Metformin Therapeutic Targets for Aortic Aneurysms: A Mendelian Randomization and Colocalization Study.

Background: Identifying effective pharmacological interventions to prevent the progressive enlargement and rupture of aortic aneurysms (AAs) is critical. Previous studies have suggested links between metformin use and a decreased incidence of AAs. In this study, we employed Mendelian randomization (MR) to investigate causal effects of metformin's targets on AA risk and to explore the underlying mechanisms underlying these effects. Methods: To examine the relationship between metformin use and AA risk, we implemented both two-sample MR and multivariable MR analyses. Utilizing genetic instrumental variables, we retrieved cis-expression quantitative trait loci (cis-eQTL) data for potential targets of metformin from the Expression Quantitative Trait Loci Genetics Consortium (eQTLGen) Consortium and Genotype-Tissue Expression (GTEx) project. Colocalization analysis was employed to ascertain the probability of shared causal genetic variants between single nucleotide polymorphisms (SNPs) associated with eQTLs and AA. Results: Our findings reveal that metformin use reduces AA risk, exhibiting a protective effect with an odds ratio (OR) of 4.88 × 10 - 3 (95% confidence interval [CI]: 7.30 × 10 - 5 -0.33, p = 0.01). Furthermore, the protective effect of type 2 diabetes on AA risk appears to be driven by metformin use ( OR MVMR = 1.34 × 10 - 4 , 95% CI: 3.97 × 10 - 8 -0.45, p = 0.03). Significant Mendelian randomization (MR) results were observed for the expression of two metformin-related genes in the bloodstream: NADH:ubiquinone oxidoreductase subunit A6 (NDUFA6) and cytochrome b5 type B (CYB5B), across two independent datasets ( OR CYB5B = 1.35, 95% CI: 1.20-1.51, p = 2.41 × 10 - 7 ; OR NDUFA6 = 1.12; 95% CI: 1.07-1.17, p = 1.69 × 10 - 6 ). The MR analysis of tissue-specific expression also demonstrated a positive correlation between increased NDUFA6 expression and heightened AA risk. Lastly, NDUFA6 exhibited evidence of colocalization with AA. Conclusions: Our study suggests that metformin may play a significant role in lowering the risk of AA. This protective effect could potentially be linked to the mitigation of mitochondrial and immune dysfunction. Overall, NDUFA6 has emerged as a potential mechanism through which metformin intervention may confer AA protection.

Efficacy and safety of mechanochemical ablation versus laser ablation in the treatment of primary great saphenous vein reflux: A randomized, open, parallel controlled clinical trial.

OBJECTIVE: To evaluate the efficacy of a new mechanochemical ablation (MOCA) device versus endovenous laser ablation (EVLA) for primary great saphenous vein (GSV) reflux. MATERIALS AND METHODS: Prospectively analyze the demographics, treatment detail and outcomes data of 57 primary GSV reflux patients. Patients were randomly assigned to MOCA or EVLA group with random envelope method. Primary endpoint was 6-month closure rate of GSV. Secondary endpoint including technical success rate, the venous clinical severity score (VCSS), chronic venous insufficiency questionnaire (CIVIQ-20) score and visual analogue scale (VAS) for pain. RESULTS: The procedures were well tolerated according to the VAS score. The 6-month closure rate was 85.71% in MOCA and 96.55% in EVLA group (p = .194). Significant changes were observed in regard of VCSS and CIVIQ-20 score at 6-month follow-up. Skin paresthesia occurred in 0 in MOCA and 5 in EVLA group. CONCLUSION: The new MOCA device is safe and effective in treating primary great saphenous vein reflux. The 6-month closure rate is non-inferior compared with EVLA. However, the long-term results need further follow-up.

Hyperuricemia promotes the progression of atherosclerosis by activating endothelial cell pyroptosis via the ROS/NLRP3 pathway.

