After reading the article “Comments on the 2018 ESC Fourth Universal Definition of Myocardial Infarction”,1 we are prompted to comment on the diagnosis of type 4a acute myocardial infarction (AMI), which describes AMI occurring after percutaneous coronary intervention (PCI). We note a major discrepancy between the definition put forward by the European Society of Cardiology (ESC)2 and the concept of “clinically relevant myocardial infarction” proposed in 2014 by the Society for Cardiovascular Angiography and Interventions (SCAI)3; we furthermore believe that this discrepancy generates conspicuous and undesirable variability in clinical practice. Guideline documents should examine this issue in greater depth, in order to establish a consensus definition and thereby eliminate this variability.
In the previous and current ESC guidelines, the key diagnostic criterion for type 4a AMI is a post-PCI elevation ≥ 5 times the 99th percentile upper reference limit for myocardial injury markers. A confirmed diagnosis requires this to be concurrent with one of the following factors: new ischemic electrocardiogram changes, new Q waves, imaging evidence of the loss of viable myocardium, or angiographic evidence of a vascular complication explaining the marker elevation.
The SCAI uses distinct criteria, defining “clinically relevant myocardial infarction” as a biomarker elevation ≥ 70 times the local laboratory upper limit of normal or ≥ 35 times that limit if accompanied by new pathological Q waves in 2 contiguous leads or new persistent left bundle branch block.3 The SCAI authors argue that the AMI definition adopted by the ESC is not clearly linked to subsequent events such as death or heart failure; widespread adoption of this biomarker threshold may therefore have serious consequences for the appropriate assessment of devices and treatments, potentially affecting clinical care pathways and leading to misinterpretation of physician competence. Thus, in place of an AMI definition sensitive to mild myonecrosis, the SCAI consensus document recommends the use of a higher biomarker elevation threshold that has shown strong links to subsequent adverse events in clinical studies.3
Likely as a consequence of this lack of consensus, current clinical practice shows an alarming variability. Moreover, in health care settings where cost concerns are more pressing, the lack of consensus and the resulting uncertain applicability of recommended thresholds to decision-making have resulted in low rates of biomarker measurement. This is evident from the US National Cardiovascular Data Registry, which shows that post-PCI biomarkers were measured in only 26% of 157 825 Medicare patients undergoing elective PCI at 711 hospitals between 2004 and 2008; the registry furthermore shows that the likelihood of postprocedure biomarker surveillance was significantly dependent on the treating hospital.4
In light of these observations, further efforts should be directed at improving the diagnosis of type 4a AMI and systematizing clinical practice. A more precise knowledge base would provide needed clarity, helping to identify those patients truly in need of biomarker analysis and providing health care savings by avoiding unnecessary biomarker determinations. Such savings are especially advisable in the current climate of escalating costs, which places a priority on dispensing with measures that do not provide value.5