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Objective To evaluate the effect of surgical treatment on extracranial supra-aortic aneurysms and summarize the experience.Methods The clinical data of 10 patients undergoing surgical treatment of extracranial supra-aortic aneurysms from May 2019 to November 2023 in the Department of Vascular Surgery of Beijing Tiantan Hospital affiliated to Capital Medical University were collected.The 10 patients included 5 patients with internal carotid artery aneurysm,2 patients with subclavian artery aneurysm,2 patients with vertebral artery aneurysm,and 1 patient with internal carotid artery aneurysm combined with ipsilateral subclavian artery aneurysm.The surgical indications,surgical regimens,clinical efficacy,and complications were retrospectively analyzed. Results All the 10 patients underwent surgery successfully,with the surgery duration range of 60-420 min and the median surgery duration of 180.0 (121.5,307.5) min.Intraoperative bleeding volume varied within 30-400 mL,with a median of 90 (50,125) mL.The time of carotid artery blocking and vertebral artery blocking varied within the ranges of 10-20 min and 20-30 min,with the medians of 15.0 (11.5,16.3) min and 25.0 (15.0,22.5) min,respectively.No cardiac accident,cerebral infarction,or cerebral hemorrhage occurred during the perioperative period.The 10 patients were followed up for 3-58 months,with the median follow-up time of 8.5 (5.3,17.0) months.One patient with subclavian artery aneurysm developed artificial vessel occlusion 20 months after surgery.One patient with internal carotid artery aneurysm developed distal carotid artery stenosis 6 months after surgery. Conclusion Surgical treatment should be actively adopted for extracranial supra-aortic aneurysms,and individualized surgical regimens should be designed according to patient conditions.
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Objective To evaluate the effect of surgical reconstruction of extracranial vertebral artery and to summarize the experience. Methods The clinical data of 15 patients undergoing surgical reconstruction of extracranial vertebral artery from September 2018 to June 2022 were collected.The operation methods,operation duration,intraoperative blood loss,operation complications,and relief of symptoms were retrospectively analyzed. Results Eleven patients underwent vertebral artery (V1 segment) to common carotid artery transposition,two patients underwent endarterectomy of V1 segment,two patients underwent V3 segment to external carotid artery bypass or transposition.The operation duration,intraoperative blood loss,and blocking time of common carotid artery varied within 120-340 min,50-300 ml,and 12-25 min,with the medians of 240 min,100 ml,and 16 min,respectively.There was no cardiac accident,cerebral hyperperfusion syndrome,cerebral hemorrhage or lymphatic leakage during the perioperative period.One patient suffered from cerebral infarction and three patients suffered from incomplete Horner's syndrome after the operation.During the follow-up (4-45 months,median of 26 months),there was no anastomotic stenosis,new cerebral infarction or cerebral ischemia. Conclusion Surgical reconstruction of extracranial vertebral artery is safe and effective,and individualized reconstruction strategy should be adopted according to different conditions.
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Isquemia Encefálica , Artéria Vertebral , Humanos , Artéria Vertebral/cirurgia , Perda Sanguínea Cirúrgica , Estudos Retrospectivos , Infarto CerebralRESUMO
Vascular restenosis after the interventional angioplasty remains the main obstacle to a favorable long-term patency. Many researches suggest cigarette smoking is one of the most important causes of restenosis. This study was designed to investigate whether melatonin could protect against the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury. Three groups of male rats (normal condition, cigarette smoke exposed, cigarette smoke exposed, and melatonin injected) were used in this study. An established balloon-induced carotid artery injury was performed, and the carotid arteries were harvested from these three groups 14 days later. The ratio of intima to media, the infiltration of inflammatory cells, the expression of inflammatory cytokines (NF-κB, IL-1ß, IL-6, TNF-α, MCP-1), adhesion molecules (ICAM-1, VCAM-1), and eNOS were measured. The results showed that cigarette smoke exposure aggravated the stenosis of the lumen, promoted the infiltration of inflammatory cells and induced the expression of the inflammatory cytokines and adhesion molecules after the balloon-induced carotid artery injury. Moreover, cigarette smoke exposure can inhibit the expression of eNOS. Particularly, we surprised that melatonin could minimize this effect caused by cigarette smoke. These results suggested that melatonin could prevent the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury and the mechanism of its protective effect may be the inhibition of the inflammatory reaction. This also implies melatonin has the potential therapeutic applicability in prevention of restenosis after the vascular angioplasty in smokers.
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Anti-Inflamatórios/farmacologia , Artérias Carótidas/efeitos dos fármacos , Estenose das Carótidas/patologia , Estenose das Carótidas/prevenção & controle , Melatonina/farmacologia , Fumaça/efeitos adversos , Angioplastia com Balão/efeitos adversos , Animais , Western Blotting , Estenose das Carótidas/etiologia , Modelos Animais de Doenças , Imuno-Histoquímica , Masculino , Ratos , Ratos Sprague-Dawley , Recidiva , Nicotiana/químicaRESUMO
When more abdominal aortic aneurysms are repaired by endovascular approaches, the post-operative endotension without endoleak increase along with the extended follow-up. An early detection of such endotension and a proper differentiation from endoleaks are particularly important for the treatment decision-making. This article reviews the mechanism, diagnosis, and management of endotension.