Hyperuricemia closely correlates with the development of atherosclerosis, but little is known of the mechanism by which atherosclerosis progression occurs in hyperuricemia. Atherosclerosis appears to involve pyroptosis, an emerging mechanism of proinflammatory regulated cell death. This study tested the hypothesis that pyroptosis underlies the relationship between hyperuricemia and atherosclerosis, using ApoE-/- mice (a model of atherosclerosis), human umbilical vein endothelial cells (HUVECs), and human atherosclerotic arterial samples. We found that hyperuricemia can aggravate the aortic atherosclerotic plaque-load in ApoE-/- mice and promote endothelial cell pyroptosis. Additionally, hyperuricemia can increase the levels of serum inflammatory factors (including IL-1ß and IL-18). Exposure to lipopolysaccharide plus a high concentration of soluble uric acid (≥12 mg/dL) induced cell pyroptosis in HUVECs, as evidenced by increased expression of pyroptosis-related proteins and elevated release of lactate dehydrogenase (a marker of tissue damage). Further, MCC950, a selective nucleotide-binding oligomerization domain (NOD)-like receptor 3 (NLRP3) inflammasome inhibitor, and N-acetyl- l-cysteine, an antioxidant, attenuated HUVEC pyroptosis by inhibiting activation of the NLRP3 inflammasome and production of intracellular reactive oxygen species (ROS). Finally, we detected significantly higher expression of pyroptosis-associated proteins in carotid specimens from patients with hyperuricemia. Collectively, our findings suggest that hyperuricemia can aggravate endothelial cell pyroptosis in aortic atherosclerotic plaques, promoting the development of atherosclerosis. Additionally, a high concentration of soluble uric acid can trigger the activation stage of the NLRP3 inflammasome, mediating endothelial cell pyroptosis, and this process is regulated by the cellular ROS level.

Radiomics Signature of Epicardial Adipose Tissue for Predicting Postoperative Atrial Fibrillation after Off-Pump Coronary Artery Bypass Surgery.

Background: Postoperative new atrial fibrillation (POAF) is a commonly observed complication after off-pump coronary artery bypass surgery (OPCABG), and models based on radiomics features of epicardial adipose tissue (EAT) on non-enhanced computer tomography (CT) to predict the occurrence of POAF after OPCABG remains unclear. This study aims to establish and validate models based on radiomics signature to predict POAF after OPCABG. Methods: Clinical characteristics, radiomics signature and features of non-enhanced CT images of 96 patients who underwent OPCABG were collected. The participants were divided into a training and a validation cohort randomly, with a ratio of 7:3. Clinical characteristics and EAT CT features with statistical significance in the multivariate logistic regression analysis were utilized to build the clinical model. The least absolute shrinkage and selection operator (LASSO) algorithm was used to identify significant radiomics features to establish the radiomics model. The combined model was constructed by integrating the clinical and radiomics models. Results: The area under the curve (AUC) of the clinical model in the training and validation cohorts were 0.761 (95% CI: 0.634-0.888) and 0.797 (95% CI: 0.587-1.000), respectively. The radiomics model showed better discrimination ability than the clinical model, with AUC of 0.884 (95% CI: 0.806-0.961) and 0.891 (95% CI: 0.772-1.000) respectively for the training and the validation cohort. The combined model performed best and exhibited the best predictive ability among the three models, with AUC of 0.922 (95% CI: 0.853-0.990) in the training cohort and 0.913 (95% CI: 0.798-1.000) in the validation cohort. The calibration curve demonstrated strong concordance between the predicted and actual observations in both cohorts. Furthermore, the Hosmer-Lemeshow test yielded p value of 0.241 and 0.277 for the training and validation cohorts, respectively, indicating satisfactory calibration. Conclusions: The superior performance of the combined model suggests that integrating of clinical characteristics, radiomics signature and features on non-enhanced CT images of EAT may enhance the accuracy of predicting POAF after OPCABG.

Inhibition of mitochondrial fission alters neo-intimal hyperplasia via PI3K/Akt signaling in arteriovenous fistulas.

