The role of cardiac troponin measurements

Troponin measurement has become the gold standard biochemical test for MI.

Cardiac troponins are only released when there is a myocardial damage (Photograph: SPL)
Cardiac troponins are only released when there is a myocardial damage (Photograph: SPL)

There are three forms of troponin - troponin T, troponin I and troponin C. Together with tropomyosin, they form the troponin-tropomyosin complex.

Troponins are found in all striated muscles. The complex is bound to the actin myofilament and acts as a molecular switch to initiate muscle contraction. When a nerve impulse arrives at the motor endplate, the muscle depolarises and calcium is released as a second messenger intracellularly. The calcium binds to troponin C, causing a conformational change that allows ATP hydrolysis and muscle contraction.

The unique genes for troponin T and troponin I produce molecularly distinct cardiac isoforms, allowing the assay of cardiac troponin T (cTnT) and cardiac troponin I (cTnI).

Advantages of measuring troponins
The advantages of measuring cTnT and cTnI over conventional cardiac enzymes, such as creatine kinase (CK) and its MB isoenzyme (CK-MB), are two-fold.

First, cardiac troponins are only released when there is cardiac damage. This means that in cases of skeletal muscle injury, such as rhabdomyolysis, road traffic accidents or even extreme physical exertion, such as running a marathon, it is possible to distinguish cardiac from skeletal muscle damage.

Second, cardiac troponins are much more sensitive as indicators of injury to the myocardium. Using currently available tests, most normal individuals have undetectable levels of cardiac troponins in the blood, so any elevation of cardiac troponin that occurs will be due to myocardial damage.

The original criteria for the diagnosis of MI were proposed by WHO.1 These included biochemical testing, but used an elevation in cardiac enzymes of more than twice the upper reference limit of the test. The cardiac enzyme to be used was not stipulated.

In the initial evaluation of cardiac troponins, it was found that approximately one-third of patients said not to have MI by WHO criteria had detectable cardiac troponin.2

A detectable troponin in these patients was associated with a much greater risk of a major adverse cardiac event, such as death, readmission with MI, readmission with unstable angina, or need for urgent revascularisation.3

This has been a consistent finding in all studies of cTnT and cTnI in patients admitted with suspected acute coronary syndromes (ACS). The measurement of cTnT and cTnI is one of the few evidence-based laboratory tests and it has been adopted as the gold standard biochemical test for MI.

Troponin in acute coronary syndromes
The measurement of cardiac troponins is used to categorise patients admitted with chest pain to confirm or exclude MI, principally in patients without characteristic ECG changes.

Cardiac troponins can be used with resting and stress electrocardiography to identify patients at high or low risk of subsequent cardiac events. Patients with a normal ECG, undetectable cardiac troponin and a negative stress test have an excellent long-term prognosis and can rapidly be discharged from hospital.

A series of studies has demonstrated that interventions, such as revascularisation, are only appropriate for patients without characteristic ECG changes if they have an elevated cardiac troponin.4-8 Troponin measurement is now incorporated in the recommended management guidelines for patients presenting with suspected ACS.9

Redefining acute MI
The use of cardiac troponin as the definitive test for MI has allowed for the development of an improved standard of care.

Cardiac troponin measurement identifies the 7 per cent of patients sent home from A&E with chest pain who are subsequently found to have experienced MI.10 Troponin measurement allows better risk stratification, resulting in some patients, previously categorised as unstable angina, being recharacterised as having had acute myocardial infarction (AMI).

Troponin elevation beyond acute MI
The advent of a sensitive, specific marker for myocardial damage has revealed that a range of clinical conditions, apart from AMI, result in cardiac damage and troponin elevation. The number of these conditions is growing. In many cases, the elevated levels of troponin are also found to predict an adverse prognosis.

Elevation of cardiac troponin may be conveniently classified into three categories (see box below).11,12 Clinical situations where troponin can be detected vary. The range of conditions illustrates the fact that the interpretation of any laboratory test can only occur in the appropriate clinical context.

Using troponin in primary care
In primary care, troponin measurement has a more limited role. It can be used in the differential diagnosis of patients with an elevated CK to exclude a cardiac cause.

Patients with cardiac-sounding chest pain should not be investigated by troponin testing in primary care. They require immediate referral to hospital or a rapid access chest pain unit, according to the clinical history and severity of symptoms.

There are two situations when troponin measurement may be of benefit in primary care. The first is when a patient presents late after suspected MI. In this case, measurement of troponin will confirm or exclude whether chest pain occurring two to three days previously was due to AMI.The second situation where troponin measurement may be of benefit is confirmatory testing in a patient who would otherwise not be admitted to hospital.

The measurement of cardiac troponins has proved a major step forward for the diagnosis and management of patients with suspected ACS. Although this is a sensitive, specific test for MI, there are other causes of myocardial damage where troponin elevation occurs.

In all cases where there is detectable troponin, an explanation must be sought because there is always underlying pathophysiology.

  • Dr Collinson is director of Clinical Blood Sciences and lead clinician in the vascular risk management clinic, department of cardiology, St George's Hospital and Medical School, London


Primary ischaemic cardiac injury

ST elevation MI, non ST elevation MI

Secondary ischaemic cardiac injury

Periprocedural cardiac injury in percutaneous coronary intervention, CABG, cocaine, pulmonary embolus, superventricular tachycardia

Non-ischaemic cardiac injury

Myocarditis, cytotoxic chemotherapy, chronic renal failure, snake or insect venom

1. Nomenclature and criteria for diagnosis of ischemic heart disease. Report of the Joint International Society and Federation of Cardiology/World Health Organization task force on standardization of clinical nomenclature. Circulation 1979; 59: 607-9.

2. Hamm CW, Ravkilde J, Gerhardt W et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med 1992; 327: 146-50.

3. Stubbs P, Collinson PO, Moseley D et al. Prospective study of the role of cardiac troponin T in patients admitted with unstable angina. BMJ 1996; 313: 262-4.

4. Lindahl B, Venge P, Wallentin L. Troponin T identifies patients with unstable coronary artery disease who benefit from long-term antithrombotic protection. J Am Coll Cardiol 1997; 29: 43-8.

5. Boersma E, Harrington RA, Moliterno DJ et al. Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomised clinical trials. Lancet 2002; 359: 189-98.

6. Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. Lancet 1999; 354: 708-15.

7. Cannon CP, Weintraub WS, Demopoulos LA et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001; 344: 1879-87.

8. De Winter RJ, Windhausen F, Cornel JH et al. Early invasive versus selectively invasive management for acute coronary syndromes. N Engl J Med 2005; 353: 1095-104.

9. Bertrand ME, Simoons ML, Fox KA et al. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2002; 23: 1809-40.

10. Collinson PO, Premachandram S, Hashemi K. Prospective audit of incidence of prognostically important myocardial damage in patients discharged from emergency department. BMJ 2000; 320: 1702-5.

11. Collinson PO, Stubbs PJ. Are troponins confusing? Heart 2003; 89: 1285-7.

12. Gaze DC, Collinson PO. Cardiac troponins as biomarkers of drugand toxin-induced cardiac toxicity and cardioprotection. Expert Opin Drug Metab Toxicol 2005; 1: 715-25.

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