BMJ  2004;329:1357-1358 (11 December), doi:10.1136/bmj.329.7479.1357

Editorial

Troponin in patients with chest pain

We need to ensure that troponin is only one element of the management algorithm

For several years the measurement of serum troponin concentration in patients presenting with acute chest pain has been routine in most hospitals in the United Kingdom. Guidelines now demarcate myocardial infarction with ST elevation from acute coronary syndromes such as unstable angina and myocardial infarction without ST elevation. Since the early 1990s studies have repeatedly confirmed that troponins are released by some patients with acute coronary syndromes and represent a marker of risk for subsequent cardiac events.^1-3 FRISC-II, TACTICS-TIMI 18, and RITA3 all indicate that early angiography and revascularisation can reduce the risk of events in this cohort, thereby improving prognosis.^4-6 As a consequence, management of acute coronary syndromes without ST elevation has changed dramatically in the United Kingdom.⁷

Formerly, patients were treated medically and considered for early revascularisation if they had ongoing ischaemia, which represents only about 10% of such a group. By contrast, current guidelines recommend early invasive treatment in patients not only with ongoing ischaemia but also those with elevated troponins with or without ST depression. In the United Kingdom we are therefore trying to manage a substantial proportion of patients with acute coronary syndromes by early angiography and revascularisation, a strategy that guarantees mismatch between demand and available resources.

This strategy necessitates a wait in hospital for transfer to a tertiary centre for most patients. Furthermore it has led to suboptimal and inequitable management for, perhaps, most patients for the following reasons. Firstly, patients awaiting transfer occupy a huge number of bed days,⁸ even when asymptomatic and mobile. This delay is detrimental to both patients and their families and the efficiency of hospitals. Secondly, as invasive facilities cannot cope with this unplanned surge in demand, patients are not being treated within the evidence based time period. FRISC-II and TACTICS-TIMI 18 randomised patients to invasive or non-invasive treatment within a few days of presentation, and ISAR-COOL⁹ shows that treating patients earlier than that is beneficial. Perhaps we are simply selecting out a group of patients at lower risk. Thirdly, we are also practising postcode medicine. A patient who has an acute coronary syndrome without ST elevation and is admitted to a hospital with facilities for revascularisation is likely to receive treatment quicker than a similar patient admitted to a hospital without such facilities.¹⁰ Similarly, in one hospital, a troponin positive patient with an acute coronary syndrome may be admitted for a few days and, if asymptomatic, be sent home, whereas in another hospital such a patient may be kept in hospital pending transfer. How can both strategies be correct?

Has measuring troponins in patients with acute chest pain been a clinical success? This measurement is flawed as a clinical tool. Firstly, our interpretation of the data may be overenthusiastic. Of studies showing a correlation between troponin concentration and outcome, the event rate, even in cohorts with the highest band of troponin is around 20%. Many centres currently refer all patients with acute coronary syndrome who have elevated troponin concentrations for early angiography. Thereafter, all these patients (fewer than 70% of whom will have an event during the follow up period) are considered for revascularisation on the basis of a reduction in the six month event rate from 12.1% to 9.4% for death or myocardial infarction in FRISC-II or 19.4% to 15.9% for death, myocardial infarction, or rehospitalisation in TACTICS-TIMI 18.^{4 5} Surely this represents a rather blunt screening tool. The second flaw in measuring troponin is that it is too eagerly perceived as a rule in or rule out test. The test has become, for many clinicians, the main component of their decision making. The final flaw is that elevation of troponin is reported in a myriad of clinical conditions that do not seem to be associated with myocardial ischaemia.

The solution is to refine the way we use the test to ensure that it is only one element of a clinically driven management algorithm. The meticulous derivation of clinical risk scores, particularly GRACE,¹¹ should be exploited. Furthermore, research that focuses on the identification of other markers of risk should be facilitated, in order to target revascularisation at those most likely to benefit. In addition, we should make use of the heterogeneous nature of current management by carefully observing outcome in patients who are not put up for inpatient angiography. Do such patients do badly? Recent data from the ICTUS trial¹² call our current strategy of early angiography for all patients with raised troponin into question.

Troponin measurement in patients with acute chest pain is a mixed blessing. We need to refine our current strategy to provide optimal treatment for such patients. Troponin is a blunt screening tool for the assessment of patients with acute coronary syndromes without ST elevation, and we should avoid compounding this by ignoring clinical factors. Above all, we need a realistic national management guideline to avoid inequity of access, pending better risk stratification tools.

