Peri-operative myocardial infarction and high sensitive cardiac troponin: A start but by no means a finish

The diagnosis of perioperative myocardial infarction (PMI) was confounded for years because creatinine kinase (CK)-MB is found to a variable extent in skeletal muscle.1 Attempts to improve the specificity of diagnosis with approaches such as the relative index (the ratio of CKMB to total CK), improved specificity but reduced sensitivity.2 This is not surprising since this metric was developed to distinguish skeletal muscle injury alone from cardiac injury alone. After the original documentation of the benefit of cardiac troponin (cTn) in detecting PMI,2 the field remained nascent until the landmark paper by Landesberg et al .3 They showed that even minor elevations above the 99th% upper reference limit (URL) in cTn were prognostic for adverse events, both short and long term. They also provided a rationale for such elevations by documenting that the majority had ischaemia that could be documented with continuous 12-lead Holter monitoring most often due to supply-demand abnormalities either intraoperatively or postoperatively.4 These data led to trials attempting to predict which patients would suffer postoperative myocardial necrosis,5 and whether there were preventive strategies to prevent PMI.6 ,7 The vast majority of these studies were unsuccessful, be they related to stress evaluations,5 drug6 or invasive therapy preoperatively.7 It was further demonstrated that most PMIs were not associated with symptoms or ECG changes.6 Although most events appeared to be due to supply-demand imbalance, the subset that was more often associated with mortality seemed to be related to plaque rupture events.8 Now, Alcock et al 9 extend the information available about this issue by evaluating how high-sensitivity cTn values impact on …