Over the last 4 months, the novel coronavirus, SARS‐CoV‐2, has caused a significant economic, political, and public health impact on a global scale. The natural history of the disease and surge in the need for invasive ventilation has required the provision of intensive care beds in London to be reallocated. NHS England have proposed the formation of a Pan‐London Emergency Cardiac surgery (PLECS) service to provide urgent and emergency cardiac surgery for the whole of London. In this initial report, we outline our experience of setting up and delivering a pan‐regional service for the delivery of urgent and emergency cardiac surgery with a focus on maintaining a COVID‐free in‐hospital environment. In doing so, we hope that other regions can use this as a starting point in developing their own region‐specific pathways if the spread of coronavirus necessitates similar measures be put in place across the United Kingdom.

The coronavirus 2019 (COVID-19) pandemic has disrupted patient care across the NHS. Following the suspension of elective surgery, priority was placed in providing urgent and emergency surgery for patients with no alternative treatment. We aim to assess the outcomes of patients undergoing cardiac surgery who have COVID-19 infection diagnosed in the early postoperative period. We identified 9 patients who developed COVID-19 infection following cardiac surgery. These patients had a significant length of hospital stay and extremely poor outcomes with mortality of 44%. In conclusion, the outcome of cardiac surgical patients who contracted COVID-19 infection perioperatively is extremely poor. In order to offer cardiac surgery, units must implement rigorous protocols aimed at maintaining a COVID-19 protective environment to minimize additional life-threatening complications related to this virus infection.

Cure of RVF can be achieved by a range of surgical approaches including abdominal and anal. A variety of different anal techniques are necessary, depending on the integrity of the anal sphincter and the presence or absence of perineal descent/internal intussusception.

Background: Epicardial adipose tissue (EAT) directly overlies the myocardium with changes in its morphology and volume associated with myriad cardiovascular and metabolic diseases. However, EAT's immune structure and cellular characterization remain incompletely described. This study aimed to define the immune phenotype of EAT in humans, and compare such profiles across lean, obese and diabetic patients. Methods: A total of 152 adult patients undergoing open chest coronary artery bypass grafting (CABG), valve repair/replacement (VR) surgery or combined CABG/valve surgery were recruited to the study. Patients' clinical and biochemical data alongside epicardial adipose tissue (EAT), subcutaneous adipose tissue (SAT) and pre-operative 3 blood samples were collected. Immune cell profiling was evaluated by flow cytometry and complemented by gene expression studies of immune mediators. Bulk RNA-seq was performed in EAT across different metabolic profiles to assess whole transcriptome changes observed in these groups.Results: Flow cytometry analysis demonstrated that EAT is highly enriched in adaptive immune (T and B) cells. Whilst overweight/obese and diabetic patients had similar EAT cellular profiles to lean control patients, the EAT exhibited significantly (P≤.01) raised expression of immune mediators including: interleukin1 (IL1), IL6, tumour necrosis factorα (TNFα) and interferonγ (IFNγ). These changes were not observed in either SAT or blood. Neither underlying coronary artery disease nor the presence of hypertension significantly altered the immune profiles observed. Bulk RNA-seq demonstrated significant alterations in metabolic and inflammatory pathways in the EAT of overweight/obese patients compared with lean controls.Conclusions: Adaptive immune cells are the predominant immune cell constituent in human EAT and SAT. The presence of underlying cardiometabolic conditions, specifically obesity and diabetes, rather than cardiac disease phenotype appears to alter the inflammatory profile of EAT. Obese states markedly alter EAT metabolic and inflammatory signalling genes, underlining the impact of obesity on the EAT transcriptome profile.