Wessex Cardiac Unit, Southampton General Hospital, Southampton SO16 6YD (nick.curzen{at}suht.swest.nhs.uk)

---

Competing interests: None declared.

References

1. Hamm CW, Ravkilde J, Gerhardt W, Jorgensen P, Peheim E, Ljungdahl L, et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med 1992;327: 146-50.[Abstract]
2. Lindhal B, Venge P, Wallentin L. Relation between troponin T and subsequent cardiac events in unstable coronary artery disease. Circulation 1996;93: 1651-7.[Abstract/Free Full Text]
3. Antman EM, Tanasijevic MJ, Thompson B, Schactman M, McCabe CH, Cannon CP, et al. Cardiac-specific troponin I levels predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;335: 1342-9.[Abstract/Free Full Text]
4. FRISC II Investigators. Invasive compared with non-invasive treatment in unstable coronary artery disease: FRISC-II prospective randomised multicentre study. Lancet 1999;354: 708-15.[CrossRef][ISI][Medline]
5. Cannon CP, Weintraub WS, Demopoulos LA, Vicari R, Frey MJ, Lakkis N, et al. TACTICS-TIMI 18 Investigators. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001;344: 1879-87.[Abstract/Free Full Text]
6. Fox KA, Poole-Wilson PA, Henderson RA, Clayton TC, Chamberlain DA, Shaw TR, et al. Randomised Intervention Trial of unstable Angina (RITA) Investigators. Interventional versus conservative treatment for patients with unstable angina or non-ST elevation MI: the BHF RITA 3 randomised trial. Lancet 2002;360: 743-51.[CrossRef][ISI][Medline]
7. Archbold RA, Curzen N. The role of revascularisation in the management of non-ST elevation acute coronary syndromes: who should you refer? Clin Med 2004;4: 32-5.[Medline]
8. Bellenger N, Eichhofer J, Crone D, Curzen N. Hospital stay in patients with non-ST elevation acute coronary syndromes. Lancet 2004;363: 1399-4000.[Medline]
9. Neumann FJ, Kastrati A, Pogatsa-Murray G, Mehilli J, Bollwein H, Beste-horn HP, et al. Evaluation of prolonged antithrombotic pre-treatment ("cooling-off" strategy) before intervention in patients with unstable coronary syndromes: a randomised controlled trial. JAMA 2003;290: 1593-9.[Abstract/Free Full Text]
10. Miller C, Lipscomb K, Curzen N. Are DGH patients with unstable angina at a disadvantage? Postgrad Med J 2003;79: 93-8.[Abstract/Free Full Text]
11. Eagle KA, Lim MJ, Dabbous OH, Pieper KS, Goldberg RJ, Van de Werf F, et al; GRACE investigators. A validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6 month post discharge death in an international registry. JAMA 2004;291: 2727-33.[Abstract/Free Full Text]
12. De Winter R. Invasive vs. conservative treatment in unstable coronary syndromes (ICTUS) trial. Oral presentation, European Society of Cardiology Congress, Munich, August 2004.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Bellenger, N G, Wells, T, Hitchcock, R, Watkins, M, Duffet, C, Jewell, D, Palliser, D, Shapland, L, Curtis, R, Scrase, S, Burns, R, Curzen, N (2006). Reducing transfer times for coronary angiography in patients with acute coronary syndromes: one solution to a national problem.. Postgrad. Med. J. 82: 411-413 [Abstract] [Full text]  

Rapid Responses:

Read all Rapid Responses

A Clinical Contribution as Screening Tool for Patients with CAD.

Sergio Stagnaro
bmj.com, 12 Dec 2004 [Full text]

Pavlovian dogs

Justin Zaman
bmj.com, 14 Dec 2004 [Full text]

A much wanted approach

Nabeela Nisar
bmj.com, 1 Jan 2005 [Full text]

Guidance on the use of troponin

J Craig, et al.
bmj.com, 12 Jan 2005 [Full text]

For the majority of Acute Coronary Syndrome patients Troponin remains the most objective and cost-effective diagnostic and risk assessment marker

Abdullah Mohammed
bmj.com, 18 Jan 2005 [Full text]