What’s Next in Troponin Testing?

The measurement of cardiac troponin has become the mainstay for diagnosing acute coronary syndrome and risk stratification. Troponin is a biomarker for myocardial necrosis. When a patient presents with symptoms consistent with acute coronary syndrome, which include myocardial infarction (heart attack), the current guidelines recommend an electrocardiogram as well as the measurement of cardiac troponin (subunit I or T).

These troponin subunits originate from genes that are specifically expressed in heart muscle. The guidelines recommend that these cardiac specific troponins be measured at the time of patient presentation as well as 3-6 hours following onset of symptoms (usually chest pain) to identify a rising and/or falling pattern. Troponin

Additional troponin levels may be obtained beyond 6 hours as per clinical judgment. Myocardial infarction (heart attack, meaning that heart muscle cells have died),” is indicated by a rising and/or falling pattern of troponin with greater or equal to a value above the 99th percentile of the upper reference level and evidence for serial increases or decreases in the levels of troponins.”1

High Sensitivity
Cardiac troponin measurements are highly sensitive and specific for detecting the death of heart muscle cells. Troponins are elevated in acute myocardial infarction within 2-4 hours after the onset of symptoms. Myocardial infarction can be confirmed in the vast majority of patients within 6 hours.

The AHA and ACC make the strong statement, “With the availability of cardiac troponin [contemporary troponin assays], CK-MB, myoglobin, and other diagnostic biomarkers are no longer necessary.”

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CK-MB is still used in some clinical trials to measure myocardial infarction (MI) size, however. In the EMBRACE STEMI study that I was recently involved in, MI size was primarily measured using CK-MB area under the curve, and troponin was a secondary outcome. There is still some controversy about troponin. For example, following a percutaneous coronary intervention such as angioplasty and stenting, there may be small increases in troponin levels in some patients. Because of the increased sensitivity of cardiac troponin, the prognostic value remains controversial following a bump with intervention.

However, in the setting of clinical myocardial infarction, there is data suggesting that troponin levels correlate with the size of the heart attack and risk of death. Patterns showing large increases may require more aggressive management. Yet not all researchers think that troponin is ideal. A paper by Maznyczka, Kaier and Marber2 stated, “high sensitivity troponin assays are recommended in early rule-out protocols for myocardial infarction, when measured at presentation and at 3-6 hours,” agreeing with the AHA/ACC guidelines, but then they go on to say:

“However, troponin is less than ideally suited for early diagnosis of acute myocardial injury because of its slow rise, late peak and low specificity for coronary plaque rupture.”

Beyond Troponin
It is important to remember that the elevation of troponin tells you that heart muscle cells have died. It does not tell you why they died, and this has to be determined by putting the whole clinical picture together.

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