BACKGROUND/OBJECTIVE: Arteriovenous fistulas (AVFs) are the preferred vascular access for hemodialysis of patients with end-stage renal disease. However, there is a high incidence of AVF failures caused by insufficient outward remodeling or venous neo-intimal hyperplasia formation. Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play an important role in many cardiovascular diseases. Abnormal VSMC proliferation and migration could be abolished by inhibition of mitochondrial division. METHOD: We found that abnormal proliferation and migration of VSMCs and increased mitochondrial fission were associated with AVF stenosis in patients. We also investigated the mechanisms, particularly the role of mitochondrial dynamics, underlying these VSMC behaviors. In vitro, we observed that inhibition of mitochondrial fission and Akt phosphorylation can diminish proliferation and migration of VSMCs induced by platelet-derived growth factor-BB (PDGF-BB). In vivo, daily intraperitoneal injections of mitochondrial division inhibitor 1 (Mdivi-1) decreased VSMC proliferation and reduced AVF wall thickness in a rat AVF model. CONCLUSION AND RESULT: Our results suggest that inhibition of mitochondrial fission improves AVF patency by reducing wall thickening through the PI3K/Akt signaling pathway. Therefore, inhibition of mitochondrial fission has the clinical potential to improve AVF patency.

WNT5B promotes vascular smooth muscle cell dedifferentiation via mitochondrial dynamics regulation in chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by proliferative vascular remodeling. Abnormal vascular smooth muscle cell (VSMC) phenotype switching is crucial to this process, highlighting the need for VSMC metabolic changes to cover cellular energy demand in CTEPH. We report that elevated Wnt family member 5B (WNT5B) expression is associated with vascular remodeling and promotes VSMC phenotype switching via mitochondrial dynamics regulation in CTEPH. Using primary culture of pulmonary artery smooth muscle cells, we show that high WNT5B expression activates VSMC proliferation and migration and results in mitochondrial fission via noncanonical Wnt signaling in CTEPH. Abnormal VSMC proliferation and migration were abolished by mitochondrial division inhibitor 1, an inhibitor of mitochondrial fission. Secreted frizzled-related protein 2, a soluble scavenger of Wnt signaling, attenuates VSMC proliferation and migration by accelerating mitochondrial fusion. These findings indicate that WNT5B is an essential regulator of mitochondrial dynamics, contributing to VSMC phenotype switching in CTEPH.

Efficacy, Safety, and Cost-Effectiveness of Intracavitary Electrocardiography-Guided Catheter Tip Placement for Totally Implantable Venous Access Port.

OBJECTIVE: Intracavitary electrocardiography (IC-ECG) has been extensively used for locating the catheter tip of the central venous access devices (CVADs) with favorable safety and accuracy. We aimed to evaluate the efficacy, safety, and cost-effectiveness of IC-ECG-guided catheter tip placement for totally implantable venous access port (TIVAP) by comparing with the standard fluoroscopy method. METHODS: A total of 231 patients who underwent TIVAP implantation from September 2019 to April 2021 were enrolled in the retrospective study. Fluoroscopy and IC-ECG were conducted intraoperatively to confirm the position of catheter tips. Demographic characteristics, surgical data, the catheter tip position, complication rate, and incidence, cost of procedures, and indwelling time were compared between the two groups. Univariate and multivariate analyses were used to identify the risk factors of TIVAP-related complications. RESULTS: There was no significance between the fluoroscopy group and the IC-ECG group in terms of the rate of ideal position (P = 0.733). Nine patients (3.9%) developed TIVAP-related complications. Complication rates and incidence were similar in the fluoroscopy group and the IC-ECG group (3.1% and 0.114/1000 catheter days vs. 4.4% and 0.105/1000 catheter days). The Kaplan-Meier curve showed that there was no significant difference in indwelling time between the 2 groups (Log Rank P = 0.634). Binary logistic regression analysis showed that body mass index (BMI) was an independent risk factor for TIVAP-related complications (OR = 1.334, 95%CI: 1.139 - 1.563, P < 0.001). The IC-ECG group was less costly than the fluoroscopy group (¥9928 ± 362 vs. ¥11762 ± 431, P < 0.001). CONCLUSIONS: IC-ECG-guided catheter tip placement for TIVAP is feasible, safe, and cost-effective, with high accuracy, low risk of complications, and lower cost. It may be considered as an alternative to the standard fluoroscopy method for catheter tip placement of TIVAP.