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Aneurisma da Aorta Abdominal/cirurgia , Complicações Pós-Operatórias , Implante de Prótese Vascular , Humanos , StentsRESUMO
OBJECTIVE: To compare the clinical efficacies of endovascular aortic repair(EVAR)and open surgical repair(OSR)for ruptured abdominal aortic aneurysm(rAAA). METHODS: The clinical data of 28 rAAA patients undergoing emergent treatment between February 2002 and February 2013 in PUMC Hospital were retrospectively reviewed. Among them 13 cases were treated by EVAR and 15 cases by OSR. RESULTS: Before the surgery,the general conditions,comorbidities,and hemodynamics were not significantly different between these two groups(all P>0.05),although the EVAR group had significantly higher mean age than OSR group(P=0.041). In the perioperative period,the EVAR group showed significantly lower 30-day mortality(P=0.044),less blood loss(P=0.005),less blood transfusion(P=0.003),less infusion quantity(P=0.000),shorter length of procedure(P=0.001),and shorter hospital stay(P=0.020). Also,the EVAR group had no severe perioperative complications and showed superior 1-year follow up survival(P<0.05). CONCLUSIONS: EVAR is an effective treatment for rAAA and can improve the clinical outcomes. EVAR may be adopted as the first-line treatment for rAAA,especially for the aged.
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Aneurisma da Aorta Abdominal/cirurgia , Ruptura Aórtica/cirurgia , Procedimentos Cirúrgicos Vasculares/métodos , Humanos , Tempo de Internação , Estudos Retrospectivos , Resultado do TratamentoRESUMO
OBJECTIVE: To establish a stable cell line overexpression heme oxygenase-1 (HO-1) mediated by a modified lentivirus system and identify its function. METHODS: The HO-1 gene was amplified by polymerase chain reaction and cloned into the modified pLentiLox3.7 expression vectors. The recombinant plasmids were transfected into HEK293T cells and the HO-1 was detected by Western blot. The recombinant plasmids were transfected into HEK293T cells to produce the viruses, with the helping plasmids including plp1, plp2, and VSVG. HEK293T cells were infected by the viruses and the cells that can express HO-1 were identified by Western blot. The reactive oxygen species were detected in the HO-1-overexpression HEK293T cells and the normal cells after the adding of hydrogen peroxide. The same experiment was performed with human umbilical vein endothelial cells. RESULTS: The stable cell line that can overexpress HO-1 was established, which was verified by Western blot. The reactive oxygen species in the HO-1-overexpression HEK293T cells and human umbilical vein endothelial cells decreased obviously after exposure to hydrogen peroxide. CONCLUSIONS: The lentivirus-carrying HO-1 was successfully packaged and the stable cell line overexpression HO-1 was established. HO-1 can play a protective role in the course of oxidative damage.
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Linhagem Celular , Heme Oxigenase-1/metabolismo , Células HEK293 , Células Endoteliais da Veia Umbilical Humana , Humanos , Plasmídeos , TransfecçãoRESUMO
Smoking is considered to be one of the primary causes of atherosclerosis and vascular injury. Previous studies have shown that nicotine in tobacco can lead to vascular inflammation and endothelial dysfunction. Perivascular adipose tissue (PVAT) is known to secrete various types of adipokines to maintain vascular homeostasis. The present study investigated whether nicotineinduced PVAT malfunction can accelerate endothelial inflammation and eventually lead to endothelial dysfunction. The levels of inflammatory adipokines, including nuclear factor (NF)κB, interleukin (IL)1ß, IL6 and tumor necrosis factor (TNF)α, the ICAM1 and VCAM1 adhesion molecules and secretion of adiponectin were assessed in mature adipocytes and endothelial cells cultured alone or in coculture under nicotine stimulation. It was found that nicotine reduced the secretion of adiponectin and stimulated secretion of the NFκB, IL1ß, IL6 and TNFα inflammatory adipokines in mature adipocytes. Although nicotine stimulated endothelial cells to secrete IL1ß and IL6, no significant increase in the secretion of TNFα was observed. The coculture of mature adipocytes with endothelial cells markedly augmented the expression of the NFκB, IL1ß, IL6 and TNFα inflammatory adipokines and the ICAM1 and VCAM1 adhesion molecules, and significantly lowered the levels of adiponectin. These findings suggested that nicotine induced mature adipocyte dysfunction, which caused the abnormal secretion of adiponectin and inflammatory adipokines, and exacerbated endothelial inflammation. These findings also suggested a mechanism whereby nicotine induced the secretion of adiponectin and inflammatory cytokines by adipocytes. The results of the present study elucidated a novel pathway induced by cigarette smoke, which contributed to atherosclerosis and vascular injury.