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.