanisms through the Oxford Nanopore Technologies (ONT) MinION platform. Overall, 9574 novel transcripts and 781 genes were identified by comparing and analysing the redundant-removed transcripts of all samples with known reference genome annotations. We characterized the alternative splicing, alternative polyadenylation events and simple sequence repeat (SSR) loci information based on full-length transcriptome data, which would help us further understand the genome annotation and gene structure of AAA. Moreover, we proved that ONT methods were suitable for the identification of lncRNAs via identifying the comprehensive expression profile of lncRNAs in AAA. The results of differentially expressed transcript (DET) analysis showed that a total of 7044 transcripts were differentially expressed, of which 4278 were upregulated and 2766 were downregulated among two groups. In the KEGG analysis, 4071 annotated DETs were involved in human diseases, organismal systems and environmental information processing. These pilot findings might provide novel insights into the pathogenesis of AAA and provide new ideas for the optimization of personalized treatment of AAA, which is worthy of further study in subsequent studies.

Background: This study evaluated aortic remodeling in highly tapered type B aortic dissection (TBAD) patients who underwent thoracic endovascular aortic repair (TEVAR) with a proximal tapered stent graft plus a distal restrictive stent graft to maximize thoracic coverage while avoiding distal excessive oversizing. Methods: Thirty-four patients presenting with highly tapered TABD were randomized to restricted TEVAR (r-TEVAR) and standard TEVAR groups. Highly tapered TBAD was defined as the maximal diameter of the true lumen at proximal and distal thoracic aorta landing zone tapers greater than 8 mm or taper ratio greater than 20%. Patients in the r-TEVAR group underwent proximal tapered stent grafts plus distal restrictive stent grafts, to match the taper ratio of the descending thoracic aorta (DTA) and extend the length of stent coverage. Patients in the standard TEVAR group underwent proximal tapered stent grafts implantation without distal restrictive stent grafts. Aortic remodeling was estimated by computed tomography angiography (CTA) during the follow-up. Results: In total, 16 patients underwent r-TEVAR, and 18 patients underwent standard TEVAR. The taper ratio of the stent graft matched the DTA in the r-TEVAR group (24.7 +/- 3.4% vs. 27.3 +/- 4.2%, P = 0.068), but did not match that in the standard TEVAR group (13.5 +/- 3.3% vs. 30.5 +/- 9.6%, P < 0.001). The length of stent graft coverage in the r-TEVAR group was longer than that in the standard TEVAR group (220.4 +/- 21.1 mm vs. 175.3 +/- 17.8 mm, P < 0.001). Compared with the standard TEVAR group, the r-TEVAR group had better complete remodeling of the DTA at 6 months (40% vs. 5.6%, P = 0.03), 12 months (60% vs. 16.7%, P = 0.027), and 24 months (78.6% vs. 41.2%, P = 0.036) after the operation. There was no difference in the cumulative survival rate between the r-TEVAR and standard TEVAR groups (P = 0.166). Conclusions: The r-TEVAR with overlapping proximal tapered stent grafts and distal restrictive stent grafts can match the taper of highly tapered TABD, extend the length of stent graft coverage, and lead to better remodeling of the DTA than standard TEVAR.

Abstract Background: For patients without arteriovenous fistula and with dysfunctional central veins caused by long indwelling tunnel-cuffed catheter (TCC), no consensus on how to achieve functional hemodialysis access has been reached. This study investigated the value of percutaneous transluminal angioplasty (PTA) of a dysfunctional central vein caused by a TCC under digital subtraction angiography (DSA) guidance. Methods: In total, thirteen patients with indwellingTCC-related complications were admitted to our institution. The TCC indwelling duration was 35.2 months (range, 6 to 70 months). The failed TCCs were removed under the support of a stiff guide wire,and an angiogram showed central vein stenosis (CVS) or occlusion. PTA was performed to recanalize the central vein, and new TCCs were placed in situ or in another central vein under DSA guidance. Results: TCCs were successfully removed in twelve patients. TCC removal failed in one patient due to severe adhesion of the TCC and the left innominate vein 4 years after implantation. PTA of central veins, including the right internal jugular vein, innominate vein, superior vena cava, and right iliac vein, was performed, and new TCCs were successfully placed in all patients. No stents were implanted in any patients. The mean follow-up was 12.9 months (range, 3 to 36 months). The new TCCs functioned well in all patients. Conclusions: Under DSA guidance, recanalization of TCC-related CVS or occlusion by PTA and implantation of anew TCC catheter in situor another central vein can establish dialysis access for patients with poorly functioning TCCs successfully.