Preoperative pulmonary vascular resistance and neutrophil-to-lymphocyte ratio predict the demand of extracorporeal membrane oxygenation after pulmonary endarterectomy.

BACKGROUND: Acute respiratory and circulatory collapse might occasionally happen after pulmonary endarterectomy (PEA). We aimed to investigate the utilization of extracorporeal membrane oxygenation (ECMO) after PEA and potential risk factors. METHODS: Demographic characteristics, clinical and surgical data were collected for all patients who underwent PEA from December 2016 to June 2022. All factors were compared between patients in the ECMO group and those in the other group. The most characteristic risk factors were obtained by least absolute shrinkage and selection operator regression and support vector machine machine learning, and receiver operating characteristics (ROC) Curve analysis was performed to verify the diagnostic value of the obtained risk factors. RESULTS: A total of 117 patients underwent PEA, and 8 (6.8%) of them received ECMO treatment intraoperatively or postoperatively. There were significant differences between the two groups in terms of cardiac function, pulmonary vascular resistance (PVR), preoperative inflammation and cardiopulmonary bypass time. The PVR and neutrophil-to-lymphocyte ratio (N/L ratio) were the most characteristic risk factors with an area under the ROC curve of 0.847 (95% confidence interval [CI] = 0.7517-0.9420, p = .005) and 0.896 (95% CI = 0.803-0.989, p = .001), respectively. The ECMO group had higher PVR (1549.4 ± 600.7 vs. 952.9 ± 466.9 dyn.s.cm-5 , p = .004) and N/L ratio (6.3 ± 5.6 vs. 2.4 ± 1.7, p = .001). CONCLUSIONS: PVR and N/L ratio can correctly predict who is likely to receive ECMO treatment after PEA. Therefore, addressing the preoperative inflammatory status might be beneficial but further research is needed.

Duration of regional cerebral oxygen saturation under 40% is a risk factor for neurological injury following pulmonary thromboendarterectomy: A prospective observational study.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) is nowadays commonly used in pulmonary thromboendarterectomy (PTE). Neurological injury related to DHCA severely impairs the prognosis of patients. However, the risk factors and predictors of neurological injury are still unclear. METHODS: We conducted a prospective observational study, including 82 patients diagnosed as chronic thromboembolic pulmonary hypertension and underwent PTE alone in our center from December 2016 to May 2021. Demographic characteristics, clinical and surgical data, and neurological adverse events were recorded prospectively. Univariate and multivariate analyses were conducted to identify the predictors of neurological injury. RESULTS: Eleven (13.4%) patients exhibited neurological injuries after surgery. Univariate analysis showed that the duration of regional cerebral oxygen saturation (rSO2 ) under 40% (p < .001), the minimum rSO2 (p = .006), and the percentage of decrease in rSO2 (p = .011) were significantly associated with neurological injury. Multivariate analysis showed that the duration of rSO2 under 40% was an independent predictor for postoperative neurological injury (odds ratio = 3.896, 95% confidence interval: 1.812-8.377, p < .001). The receiver operating characteristic curve showed that when the cut-off value was 1.25 min, its sensitivity for predicting neurological injury was 63.6% with a specificity of 88.7%. CONCLUSIONS: The duration of rSO2 under 40% is an independent predictor for neurological injury following PTE. For complicated lesions, more times of circulatory arrest were much safer and more reliable than a prolonged time of a single circulatory arrest. The circulation should be restored as soon as possible, when the rSO2 under 40% is detected, rather than waiting for 5 min.

