Myocardial inflammation after major non-cardiac thoracic surgery

Following major non-cardiac surgery, large numbers of patients have biochemical evidence perioperative myocardial injury (PMI) associated with increased and long-term morbidity mortality.1 Recent work suggests inflammation is a driver PMI.2 Our research group previously demonstrated right (but not left) ventricular dysfunction in undergoing lung resection hypothesised that an inflammatory to the ventricle (RV) was implicated its aetiology. With informed consent ethical approval, 15 lobectomy underwent T1-weighted cardiac magnetic resonance imaging (CMR) pre post contrast; pre-operatively, post-operative day two (POD2) at 2-months. Imaging correlates inflammation, native T1 time extra-cellular volume (ECV) were measured on CMR LV RV (at insertion points) using Circle cvi42 (Calgary, Canada) post-processing software. As reported, ejection fraction fell postoperatively from 62.3% (9.2) pre-op 51.7% (9.6) POD2 (p=0.001) whilst left unchanged over (p=0.90). Both ECV significantly RV, but (T1 changes depicted Fig. 2); rose 25.9% (3.2) pre-operatively 43% (4.4) (p=0.001), no change (p=0.50). This first study demonstrate surgery supporting hypothesis drives PMI. Changes restricted RV; it plausible pulmonary vascular effects drive through afterload this patient group. Further required explore role PMI other forms surgery. References1. Ackland GL, Abbott TEF, Jones TF, et al. BJA 2020;124(5):535-543.2. May SM, Del Arroyo AG, 2020;125(5):661-671.