The introduction of troponin (cTn) testing in the early 1990s has led to many questions about the clinical significance of elevated values. What has become clear in the past several years is that an elevated troponin in and of itself does not indicate myocardial infarction (MI); rather it is a finding that represents the likely occurrence of myocardial necrosis and of itself does not provide any indication of the etiology. It is extremely important for all practitioners to fully understand the implications of an elevated troponin in order to initiate the appropriate treatment and optimize outcomes.
The term MI should only be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. The definition should include a rise and/or fall of cardiac markers (preferably cardiac troponin cTn) with at least one value above the 99th percentile upper reference limit (URL) and at least one of the following:
A 2012 expert consensus document, developed by the European Society of Cardiology, American College of Cardiology, American Heart Association, and World Heart Foundation, maintains the pathological definition of acute MI as myocardial cell death due to prolonged myocardial ischemia. Their definition also classified AMI into 5 types, based on pathological, clinical and prognostic differences:
For further assistance in determining the etiology of the elevated troponin level (ischemic versus non-ischemic) and appropriate patient diagnosis (myocardial infarction versus non-myocardial infarction), please refer to Figure 1 in the reference listed below.
Remember, any time an MI diagnosis is documented, all AMI core measures must be met, including:
References: American College of Cardiology Foundation 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations: A Report of the American College of Cardiology Foundation Task Force on clinical expert consensus documents.