Resting heart rate as a preoperative predictor of postoperative atrial fibrillation after pulmonary thromboendarterectomy.

BACKGROUND: As a marker of the autonomic nervous system, resting heart rate is a predictor of postoperative atrial fibrillation (POAF). However, its predictive value for POAF after pulmonary thromboendarterectomy (PTE) has not been adequately studied. METHODS: We enrolled 97 patients who underwent PTE in our hospital from December 2016 to November 2021 in this retrospective study. Almost all preoperative characteristics, including electrocardiogram, demographics, hematologic and biochemical indices, echocardiography, and pulmonary hemodynamics, were compared between patients with and without POAF. Multivariate logistic regression analysis was used to identify the independent risk factors for POAF after PTE. RESULTS: Overall, 21 patients (21.6%) suffered from POAF after PTE. Compared with patients without POAF, those with POAF were older (p = .049), with a higher resting heart rate (p = .012), and higher platelet count (p = .040). In the binary logistic regression analysis, the resting heart rate (odds ratio [OR] = 1.043, 95% confidence interval [CI] = 1.009-1.078, p = .012) and age (OR = 1.051, 95% CI = 1.003-1.102, p = .037) were independent risk factors for POAF after PTE. The optimal cutoff point of resting heart rate was 89.5 with sensitivity and specificity of 47.6% and 77.6%. When the cutoff value of the age was 54.5, its sensitivity for predicting POAF was 71.4%, with a specificity of 59.2%. CONCLUSIONS: POAF is common after PTE surgery, and the incidence may be underestimated. The resting heart rate and age are independent preoperative risk factors for POAF after PTE. Considering the lower predictive power of the resting heart and age, further large-scale studies are needed.

Role of pyroptosis in atherosclerosis and its therapeutic implications.

Atherosclerosis is a significant cardiovascular burden and a leading cause of death worldwide, recognized as a chronic sterile inflammatory disease. Pyroptosis is a novel proinflammatory regulated cell death, characterized by cell swelling, plasma membrane bubbling, and robust release of proinflammatory cytokines (such as interleukin IL-1ß and IL-18). Mounting studies have addressed the crucial contribution of pyroptosis to atherosclerosis and clarified the candidate therapeutic agents targeting pyroptosis for atherosclerosis. Herein, we review the initial characterization of pyroptosis, the detailed mechanisms of pyroptosis, current evidence about pyroptosis and atherosclerosis, and potential therapeutic strategies that target pyroptosis in the development of atherosclerosis.

One-year outcomes of drug-coated balloon treatment for long femoropopliteal lesions: a multicentre cohort and real-world study.

BACKGROUND: Drug-coated balloons (DCBs) have shown superiority in the endovascular treatment of short femoropopliteal artery disease. Few studies have focused on outcomes in long lesions. This study aimed to evaluate the safety and effectiveness of Orchid® DCBs in long lesions over 1 year of follow-up. METHODS: This study is a multicentre cohort and real-world study. The patients had lesions longer than or equal to 150 mm of the femoropopliteal artery and were revascularized with DCBs. The primary endpoints were primary patency, freedom from clinically driven target lesion revascularization (TLR) at 12 months and major adverse events (all-cause death and major target limb amputation). The secondary endpoints were the changes in Rutherford classification and the ankle brachial index (ABI). RESULTS: One hundred fifteen lesions in 109 patients (mean age 67 ± 11 years, male proportion 71.6%) were included in this study. The mean lesion length was 252.3 ± 55.4 mm, and 78.3% of the lesions were chronic total occlusion (CTO). Primary patency by Kaplan-Meier estimation was 98.1% at 6 months and 82.1% at 12 months. The rate of freedom from TLR by Kaplan-Meier estimation was 88.4% through 12 months. There were no procedure- or device-related deaths through 12 months. The rate of all-cause death was 2.8%. Cox regression analysis suggested that renal failure and critical limb ischaemia (CLI) were statistically significant predictors of the primary patency endpoint. CONCLUSION: In our real-world study, DCBs were safe and effective when used in long femoropopliteal lesions, and the primary patency rate at 12 months by Kaplan-Meier estimation was 82.1%.

