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Introduction. Aortic graft infection (AGI) is a rare complication following AAA repair and is associated with high morbidity and mortality. Management is variable, and there are no evidence-based guidelines. The aim of this study was to systematically review and analyse management options for AGI. METHODS: Data was collected between July and August 2018. A full HDAS search was conducted on the following databases: MEDLINE, EMBASE, CINAHL, and PUBMED. Meta-analysis was conducted using RevMan 5 software. RESULTS: 1,365 patient outcomes were assessed (10 cohort studies and 12 comparative studies). The most common treatment was in situ replacement of the graft (ISR) followed by extra-anatomical replacement (EAR). Various grafts were used for ISR, such as fresh/cryopreserved allograft, venous graft, and prosthetic grafts. No graft material was shown to be superior. Axillobifemoral graft was the commonest type of EAR used. In the majority of cohort studies, ISR was the main treatment for AGI. There was no significant difference in the overall mortality rate (ISR n = 70/176 vs. EAR n = 70/176 vs. EAR P = 0.87). Graft occlusion rate was significantly lower in the ISR group vs. the EAR group (n = 70/176 vs. EAR n = 70/176 vs. EAR P = 0.87). Graft occlusion rate was significantly lower in the ISR group vs. the EAR group (n = 70/176 vs. EAR n = 70/176 vs. EAR P = 0.87). Graft occlusion rate was significantly lower in the ISR group vs. the EAR group (Discussion. In situ replacement is the preferred method of treatment as it had lower rates of occlusion. Further strong evidence is required, such as a multicentre trial to establish a management pathway for the condition.

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AIM: To investigate the risk of endoleak during endovascular aneurysm repair (EVAR) involving the distal common iliac artery (CIA) when the internal iliac artery (IIA) is covered without prior coil embolization. MATERIALS AND METHODS: Retrospective analysis of 145 (125 men, 20 women) consecutive EVAR cases. Clinical notes and radiological images were reviewed, and data collected on patient demographics, aneurysm morphology, covering of the IIA with or without embolization, presence of endoleaks, and patient symptoms relating to IIA ischaemia. RESULTS: A total of 29 IIAs (10%) were covered in a total of 25 patients. Seven IIAs (24%) were embolized before stent covering (Embolization group), and 22 IIAs (76%) were covered only without embolization (Cover group). There was no statistically significant difference in the mean size of the abdominal aortic aneurysm diameter or CIA diameter between each group. No endoleaks from IIA retrograde filling were found in either group. CONCLUSION: The results of the present study do not support the traditional view that coverage of the IIA without prior embolization carries a high risk of endoleak, with no endoleaks seen in all 22 cases. Large-scale trials are required. However, the advent of branched-stenting techniques and the emergence of their success in long-term follow-up may preclude the former.

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1. The glycosaminoglycan heparin inhibits vascular smooth muscle cell (VSMC) proliferation and migration, but the mechanism of its antiproliferative action remains unclear. Heparin has been reported to bind to high affinity cell surface sites on animal VSMC before undergoing receptor mediated endocytosis resulting in signal transduction into the cytoplasm and modulation of genes involved in proliferation. In this study, we have characterized the binding of [3H]-heparin to human saphenous vein-derived VSMC and examined whether there is any relationship between the affinity of [3H]-heparin binding and the inhibitory effect of heparin and its structural analogues on DNA synthesis. 2. At 4 degrees C [3H]-heparin binding to human VSMC occurred in a specific, time and concentration-dependent manner and was not influenced by the removal of calcium ions. Binding of the ligand appeared to occur to the cell surface and was both saturable and reversible. Kinetic and steady state data indicated a single class of binding sites. 3. The pharmacology of [3H]-heparin binding was examined in displacement studies using unlabelled heparin and structural analogues. A comparison of the rank potencies of heparin, heparan sulphate fraction II, low molecular weight heparin and trehalose octasulphate showed that there was a marked discrepancy between their estimated affinities in the binding assays and their effect on DNA synthesis. 4. In summary, we have characterized the heparin binding site on human saphenous vein-derived VSMC. Our findings suggest that the action of heparin and its analogues on DNA synthesis does not simply reflect an interaction with the cell-associated heparin binding site defined in these studies, but may also be determined by the internalization and metabolism of the glycosaminoglycan(s).