Objectives: Endoleaks may be present in up to 25% of patients after endovascular abdominal aortic aneurysm repair (EVAR) and there is no clear consensus on valuable biomarkers to determine endoleak presence. The aim of this study was to examine the potential value of plasma tumor necrosis factor-alpha converting enzyme (TACE) and Notch1 concentrations in determining endoleak presence after EVAR. Methods: A total of 110 patients with abdominal aortic aneurysm who underwent EVAR were enrolled in our study, and plasma TACE and Notch1 concentrations were measured prior to and 6 months after EVAR. Logistic regression was performed to assess the association of postoperative plasma TACE and Notch1 concentrations with endoleak after adjusting for potential confounders. The ability of plasma TACE and Notch1 concentrations to determine endoleak presence was assessed using receiver operating characteristic curves and area under the curve (AUC). Results: Twenty-four patients developed endoleaks 6 months after EVAR. Both postoperative plasma TACE and Notch1 concentrations were higher in patients with endoleak than in those without endoleak (2376.4 +/- 28.1 pg/ml vs. 2094.1 +/- 27.3 pg/ml, P < 0.01; 218.6 +/- 1.9 pg/ml vs. 195.0 +/- 2.1 pg/ml, P < 0.01, respectively). The AUCs from receiver operating characteristic curve analysis of plasma TACE and Notch1 concentrations in determining endoleak presence were 0.844 (95% CI 0.771 to 0.918, P < 0.01) and 0.860 (95% CI 0.791 to 0.930, P < 0.01), respectively. Combining the detection of plasma Notch1 and TACE concentrations could improve the accuracy in determining endoleak presence (AUC 0.930, 95% CI 0.883 to 0.978, P < 0.01). The predicted probability cutoff of 0.22 yielded a sensitivity of 95.8% and a specificity of 82.6% for endoleak presence. Conclusions: Plasma TACE and Notch1 levels can discriminate patients with and without endoleak 6 months after EVAR, and have a potential role in screening patients requiring computed tomography angiography.

Clear cell renal cell carcinoma (CCRCC) with sarcomatoid differentiation (CCRCCS) displays invasive behavior, poor prognosis, and poor therapeutic response. The present study was aimed to gain new insights into the molecular mechanisms of sarcomatoid transformation, and identify new prognostic and therapeutic targets for CCRCCS. Whole exome sequencing was performed on matched carcinomatous and sarcomatoid elements from five specimens with CCRCCS. A non‑synonymous single‑nucleotide polymorphism (SNP) of cadherin 23 (CDH23) was further studied through Sanger sequencing in expanded 40 specimens with CCRCCS and 50 specimens with CCRCC. Carcinomatous and sarcomatoid elements shared most somatic single‑nucleotide variants (SSNVs) as revealed through whole exome sequencing. Sarcomatoid element had higher overall SSNVs than carcinomatous element. A highly frequent mutation of CDH23 (rs3802711) was observed in CCRCCS that resulted in an alteration in the highly conserved calcium‑binding site in the three‑dimensional (3D) structure mediating the functions of cadherins. In the expanded 90 specimens, CDH23 SNP (rs3802711) was a highly frequent mutation in CCRCCS than that in all CCRCC samples and even high grade CCRCC. Cox multivariate analysis indicated that CDH23 (rs3802711) genotype was an independent prognostic factor affecting the overall survival of the cohort. CDH23 gene and protein were negatively or weakly expressed in most CCRCCS specimens with CDH23 mutation. The present study revealed, for the first time, that the CDH23 (rs3802711) was a highly genetic risk factor for CCRCCS. It was associated with the decreased expression of CDH23 protein, resulting in the absence of cadherin function of CDH23, indicating that the CDH23 mutation may be involved in the sarcomatoid transformation in CCRCCS. Collectively, a novel and specific SNP of CDH23 was identified in CCRCCS and a new candidate cadherin involved in EMT was revealed. Furthermore, a new prognostic evaluation factor and potential therapeutic target for CCRCCS was identified.

The aim of this meta‐analysis was to evaluate the mortality, amputation and complication rates in patients with peripheral lower limb arterial disease undergoing bypass surgery with or without a prior history of endovascular opera‐ tion. A systematic literature screen was performed according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines on four academic databases, Medline, Scopus, Embase and Cochrane Central Register of Controlled Trials. Out of 1,072 records, six articles involving 11,420 patients (mean age, 68.1±2.0 years) met the inclu‐ sion criteria. The findings presented a 2b level of evidence (i.e. overall evidence represents data from individual cohort study or low quality randomized controlled trials) and suggested lower mortality, amputation and complication rates for patients undergoing bypass surgery without any history of endovascular operation, compared with those with a history of prior endovascular operation. Moreover, a random‐effect meta‐analysis suggested a small, positive reduction in mortality (Hedge's g=0.08), amputation (Hedge's g=0.18) and complication rates (Hedge's g=0.05) for patients undergoing bypass surgery without any history of endovascular opera‐ tion. Nevertheless, owing to the scarcity of high‐quality data, further studies and randomized clinical trials are needed to confirm these effects.

