The Third Universal Definition of Myocardial Infarction—Moving Forward

The third iteration of the Universal Definition of Acute Myocardial Infarction (AMI) was recently published (1). The guidelines expand on previous information. Salient features include: Cardiac troponin remains the biomarker of choice for the diagnosis of each type of AMI. Criteria for AMI include a rising and/or falling pattern of troponin values with at least 1 >99th percentile value. Assays should ideally have a 10% CV at the 99th percentile to best maximize the ability to define significant changes; however, assays with CVs up to 20% do not cause false-positive values and are clinically usable. Because troponin criteria for a rising and/or falling pattern are assay dependent, generalized concentration or percentage changes could not be specified. With high-sensitivity assays, sex-specific 99th percentile values are necessary. Five subtypes of AMI are recognized. Type 1: AMI due to acute plaque rupture. Type 2: AMI due to supply–demand imbalance and/or abnormalities in cardiac vasomotion and/or dissection. Type 3: AMI that is classically documented by electrocardiogram or angiography, or autopsy in cases in which the patient succumbs before biomarker values can be obtained or before a diagnostic pattern can be recognized. Type 4: AMI related to percutaneous intervention. If the baseline troponin is within the reference interval (<99th percentile), a 5-fold increase in values in association with clinical signs and/or symptoms or documented angiographic complications is necessary to make the diagnosis of AMI. If the baseline is increased but stable or falling, a 20% increase is sufficient for the diagnosis. Subsets of patients with acute stent thrombosis and in-stent restenosis are acknowledged. Such events are diagnosed according to the metrics in number 2 above. Type 5: Coronary artery bypass graft AMI. This type requires a baseline value within the reference interval, with a 10-fold increase and additional findings by electrocardiogram or imaging to make the diagnosis. For the present these criteria should be used for new novel procedures such as transcatheter aortic valve implantation. Increases of troponin can occur for a variety of reasons in the absence of ischemic heart disease. In these situations, the term cardiac injury can be applied. Increases of troponin are common in critically ill patients and noncardiac postoperative patients. Often these increases are due to supply–demand imbalance and thus indicate type 2 AMIs. Autopsy studies, however, suggest that many of the more morbid events are more often type 1 AMIs. Troponin is often increased with acute or chronic heart failure. Such increases could be due to acute ischemia but may also be due to other processes. Thus, all such increases do not warrant a diagnosis of AMI. The findings of clinical trials should be reported by using the above classification system and the reports should provide results in multiples of the 99th percentile so that comparisons can be made across studies.