Drug-Coated Balloon versus Bare Nitinol Stent in Femoropopliteal Artery: 12 Months Outcome from a Single Center in China.

OBJECT: The study sought to compare the safety and effectiveness of drug-coated balloon (DCB) with bare nitinol stent in patients with complex femoropopliteal(FP) lesions in real-world practice. METHODS: Patients with symptomatic (Rutherford stage 2 to 5) femoropopliteal lesions who underwent DCB or bare nitinol stent implantation at the Department of Cardiovascular Surgery of China-Japan Friendship Hospital from June 2016 to September 2017 were included. Demographics, angiographic and procedural variables were included. Freedom from target lesion revascularization (TLR), primary patency and major adverse events were obtained from follow-up results at 3,6 and12 months. Descriptive analysis was performed on all variables. RESULTS: A total of 90 eligible patients were enrolled, which included 51 DCB subjects (mean age, 63.1 ± 13.2 years; 76.5% male) with 55 lesions and 39 nitinol stent subjects (mean age, 66.5 ± 10.5 years; 61.5% male) with 42 lesions. Significant higher primary patency was observed in the DCB group compared with the stent group (74.5% vs. 52.4%; log-rank test P = 0.018; HR 0.335, 95%CI 0.124-0.903, P = 0.031). The rates of freedom from TLR (f-TLR) were 78.2% and 59.5% (log-rank test P = 0.032) for the DCB group and the stent group, respectively, at 12 months. CD-TLR rates were 18.2% vs. 38.1% with a P-value of 0.023. Female sex (HR 6.122, 95%CI 1.880-19.934, P = 0.003), lesion length over 20 cm (HR 5.514, 95%CI 2.312-13.148, P < 0.001) and renal insufficiency (HR 2.609, 95%CI 1.087-6.260, P = 0.032) were suggested as independent risk factors of reducing primary patency. There were no significant differences in major adverse events between the 2 groups. CONCLUSION: The result above demonstrates that DCB treatment has higher primary patency and lower TLR at 12 months than nitinol stent. These data confirm the safety and effectiveness of the DCB for patients with complex femoropopliteal lesions.

LncRNA-RP11-714G18.1 suppresses vascular cell migration via directly targeting LRP2BP.

Atherosclerotic cardiovascular disease is considered as the leading cause of mortality and morbidity worldwide. Accumulating evidence supports an important role for long noncoding RNA (lncRNA) in the pathogenesis of atherosclerosis. Nevertheless, the role of lncRNA in atherosclerosis-associated vascular dysfunction and the underlying mechanism remain elusive. Here, using microarray analysis, we identified a novel lncRNA RP11-714G18.1 with significant reduced expression in human advanced atherosclerotic plaque tissues. We demonstrated in both human vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) that RP11-714G18.1 impaired cell migration, reduced the adhesion of ECs to monocytes, suppressed the neoangiogenesis, decreased apoptosis of VSMCs and promoted nitric oxide production. Mechanistically, RP11-714G18.1 could directly bind to its nearby gene LRP2BP and increased the expression of LRP2BP. Moreover, we showed that RP11-714G18.1 impaired cell migration through LRP2BP-mediated downregulation of matrix metalloproteinase (MMP)1 in both ECs and VSMCs. In atherosclerotic patients, the serum levels of LRP2BP were positively correlated with high-density lipoprotein cholesterol, but negatively correlated with cardiac troponin I. Our study suggests that RP11-714G18.1 may play an athero-protective role by inhibiting vascular cell migration via RP11-714G18.1/LRP2BP/MMP1 signaling pathway, and targeting the pathway may provide new therapeutic approaches for atherosclerosis.

