The advent of the measurement of cardiac troponins, cardiac troponin T and cardiac troponin I, offered the clinician and the laboratory a new tool to detect myocardial injury in patients suspected of acute myocardial infarction (AMI). The new tests were both more sensitive and specific than the biomarkers they replaced due to their absolute specificity for myocardial injury. The ability to predict an adverse prognosis in patients previously considered to have unstable angina and the ability to guide therapy led to their widespread adoption and ultimately to the redefinition of AMI to incorporate troponin measurement. The original redefinition of myocardial infarction (MI) does not contain any mention of subtypes of AMI.1 It only recommends the use of cardiac troponin as the preferred biomarker in the presence of other features which clinicians recognise as being indicative of myocardial ischaemia. The first appearance of the fivefold classification of AMI appears in the universal definition of MI and has been elaborated subsequently through the two recent redefinitions.2

The universal definition of MI provides five subtypes of AMI. Type 1 is what is generally understood to be a ‘heart attack’. Type 3 is the diagnosis when there is no biomarker information available. Type 4a (postpercutaneous intervention MI) and type 5 MI are arbitrary and constructs judged by biomarker elevation alone where a decision threshold has been selected to delineate whether significant or insignificant myocardial injury has occurred. Type 4b MI has a more rational pathophysiological basis as it is a combination of a cardiac troponin above the …