#incomplete see: [2025 ACS guideline - Biomarkers](https://www.heartfoundation.org.au/for-professionals/acs-guideline?tab=2#Biomarkers) > [!key points]- Reflection > I remember listening to the Goljan audio lectures in med school where he enthusiastically looks forward to new-fangled troponin testing that he hopes will replace CK testing soon and thinking 'wow, medicine changes quickly' because troponin testing had become well-codified into the assessment of ACS by the time I was in med school. High sensitivity troponin testing came into vogue while I was a junior doctor and now in 2025 we have even codified single troponin, 0/1, and 0/2 hour troponin testing into the Australian guidelines, all in an effort to reduce ED times for patients who can be safely identified as being low, or very low, risk for ACS. Hopefully in a few years this message will itself be dated as quality Point-of-care high sensitivity troponin assays become more reliable and available. > > For some reason, there is tremendously less aversion to "unnecessary" troponin testing than there is for D-dimer testing. If you eliminate the specific radiation risks of an "unnecessary" CTPA for exclude PE in a positive D-dimer, troponin testing actually generates far more bloat in the ED system than D-dimer testing. This is all getting better though, and by and large, it is very nice that we can quickly screen for NSTEMI. > > The reality is that high sensitivity troponin testing is truely a trigger-happy [[Statistics and research methods overview#sensitivity/specificity, PPV, likelihood ratio|sensitive]] screening test for myocardial ischaemia. When you then put it into the context of "what do we need to do about a positive troponin?" the reality is that not all elevated troponins need discussion with cardiology. IF the test was attended pursuant to screening for an acute coronary syndrome, then yes, needs discussion with cardiology about PCI timing (assuming the ECG didn't show a [[STEMI ECG patterns|STEMI]] or [[STEMI equivalents|STEMI equivalent]]), otherwise need to treat the underlying cause. Regardless, an elevated troponin, while not *specific* for a treatable myocardial lesion, is nonetheless biochemical evidence of myocardial ischaemia and an independent predictor of overall poor health. ## Causes of elevated troponin - MI with acute coronary occlusion - plaque rupture/erosion - spontaneous coronary artery dissection - coronary embolism - vasospasm/mycovascular dysfunction - MI due to oxygen supply/demand mismatch without acute coronary occlusion - with or without fixed obstructive coronary artery disease - Acute myocardial injury - acute heart failure - [[Myocarditis]] - Chronic myocardial injury - structural heart disease - chronic kidney disease ## Differences between troponin T and I assays High-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT) have comparable accuracy for the early detection and diagnoses of MI. Troponin T is more likely to be elevated among people with poor [renal function](https://www.heartfoundation.org.au/for-professionals/acs-guideline?tab=2#renal-disease) and chronic muscular diseases (e.g. chronic myopathy, myositis). This is possibly due to re-expression of cTnT in the diseased muscle or due to cross reactivity of the cTnT assay with skeletal muscle troponin T. ## false positives and negatives False positive or negative cTn results are rare but possible. False positives may occur due to antibody interference, such as macrotroponins – high molecular weight complexes of cTn fragments and immunoglobulins (cTn autoantibodies) – which delay troponin clearance and cause artificially elevated readings. Heterophilic antibodies cause another type of interference, as these can bind to test antibodies and yield a positive result without actual cTn elevation. While the exact cause of heterophilic antibodies is unclear, they are sometimes associated with conditions like rheumatoid arthritis or viral infections, including Epstein–Barr virus and CMV. Conversely, severe haemolysis or plasma substances like biotin can lead to false negatives. If troponin levels do not align with the clinical presentation, consulting the hospital laboratory is essential to rule out these rare false positive cTn results ## Troponin assay cutoffs ![[Pasted image 20250513092040.png]] > [!caption] hs-cTn 0/2-hour testing recommendations. Note: the 0/2-hour time points are shown in this figure. If using a 0/1-hour strategy, change timeframes accordingly. Refer to Table 7 interpretation of cTn assay-specific values and sex-specific 99th percentiles. *All people with symptom onset <2 hours need serial testing.* People with ongoing symptoms should be assessed according to high-risk criteria. ![[Pasted image 20250513092154.png]]