A Systematic Review of Early Results Following Synchronous or Staged Carotid Artery Stenting and Coronary Artery Bypass Grafting.

Background The optimal management of patients with concomitant coronary artery disease (CAD) and severe carotid artery stenosis remains a controversy. We performed a systematic review of studies comparing early outcomes of synchronous or staged carotid artery stenting (CAS) and coronary artery bypass grafting (CABG) in the treatment of patients with concomitant CAD and severe carotid artery stenosis. Methods Multiple databases were systematically searched to identify studies of synchronous or staged CAS and CABG in the treatment of concomitant severe carotid and coronary artery disease published from 2005 to 2015. The quality of studies was assessed using the MINORS scale. The demographic data, risk factors, 30-day outcomes, and antiplatelet strategy were extracted. Results 23 studies were identified with a total of 873 and 459 patients in the staged and synchronous group, respectively. The observed overall death/stroke/MI rate was 8.5% (95% CI: 7.6-9.4%) in staged group and 4.8% (95% CI: 3.8-5.8%) in synchronous group. It seems that the synchronous group has better 30-day outcomes, but these data could not be compared statistically. Conclusion Our systematic review suggests either synchronous or staged CAS and CABG can be chosen for the treatment of concomitant carotid and coronary artery disease. It seems that the synchronous approach is relatively convenient and the antiplatelet strategy is relatively definite. For these patients, hybrid revascularization by synchronous CAS and CABG might be a feasible and promising therapeutic strategy. Our conclusions and the quality of the existing data suggest that a randomized controlled trial is needed to define the best treatment for patients with concomitant carotid and coronary artery disease.

Feasibility and Safety of Simultaneous Carotid Endarterectomy and Carotid Stenting for Bilateral Carotid Stenosis: A Single-Center Experience using a Hybrid Procedure.

BACKGROUND: The treatment for bilateral carotid stenosis (BCS) is challenging, and the optimal treatment strategy is not clear. We report our experience of treating 8 patients with BCS by simultaneous carotid endarterectomy (CEA) and carotid stenting (CAS), thereby providing an alternative for vascular surgeons. METHODS: Between October 2010 and August 2014, 8 patients (5 males and 3 females; range, 53-82 years; mean, 69 ± 8.8 years) underwent simultaneous CEA and CAS in our hospital. CEA before CAS was done in 5 patients, and CAS before CEA was done in 3 patients. One patient also underwent simultaneous coronary artery bypass grafting due to unstable angina. Intraoperative transcranial Doppler ultrasonography, carotid shunts, patches, and embolic protection devices were used in all patients. Instances of hyperperfusion syndrome (HPS), hemodynamic depression, stroke, myocardial infarction (MI), and death were recorded. RESULTS: All patients completed the procedure. One patient developed postprocedural HPS. After systemic treatment, he recovered completely. There were no deaths, major and/or minor strokes, or MI, nor did any patient exhibit lower palsy in cranial nerves in the perioperative period (<30 days) or on clinical follow-up (3 and 6 months). We observed no restenosis and no recurrent symptoms during follow-up. CONCLUSIONS: After careful preoperative assessment and preparation, simultaneous CEA and CAS for high-grade BCS may be considered as an alternative management strategy in carefully selected patients.

[Clinical outcomes of synchronous revascularization on patients concomitant carotid and coronary artery severe stenosis].