Duodenal polyposis is found in the majority of patients with familial adenomatous polyposis. Endoscopic surveillance programmes grade the severity of duodenal disease according to the Spigelman classification (stages 0-IV) to identify patients at risk of developing adenocarcinoma. To evaluate the progression of duodenal polyposis in patients with a previous diagnosis of Spigelman stage IV disease who have been downstaged by endoscopic or pharmacological means. A database search of a large polyposis registry identified patients who had been downstaged from stage IV disease and had further opportunity for disease progression. These patients were divided into three groups according to their new Spigelman stage. A measure of a patient's disease progression was obtained by the increase in stage over the recommended follow up time period for their new, reduced, Spigelman stage. Group 1 (n = 16) were downstaged to stage III disease, with 50 % progressing back to stage IV over the recommended 1-year follow up period. Group 2 (n = 19) were downstaged to stage II disease, with 84 % progressing over the recommended 3-year follow up period. Group 3 (n = 6) were downstaged to stage I disease, with 100 % progressing over the recommended 5-year follow up period. Patients downstaged from Spigelman stage IV demonstrate an increased rate of disease progression in comparison to reported rates of primary disease progression. An amendment to the current endoscopic surveillance protocol is recommended to ensure that once a patient has been diagnosed with stage IV disease they are treated as a high-risk patient in perpetuity.

A best evidence topic was constructed according to a structured protocol. The question addressed was whether, in patients undergoing minimally invasive aortic valve replacement (AVR), right anterior thoracotomy (RT) or mini-sternotomy (MS) was superior in terms of postoperative outcome? A total of 840 publications were found using the reported search. Of these, 6 represented the best available evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. In all, except 1 study, the primary outcome was early mortality, ranging from in-hospital mortality to 90 days postoperatively. The remaining study was a cost-benefit analysis. Four studies were non-randomized observational studies, one of which was multicentre. Two were meta-analyses of studies comparing minithoracotomy or MS with conventional sternotomy for AVR, rather than direct comparisons of the 2 minimal access techniques. We conclude that there is a lack of high-quality evidence comparing RT and MS for minimally invasive AVR, with no randomized controlled trials to date. The available evidence shows no difference in early mortality between RT and MS for surgical AVR. In studies that directly compared RT and MS, RT was found to be associated with reduced length of hospital stay, despite longer cardiopulmonary bypass times and cross-clamp times. One study reported groin complications (10.8%) with the RT group, where peripheral cannulation was used, while the other 5 studies did not comment on groin complications associated with peripheral cannulation. In the only cost-benefit analysis, RT was found to carry considerably more cost than MS over and above conventional AVR.

Despite being recognised over a century ago, the aetiology and pathogenesis of large vessel vasculitis (LVV) still remains elusive. Takayasu's arteritis (TA) and giant cell arteritis (GCA) represent the two major categories of LVV, each with distinctive clinical features. Over the last 10 years an increased understanding of the immunopathogenesis of the inflammatory cascade within the aortic wall has revived the view that LVVs may represent subtypes of the same pathological process, with implications in the treatment of this disease. In this review, the histological, genetic and immunopathological features of TA and GCA will be discussed and the evidence for a common underlying disease mechanism examined. Novel markers of disease activity and therapies based on advances in our understanding of the immunopathogenesis of these conditions will also be discussed.

Thoracic aortic aneurysm (TAA) represents a major cause of mortality and morbidity in Western countries. The natural history of TAA is indolent, with patients usually being asymptomatic until a catastrophic event such as rupture or dissection ensues. As such, early diagnosis is crucial and the search is ongoing for a biomarker that can indicate the presence of TAA with sufficient accuracy to act as a screening tool. To date, no such marker has been developed for the diagnosis of non-familial or 'sporadic' TAA. However, our increased understanding of the pathogenesis of both familial and sporadic TAA has suggested potential candidates for diagnostic biomarkers. Many markers/pathways have been shown to have differential activity levels or expression in the aortic tissue of TAA. However, priority is given to markers that have shown differential levels in blood plasma, as blood tests represent the easiest route for mass screening for TAA. This review aims to evaluate the efficacy of clinical tests already in use in diagnosing TAA, explore novel proposed biomarkers and identify key areas of future interest.