The aim of this meta-analysis was to evaluate the mortality, amputation and complication rates in patients with peripheral lower limb arterial disease undergoing bypass surgery with or without a prior history of endovascular operation. A systematic literature screen was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines on four academic databases, Medline, Scopus, Embase and Cochrane Central Register of Controlled Trials. Out of 1,072 records, six articles involving 11,420 patients (mean age, 68.1±2.0 years) met the inclusion criteria. The findings presented a 2b level of evidence (i.e. overall evidence represents data from individual cohort study or low quality randomized controlled trials) and suggested lower mortality, amputation and complication rates for patients undergoing bypass surgery without any history of endovascular operation, compared with those with a history of prior endovascular operation. Moreover, a random-effect meta-analysis suggested a small, positive reduction in mortality (Hedge's g=0.08), amputation (Hedge's g=0.18) and complication rates (Hedge's g=0.05) for patients undergoing bypass surgery without any history of endovascular operation. Nevertheless, owing to the scarcity of high-quality data, further studies and randomized clinical trials are needed to confirm these effects.

Background: Migration of the iliac limb after endovascular abdominal aortic aneurysm repair (EVAR) can result in type 1 b and 3 endoleaks, which are relatively common causes of reintervention after EVAR. The aim of the present study was to investigate the factors influencing migration of the iliac limb and methods of treatment. Methods: From April 2012 to September 2017, 4 patients experienced migration of the iliac limb, requiring additional iliac stent graft implantation intraoperatively or at follow-up at our institute. Patient 1 was a 74-year-old man in whom preoperative computed tomography angiography (CTA) revealed a large aneurysm. The patient underwent EVAR with a bifurcated stent graft, and the left iliac stent graft migrated into the aneurysm sac. Patient 2 was a 53-year-old man in whom CTA revealed a large abdominal aortic aneurysm (AAA) involving the bilateral common iliac artery (CIA), with occlusion of the left hypogastric artery. An iliac stent graft was deployed to the right CIA to preserve the hypogastric artery. CTA, at 5 years of follow-up, showed migration of the right iliac limb and impending rupture. Patient 3 was a 61-year-old man with a ruptured AAA, and CTA revealed a large AAA and dilated CIA. The patient underwent EVAR with a bifurcated stent graft. Three years after EVAR, CTA showed that the right iliac limb migrated and kinked, with rupture of the stent graft. Patient 4 was an 80-year-old man with a ruptured AAA and aortocaval fistula. CTA revealed a large aneurysm involving the bilateral CIA. The patient underwent urgent EVAR with a bifurcated stent graft, and a cuff was deployed to seal the landing zone of the left CIA to preserve the hypogastric artery. Type 3 endoleak occurred because of the migration and detachment of the left iliac limb. All 4 patients underwent additional iliac stent graft implantation to connect or reline the iliac limb. Results: The mean diameter of the aneurysms was 85.3 +/- 18.9 mm, and 2 patients were diagnosed with ruptured AAAs. The mean diameter, length, and proportional engagement rate of the CIA that experienced migration of the iliac limb were 25.50 +/- 11.1 mm, 32.8 +/- 6.6 mm, and 72.75% +/- 17.88%, respectively. Oversizing of the iliac stent graft was 10-20% in 2 patients and was less than 10% in the other 2 patients. The migrated iliac limbs were bell-bottom stent grafts. All patients underwent additional iliac stent graft implantation successfully, and there were no deaths or complications perioperatively. The patients were followed up from 7 months to 3 years and remained in good condition. Conclusions: Migration of the iliac limb after EVAR was influenced by a complex combination of several factors including a large aneurysm (>60 mm in diameter), dilated or aneurysmal CIA (>18 mm in diameter), short length of fixation (<70%), lower degree of iliac limb oversizing (<10-20%), and bell-bottom of the iliac limb. Patients with these factors require more vigorous surveillance after EVAR. The implantation of an additional stent graft is effective and is the most common reintervention procedure.

Xp11.2 translocation/TFE3 rearrangement-associated renal cell carcinoma (RCC) and Xp11 translocation renal mesenchymal tumor are distinct tumor entity. To broaden the spectrum of Xp11 neoplasms, we investigated a novel tumor exhibiting morphologies overlapping Xp11.2 translocation/TFE3 rearrangement-associated RCC and the mesenchymal counterpart with melanocytic differentiation by immunohistochemistry, fluorescence in situ hybridization (FISH) and RNA sequencing, as well as literature review. Histologically, the tumor was composed of three different types of tumor cells, including a large proportion of clear cells, small round cells, and a few spindle cells, presenting a relatively clear border in the majority area. The nuclei of all tumor cells showed extensively and strong positive expressions of TFE3. Whereas, the clear cells positively expressed the RCC-related markers including PAX8, RCC marker and CD10, and negatively expressed HMB45; On the contrary, the small round cells and spindle cells positively expressed melanocytic marker HMB45, and negatively expressed PAX8, RCC marker and CD10. The ki67 index was higher in the small round cells and spindle cells than that in the clear cells. FISH revealed the rearrangement of TFE3 gene in all the three types of cells. The NONO-TFE3 fusion gene was detected in all tumor cells by RNA sequencing. This unique Xp11 translocation-associated neoplasm might represent a distinct entity overlapping Xp11 translocation RCC and the mesenchymal counterpart with melanocytic differentiation, broadening the spectrum of Xp11 neoplasms. The patient died of tumor recurrence and lung metastasis after seven months after the surgery suggesting those tumors have an unfavorable prognosis.

