EP.WE.906Endovascular Repair of Abdominal Aortic Aneurysm – A Retrospective Analysis of Outcomes from a UK Teaching Hospital

Aims Endovascular Repair of Abdominal Aortic Aneurysm (EVAR) is a minimally invasive technique that has become increasingly popular in the past few years. Recent evidence questioned the long term durability of the technique and highlighted the relevance of long term complications and reinterventions. The aim of this paper is to evaluate long term outcomes of EVAR with a focus on survival and aneurysm related reinterventions. Methods We retrospectively analysed all elective EVAR procedures performed for Abdominal Aortic Aneurysm (AAA) between May 2010 and June 2016 in our institution. Data collected included - comorbidities, post operative survival and post operative aneurysm related interventions. Survival analysis was performed using the Kaplan-Meyer method. We build a Cox Proportional-Hazard model to identify factors associated with increased mortality. Results 182 patients were included in our analysis. Median age was 77 years (50-92). Median follow up was 65 months (31-104). During the follow up period we recorded 41 deaths. 30 day mortality was 0.5% (1), 2 year mortality was 8.7% (16). 17 patients (9.3%) required reintervention during the follow up period (2.4 reinterventions per 100 patient-years). Conclusions Our medium and long term outcomes following EVAR are comparable with what has been reported in the literature. A higher ASA grade and advanced age were associated with increased mortality in our cohort.

EXPRESS: Pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension: state-of-the-art 2020

Pulmonary endarterectomy (PEA) is the treatment of choice for patients with operable CTEPH as it is potentially curative. In expert centers that conduct > 50 PEA procedures per year, peri- and post-surgical mortality rates are very low and long-term outcomes are excellent, with 3-year post-operative survival of > 80%. Therapeutic decisions in CTEPH are based largely on the location of the arterial obstruction, with PEA for obstructions in main, lobar, and segmental vessels, and balloon pulmonary angioplasty (BPA) and medical therapy for small-vessel disease. Medical therapy is also an option for patients with persistent/recurrent pulmonary hypertension after PEA or BPA. With increasing surgical experience and improvements in instruments and procedures, an increasing number of patients are now considered operable who would previously have been inoperable, including some patients with subsegmental disease. At our University, around 200 PEA procedures are performed every year and several advances have been developed, including resection of more distal disease, availability of PEA to patients previously considered to be at too high risk for surgery, improved management of post-PEA complications, and minimally invasive PEA. PEA can be combined with other treatment modalities, including BPA, medical therapy for persistent/recurrent pulmonary hypertension after PEA, and medical therapy or BPA as bridging therapy before surgery. Data on these combinations are, however, limited. Combination treatment should therefore be considered on an individual patient basis. In the future, however, multimodal therapy with PEA, BPA, and/or medical therapy is likely to be an important treatment option for many patients.

Examining the Role of Specialized DNA Polymerases in the Development of Temozolomide Resistance in Glioblastoma Multiforme

Glioblastoma multiforme (GBM) is an extremely malignant type of primary brain tumor that exhibits a high mortality rate. Current standard therapy involves surgery followed by radiation and treatment with the DNA-alkylating agent, temozolomide (TMZ). While TMZ treatment can extend post-operative survival, most patients develop resistance to TMZ which leads to a significant increase in mortality. At the molecular level, TMZ produces a variety of different DNA lesions including N7-methylguanine, N3-methyladenine, and O6-methylguanine. Although each DNA lesion possesses a unique molecular structure, they all elicit cytostatic and cytotoxic effects against GBM cells. This review article describes the molecular and cellular mechanisms accounting for the anti-cancer activity of TMZ as well as the mechanisms responsible for both inherent and TMZ-induced drug resistance. Special emphasis is placed on understanding the roles that various DNA polymerases play toward the initiation and progression of GBM in addition to mediating resistance to TMZ. This review concludes with discussions on several new approaches that show promise in combating TMZ-resistance, specifically using small molecules to block the replication of DNA lesions catalyzed by various DNA polymerases.