BEST PRACTICES :: UNDERSTANDING ELEVATED TROPONIN
The ongoing troponin conundrum: Understanding an elevated troponin
By Kalen Nissen, PhD, DABCC, FAACC A
s laboratory assays have evolved with improved per- formance, the clinical use of cardiac troponin (cTn) has also evolved beyond the context of myocardial infarction
(MI). The release of high sensitivity (hs) cTn assays has led to even more changes in clinical and laboratory guidelines for cTn use and expanding data on additional clinical uses. As defined in the Fourth Universal Definition of Myocardial Infarction,1 “the clinical definition of MI denotes the presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischaemia.” The preferred biomarkers for myocardial injury evaluation are cTnI and cTnT, with hs-cTn assays recommended for routine clinical use.1,2
of accommodating the differential diagnosis for different types of myocardial infarction and injury that release troponin into the blood, so as not to contribute to unnecessary work-ups and procedures. Data on risk stratification using cTn, including when below the 99th percentile URL, is being studied, to elucidate appropriate cutoffs and interpretation.
Myocardial injury is defined by an elevated cTn value,
with at least one value above the upper reference limit (URL), as defined by the 99th percentile of a health population. Therefore, MI is a type of myocardial injury, but not every myocardial injury is an MI. With the advent of hs-cTn assays, as required to qualify an
assay as being highly sensitive, now more than 50% of healthy individuals (>80% for some assays) will have a detectable tro- ponin. Gone are the days when any detectable troponin was an indicator of a potential evolving health emergency or poor prognosis. Now, clinicians must be able to assess a troponin result in consideration of the many causes of troponin elevation and patterns over time. Clinical decisions for interpretating hs-cTn elevations, including potential use of rule-in/rule-out algorithms, make it critical to have accurate cTn results and to interpret the results in the context of the patient’s presentation, clinical history, and other assessments (e.g., ECG results). This high sensitivity in more healthy individuals brings a challenge
38 | SEPTEMBER 2023
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Across the continuum of myocardial injury Serial testing of cTn in patients needing testing has grown in importance with the shift to hs-cTn assays, to help identify presence of an acute (rising and/or falling pattern) versus chronic elevation of cTn (see later section “Biological-related cardiac troponin elevations”). Additionally, there is an increased need to understand different clinical classifications of MI beyond the ST-segment elevation (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina paradigm. More nuanced classifications describe various types of MI, based on their pathological, clinical, and prognostic differences along with associated differences in treatment strategy. The criteria for type 1 MI includes a rise and/or fall of cTn values with at least one value above the 99th percentile, and at least one related appropriate sign of artherothrombotic coronary artery disease (Figure 1).1
This “traditional” type of MI must be distinguished
from another group of diseases that cause acute myocardi- al ischemia but due to another reason. Type 2 MI involves ischemic myocardial injury caused by an oxygen supply and demand mismatch, also requiring similar cTn criteria as type I with evidence of the mismatch from symptoms, imaging, or ECG changes. Some examples of type 2 MI include coronary embolism, hypotension or shock, and respiratory failure.
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