What do I do with a high sensitivity troponin?

Newer high-sensitivity troponin tests can be positive in patients who would have negative tests with the ‘traditional’ assay, which can result in confusion about what to do with the patient, particularly those patients without an obvious cardiac presentation. A recent study1 shows that the majority of patients that fall into this group had non-cardiac discharge diagnoses.



Background: High sensitivity troponin T (hsTnT) detects lower levels of troponin T with greater precision than the 4th generation (cTnT) assay. However, the clinical implications of this are uncertain.


Objectives: Primary: Describe the proportion of patients who test ‘positive’ with hsTnT but negative with cTnT. Secondary: Determine proportion in each group with an adverse event (representation, AMI or died) within 90 days of the index test.


Method: 161 patients samples were tested with cTnT and hsTNT assays. McNemar’s test was used to compare paired samples. Electronic medical records were reviewed, with discharge diagnosis and 90 day outcomes determined blind to hsTnT results. Patients were then classified as ‘TnT negative’ (hsTnT was <0.014 mcg/mL), 'new positive' (hsTnT was ≥0.014 mcg/mL and cTnT <0.03 mcg/mL) and 'TnT positive' (cTNT was ≥0.03 mcg/mL)


Results: Positive results more than doubled with the hsTnT assay (50% vs 22%, P < 0.001). 81 patients were ‘TnT negative’, 44 were ‘new positive’ and 36 ‘cTnT positive’. The discharge diagnosis for ‘new positives’ was AMI in 4 (9%), other cardiac in 13 (30%) and non-cardiac in 27 (61%). At 90 days adverse events occurred in 30%, 54% and 50% of the groups respectively. There were no late cases of AMI or cardiovascular death in ‘new positive’ patients.


Conclusion: Many patients with diagnoses other than AMI will have hsTNT above the reference level. Indiscriminate testing with hsTnT might lead to more patients requiring serial troponin testing and/or invasive further tests, which will have process and resource implications for EDs and health services.


An accompanying editorial2 highlights that:

Elevations are seen in pathological conditions, including structural heart disease, renal impairment and pulmonary embolism, but might also be seen in extreme exertion, such as marathon runners. It is now clear that when using a highly sensitive assay, circulating levels of troponin will be detected in many normal people.

The editorial makes the interesting observation that the duration of rise may help elucidate the cause; ischaemic elevation of troponin falls rapidly, since the rise might be due to the release of small amounts of troponin that exist free within the cytoplasm, in contrast to the more persistent elevation seen with myocardial necrosis. The editorialist provides the following caution:


Overall, our practice for ordering troponin will need to be urgently reviewed. Single troponin values will continue to be of little to no use in defining disease states in the ED. Identifying a chronic versus an acute elevation will only be revealed by serial troponin testing. The time interval between testing is currently contentious.

High sensitivity troponins are referred to in the newly published 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes (full text link below)3:

RECOMMENDED PROTOCOL FOR TROPONIN TESTING USING HIGH SENSITIVITY ASSAYS IN “RULING-OUT” ACS
  • All patients with a suspected ACS should undergo troponin testing on arrival at ED to ‘rule in’ ACS within the differential diagnosis
  • For a patient with a positive troponin result or a change in troponin levels over time, neither ACS nor other significant pathology (e.g. pulmonary embolus, aortic dissection, and sepsis) can be excluded. These patients are at higher risk of subsequent events. A positive result should be considered within the entire clinical context (history, examination, ECG findings and other investigations). Further investigations directed at all plausible clinical diagnoses should be considered and, if ACS is thought to be the likely cause, these patients may require cardiology assessment.
  • All patients with a negative result should undergo repeat testing 3–4 hours later.
  • The testing interval to ‘rule out’ MI may be reduced to 3 hours, provided that one sample is taken at least 6 hours after symptom onset:
  • Patients with a negative result at 3 hours after presentation and at least 6 hours after the onset of pain should be considered for early assessment by non-invasive anatomic or functional testing, as determined by local availability.
  • For patients presenting more than 6 hours after pain onset, a single high sensitivity troponin assay is sufficient to rule out myocardial infarction in the absence of ongoing chest pain.

High sensitivity troponin assays have an increased sensitivity for the detection of “myonecrosis”, but a reduced specificity for the diagnosis of “MI”. A positive result (≥99th centile for reference population OR where there is a change of ≥50% above an initial baseline level) should be interpreted in the context of the entire clinical presentation and does not necessarily represent an indication for coronary angiography. The management MI secondary to other conditions (e.g. anaemia, thyrotoxicosis, and sepsis) should be primarily directed at those conditions.
The finding of troponin concentrations that remain stable over time suggests that the presence of troponin is due to chronic disease. Acute exacerbations of chronic disease that result in elevated troponin levels can mimic an MI release pattern.

1. Clinical diagnosis and outcomes for Troponin T ‘positive’ patients assessed by a high sensitivity compared with a 4th generation assay
Emerg Med Australas. 2011 Aug;23(4):490-501

2. Troponin: A risk-defining biomarker for emergency department physicians
Emerg Med Australas. 2011 Aug;23(4):391-4

3. 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes
Heart, Lung and Circulation 2011 Aug;28(8):487-502 Free Full Text