Predicting cardiac surgical site infection: development and validation of the Barts Surgical Infection Risk tool

Objective: To develop and validate a new risk tool (Barts Surgical Infection Risk (B-SIR)) to predict surgical site infection (SSI) risk after all types of adult cardiac surgery, and compare its predictive ability against existing (but procedure specific) tools: Brompton-Harefield Infection Score (BHIS), Australian Clinical Risk Index (ACRI), National Nosocomial Infection Surveillance (NNIS). Design: Single-centre retrospective analysis of prospectively collected data. Patients and Setting: Data from 2,449 patients undergoing cardiac surgery between January 2016 and December 2017 from one European tertiary centre were included. Methods: Thirty-four variables associated with SSI risk after cardiac surgery, identified from the literature, were collated from three local databases. Independent predictors were identified using stepwise multivariate logistic regression. Bootstrap resampling was conducted to validate the model. Hosmer-Lemeshow goodness of fit test was performed to assess calibration of scores. A p-value of <0.05 was considered statistically significant for all analyses. Results: The B-SIR model was constructed from six independent predictors (female gender, body mass index (BMI) >35, diabetes, left ventricular ejection fraction (LVEF) <45%, peripheral vascular disease (PVD) and operation type, and the risk estimates were derived. The Receiver Operating Characteristics curve for B-SIR was 0.679, vs 0.603 for BHIS, 0.618 for ACRI and 0.482 for the NNIS tool. Conclusion: B-SIR provides greater predictive power of SSI risk after cardiac surgery compared with existing tools in our population. Further studies are needed to validate B-SIR on other cardiac populations and specific cardiac patient groups

Obesity and diabetes are major risk factors for epicardial adipose tissue inflammation

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. We aimed to define the immune phenotype of EAT in humans and compare such profiles across lean, obese, and diabetic patients. METHODS: We recruited 152 patients undergoing open-chest coronary artery bypass grafting (CABG), valve repair/replacement (VR) surgery, or combined CABG/VR. Patients’ clinical and biochemical data and EAT, subcutaneous adipose tissue (SAT), and preoperative 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 metabolic profiles to assess whole-transcriptome changes observed in lean, obese, and diabetic groups. RESULTS: Flow cytometry analysis demonstrated EAT was highly enriched in adaptive immune (T and B) cells. Although overweight/obese and diabetic patients had similar EAT cellular profiles to lean control patients, the EAT exhibited significantly (P ≤ 0.01) raised expression of immune mediators, including IL-1, IL-6, TNF-α, and IFN-γ. These changes were not observed in 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. CONCLUSION: 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 signaling genes, underlining the impact of obesity on the EAT transcriptome profile. FUNDING: Barts Charity MGU0413, Abbott, Medical Research Council MR/T008059/1, and British Heart Foundation FS/13/49/30421 and PG/16/79/32419