OBJECTIVESCervical aortic arch with aneurysm formation is considered an extremely rare condition. Here, we summarize our experience in treating 8 patients. We validated extra-anatomic ascending-to-infrarenal abdominal aorta bypass through the retroperitoneal cavity without circulatory arrest as an alternative treatment for patients with a tortuous arch that was unsuitable for endovascular repair.METHODSFrom March 2015 to April 2018, 8 patients (7 women; median age 46 years) diagnosed with cervical aortic arch complicated with aneurysm formation were treated at Peking Union Medical College Hospital and the Affiliated Hospital of Qingdao University. After assessment of the anatomical characteristics, 4 patients underwent endovascular repair. Three patients with a tortuous aortic arch and saccular aneurysm formation between the left common carotid artery and the left subclavian artery were treated with an extra-anatomic ascending-to-infrarenal abdominal aorta bypass and aneurysm indwelling. One patient refused surgical intervention and is being followed up on a yearly basis at our outpatient clinic. No circulatory arrest was required during surgery.RESULTSNo severe postoperative complications were observed during follow-up (6-36 months). Postoperative computed tomography angiography revealed patent blood flow in the prosthetic aortic graft bypass. No endoleak, migration or stenosis of the stent grafts was observed in patients following endovascular repair. The left subclavian artery was preserved in 3 patients. Follow-up computed tomography angiography revealed satisfactory postoperative results in all patients, with no signs of aortic dilation or coarctation.CONCLUSIONSAscending-to-infrarenal abdominal aorta bypass through the retroperitoneal cavity is a safe and effective treatment for cervical aortic arch with a tortuous aorta complicated by aneurysm formation and coarctation.

Background: Persistent sciatic artery is a rare embryological vascular anomaly, with an incidence of 0.01%–0.05%. Up to 60% of persistent sciatic artery patients will develop aneurysms that can subsequently lead to distal embolization and a high risk of limb loss. Method: Here we report a case with acute limb ischemia caused by thrombus in a right persistent sciatic artery aneurysm. The patient underwent endovascular treatment by deploying a 10 × 150 mm stent graft (Viabahn) in the persistent sciatic artery and two self-expanding bare stents (10 × 40 mm, 10 × 60 mm, SMART) in the stent graft to reinforce the radial resistive force. In addition, we conducted a literature review of articles published in PubMed from 2001 to 2018 regarding stent graft repair of complete persistent sciatic artery aneurysms. A total of 13 articles reported 13 patients with complete persistent sciatic artery aneurysms who underwent endovascular stent graft repair. Result: A favorable result was obtained for this patient, and computed tomographic angiography at 6 months of follow-up revealed patent stent graft. Most articles reported favorable results. Conclusion: Favorable results can be achieved with endovascular stent graft repair and anticoagulation therapy for complete persistent sciatic artery aneurysms.

目的 了解紫杉醇药物涂层球囊(BCD)治疗下肢动脉粥样硬化性闭塞症的安全性和有效性.方法 对股腘动脉腔内治疗69例病人的临床资料进行回顾性分析,其中应用紫杉醇DCB病人30例(30条患肢),应用经皮腔内血管成形术(PTA)+支架成形病人39例(39条患肢),卢瑟福分级均为3～5级.术后6个月进行随访,观察两组病人踝臂指数(ABI)变化、靶病变血管再狭窄率、卢瑟福分级变化、跛行距离、治疗侧下肢是否截肢,以及围手术期、随访期间病人死亡情况.结果 术后6个月,两组病人ABI均较术前升高,差异有统计学意义(t=4.305、14.175,P＜0.05);两组手术前后ABI差值比较,差异无统计学意义(P＞0.05).两组治疗前后跛行距离差值比较差异有统计学意义(t=15.977,P＜0.05).两组病人卢瑟福分级均不同程度提高,围手术期、随访期间无截肢病人、无病人死亡.靶病变血管再狭窄DCB组3例,PTA+支架成形组5例.结论 紫杉醇DCB治疗下肢动脉粥样硬化性闭塞症安全、有效.