In the beginning of the 20th century, the first reports of the clinical manifestations of myocardial infarction (MI) appeared, followed around a decade later by reports regarding the electrocardiographic (ECG) changes associated with MI (figure 1). From the middle of the 20th century, the application of assays for muscle enzymes for the diagnosis of MI became widespread, culminating in the WHO definition of MI based on clinical, ECG and cardiac enzyme criteria. Towards the end of the 20th century, the assays for cardiac troponins (I and T) became refined and were rapidly adopted by the cardiology community, allowing for more accurate diagnosis of MI. Accordingly, an American/European consensus document redefining MI was adopted for the first time, defining MI as clinical evidence of cardiac ischaemia and maximal concentration of troponin T or I exceeding the decision limit (99th percentile of the values for a reference control group) on at least one occasion during the first 24 hours after the index clinical event.1 Since then, there have been three more iterations to this document, with the latest fourth universal definition of MI published in 2018 and adopted by cardiac societies around the globe, accounting for five different types of MI (table 1).2 The principle that MI is defined by a clinical scenario of ischaemia and evidence of myocardial injury was loosely preserved in the different iterations. Several key caveats have arisen regarding the use of this latest definition.

The evolution of the diagnosis of MI over the years. AST, aspartte transferase; CK, creatine kinase; CK-MB, creatine kinase …