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BACKGROUND: Vascular smooth muscle cell (VMSC) proliferation is an essential component of myointimal hyperplasia, which is implicated in the failure of 30% to 50% of vascular interventions, such as coronary angioplasty and peripheral vein grafting. We have shown that cells derived from stenotic lesions in infrainguinal vein grafts were significantly more resistant than controls to growth inhibition by heparin. METHODS AND RESULTS: In a prospective study, we correlated antiproliferative responses to heparin in vitro with graft patency after 1 year. Sixty-two patients with infrainguinal vein grafts were entered into a graft surveillance program for > or = 1 year. At operation, saphenous vein segments were explanted for VSMC culture. Cell proliferation in response to fetal calf serum was later determined in the presence and absence of heparin. In 35 cell cultures, including 13 from the above-mentioned patients, [3H]heparin binding was also estimated. VSMCs from patients with patent grafts were significantly more sensitive to growth inhibition by heparin than cells from patients with stenoses (median, 54% versus 20.9%, P<0.001), and [3H]heparin binding was strongly correlated with inhibition of proliferation (r=0.81). CONCLUSIONS: Responsiveness to heparin in cultured VSMCs is a strong predictor of outcome for infrainguinal vein grafts, and reduced sensitivity to heparin is correlated with decreased heparin binding. Relative resistance to the antiproliferative action of heparin may be a marker for aberrant regulation of VSMC growth.

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The effect of the three platelet-derived growth factor (PDGF) isoforms AA, AB, and BB on migration was investigated in cultured human saphenous vein smooth muscle cells. The modified Boyden chamber technique yielded efficacies BB >> AB, AA = 0. However, the BB concentration-response relationship displayed a pronounced peak, occurring between 1 and 10 ng/mL, with no response above this range. Checkerboard analysis showed that the promotion of migration at low concentrations was chemotactic in nature but that the downturn was independent of gradient. Furthermore, at high concentrations BB was able to prevent chemotaxis induced by fetal calf serum and epidermal growth factor (EGF). Experiments using low concentrations of BB in combination with high concentrations of AA to saturate PDGF alpha-receptors in the presence and absence of a neutralizing antibody to alpha-receptors revealed that alpha-receptor activation induced partial inhibition of chemotaxis but this did not account for the inhibition of migration by high concentrations of BB. Despite possessing no significant chemotactic action itself, high concentrations of the AB isoform completely inhibited BB induced chemotaxis. Taken together these results suggest that the chemotactic signal induced by PDGF is dominated by PDGF beta-receptors and switches from positive at low concentrations to negative at higher concentrations. Stimulation of DNA synthesis by the three isoforms (as measured by [3H] thymidine incorporation) yielded saturable responses for the AB and BB isoforms, with similar efficacy and weak or no response for the AA isoform. Concentration-dependent patterns of tyrosine phosphorylation of certain proteins mirrored the form of the chemotactic response and suggest one possible underlying regulatory mechanism to account for the disparity between PDGF-induced chemotaxis and DNA synthesis.

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1. PDGF is a highly hydrophilic cationic glycoprotein (M(r) 28-35kDa) produced by platelets, monocyte/macrophages, endothelial cells and vascular smooth muscle cells under some conditions. 2. Since its original description, PDGF has attracted much attention and it is currently believed to play a role in atherosclerosis and other vascular pathologies. 3. This review describes the vascular biology of PDGF. It particularly focuses on recent findings regarding the intracellular signals activated by PDGF in the context of vascular smooth muscle cell proliferation, migration and, contraction.

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