OBJECTIVE: To analyze the outcomes of synchronous revascularization for patients concomitant carotid and coronary artery severe stenosis. METHODS: From May 2012 to April 2014, 12 cases who received one-stage operation was retrospective analyzed, including the characteristics, methods of treatment, perioperative complications and health survey 30 days post procedure. Two subgroups were divided according to the different treatment methods on carotid artery, WIC and SF-36 scale were applied to compare the basic condition and recovery situation between 2 groups, the hospital stay time, costs, ventilation time, drainage and blood transfusion volume were also be compared. RESULTS: Totally 30 coronary vessels 8 carotid endarterectomy (CEA) and 5 carotid artery stenting (CAS) were performed on 12 patients. One patient also received coronary artery bypass grafting and bilateral carotid artery revascularization (CEA on right and CAS on left). Two (16.67%) minor stroke, 1 (8.33%) TIA, 1 wound infection occurred within 30 days post procedure, and 11 (91.67%) received blood component transfusion. No myocardial infarction and death occured. The average hospital stay time were (36.5 ± 25.3) days, ventilator application (37.5 ± 31.2) hours, postoperative drainage volume from pericardial and mediastinal was (347.92 ± 105.69) ml, infusion of concentrated red cell was 4.3 U. WIC was (5.57 ± 1.51) in CEA and (4.25 ± 1.50) in CAS subgroup, there was no significantly statistical difference (t = 1.40, P > 0.05). the results of SF-36 was (3.63 ± 1.76) and (5.44 ± 1.05) in CEA and CAS subgroup, there was no significantly statistical difference (t = -1.85, P > 0.05). In hospital stay time, ventilator application time, transfusion and drainage volume, hospitalization costs were also no significant statistical difference between two groups. CONCLUSIONS: The early outcome of synchronous revascularization on concomitant carotid and coronary severe stenosis disease is satisfactory. The clinical results are similar in the CEA and CAS subgroup.

New-onset postoperative atrial fibrillation after pulmonary endarterectomy is associated with adverse outcomes.

Background: New-onset postoperative atrial fibrillation (POAF) is a common complication after pulmonary thromboendarterectomy (PEA), yet the risk factors and their impact on prognosis remain poorly understood. This study aims to investigate the risk factors associated with new-onset POAF after PEA and elucidate its underlying connection with adverse postoperative outcomes. Methods: A retrospective analysis included 129 consecutive chronic thromboembolic pulmonary hypertension (CTEPH) patients and 16 sarcoma patients undergoing PEA. Univariate and multivariate analyses were conducted to examine the potential effects of preoperative and intraoperative variables on new-onset POAF following PEA. Propensity score matching (PSM) was then employed to adjust for confounding factors. Results: Binary logistic regression revealed that age (odds ratio [OR] = 1.041, 95% confidence interval [CI] = 1.008-1.075, p = 0.014) and left atrial diameter[LAD] (OR = 1.105, 95% CI = 1.025-1.191, p = 0.009) were independent risk factors for new-onset POAF after PEA. The receiver operating characteristic (ROC) curve indicated that the predictive abilities of age and LAD for new-onset POAF were 0.652 and 0.684, respectively. Patients with new-onset POAF, compared with those without, exhibited a higher incidence of adverse outcomes (in-hospital mortality, acute heart failure, acute kidney insufficiency, reperfusion pulmonary edema). Propensity score matching (PSM) analyses confirmed the results. Conclusion: Advanced age and LAD independently contribute to the risk of new-onset POAF after PEA. Patients with new-onset POAF are more prone to adverse outcomes. Therefore, heightened vigilance and careful monitoring of POAF after PEA are warranted.

Endovascular comprehensive treatment of post-traumatic superior mesenteric arteriovenous fistula: case report and literature review.

Background: Superior mesenteric arteriovenous fistula is a rare and difficult complication after abdominal trauma. Utilizing comprehensive endovascular treatment represents an effective approach to managing this condition. Case presentation: We report a case involving a 53-year-old female with a history of trauma who presented with complaints of abdominal pain, malaise, and melena. A computed tomographic scan revealed the presence of a superior mesenteric arteriovenous fistula. The fistula was occluded using four Interlock detachable coils, and a covered stent was positioned over the arteriovenous fistula in the superior mesenteric artery. Following endovascular treatment, the patient's abdominal pain and melena symptoms disappeared. Conclusion: Utilizing covered stents and Interlock detachable coils for endovascular treatment of a superior mesenteric arteriovenous fistula proves to be both feasible and highly effective.