Late onset infection of covered and bare metal arterial stents

Objective The objective was to present the case of a late covered iliac stent late infection and report a comprehensive literature review on diagnosis and outcomes in this setting. Methods A comprehensive review of the literature was performed through MedLine by two independent reviewers from 1990 to 2020 on reported cases of arterial stent late onset infection over arterial stents. The data about on the risk factors, clinical presentation, treatment and outcomes were collected. Results Twenty-two studies were selected as pertinent for the analysis, totalling 24 patients including the indexed case. Infection occurred at a median of 22 months postoperatively (range 2–120 months) over a bare metal stent in 66.7% ( n 16) of cases versus 33.3% ( n 8) over a covered stent. Clinical presentation included local symptoms (local pain, oedema, petechiae or skin rash) in 21 (87.5%) cases and non-specific systemic symptoms (fever, sepsis, chills and leucocytosis) in 8 cases (33.3%). In 4 cases (16.7%), patients presented with haemorrhagic shock upon arterial rupture. The bacteria most frequently encountered were S. aureus (54.2% of cases). Several factors were supposed to be responsible for the infection including among which procedure-related (non-aseptic technique, lack of prophylactic antibiotics and repetitive punctures at the access site) or related to pre-existing patient’s clinical conditions (immunosuppression, diabetes and concurrent infection) have been considered responsible for the infection. Treatment consisted in antibiotics alone (2 patients, 8.3%) or in association with surgical explant, both with or and without revascularization ( n 21, 87.5%). In one case, an endovascular coiling was performed. Complications occurred in 29.2% ( n 7) of cases and included the need for amputation, bowel resection, endocarditis, pulmonary failure or pneumonia. Overall, three patients (12.5%) died from a septic shock or multi-organ failure. Conclusions Intravascular stent infection is a rare but fearsome condition associated with high morbidity and mortality.

Successful removal of a central venous catheter misplaced in the right subclavian artery using an intravascular stent: a case report

Background Cannulation of a central venous catheter is sometimes associated with serious complications. When arterial cannulation occurs, attention must be given to removal of a catheter. Case presentation A 62-year-old man was planned for emergency thoracic endovascular aortic repair. After the induction of anesthesia, a central venous catheter was unintentionally inserted into the right subclavian artery. We planned to remove the catheter. Since we considered that surgical repair would be highly invasive for the patient, we decided to remove it using a percutaneous intravascular stent. A stent was inserted through the right axillary artery. The stent was expanded immediately after the catheter was removed. Post-procedural angiography revealed no leakage from the catheter insertion site and no occlusion of the right subclavian and vertebral arteries. There were no obvious hematoma or thrombotic complications. Conclusions A catheter that has been misplaced into the right subclavian artery was safely removed using an intravascular stent.

Neurotrophin-3 accelerates reendothelialization through inducing EPC mobilization and homing

Rapid endothelialization is an effective way to treat intimal hyperplasia after intravascular stent implantation. Blood vessels and nerves coordinate with each other in function, while neurotrophin-3 (NT-3) is an important class of nerve growth factors. Our study found that NT-3 promoted endothelial progenitor cell (EPC) mobilization, and the proportion of EPCs in peripheral blood was increased by 1.774 times compared with the control group. Besides, NT-3 promoted the expression of stromal cell-derived factor-1α (SDF-1α), matrix metalloproteinase-9 (MMP9), and chemokine (C-X-C motif) receptor 4 (CXCR4) in EPCs, which increased by 59.89%, 74.46%, and 107.7%, respectively, compared with the control group. Transwell experiments showed that NT-3 enhanced the migration of EPCs by 1.31 times. Flow chamber experiments demonstrated that NT-3 captured more circulating EPCs. As shown by ELISA results, NT-3 can promote the paracrine of vascular endothelial growth factor, interleukin-8, MMP-9, and SDF-1 from EPCs. Such increased angiogenic growth factors further accelerated the closure of endothelial cell scratches. Additionally, EPC-conditioned medium in the NT-3 group significantly inhibited the proliferation of vascular smooth muscle cells. Then animal experiments also illustrated that NT-3 prominently accelerated the endothelialization of injured carotid artery. In short, NT-3 accelerated rapid reendothelialization of injured carotid artery through promoting EPC mobilization and homing.