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Cardiac troponin I and T are well known as biomarkers in the assessment of myocardial injury. An appreciation and understanding the pathophysiology of troponin and the timing of troponin testing is fundamental in the clinical utility of these biomarkers, as troponin and its kinetics are central to the universal definition of acute myocardial infarction (AMI).
Troponin levels become elevated in serum within hours of an AMI, remaining elevated for up to 7-10 days. There are other conditions that result in elevated troponin concentrations, so it is essential that the results of troponin tests are interpreted in conjunction with clinical findings and electrocardiography results.
The dynamics of troponin levels help distinguish AMI from non-AMI conditions, thus serial troponin testing is a well-documented approach in the assessment of patients with suspected acute coronary syndrome (ACS).
Troponin testing within the community is complex with ACS management guidelines recommending a troponin test result be available within 60 minutes of blood being drawn or point-of-care testing be available if the former is difficult. Appreciably this is difficult for large pathology networks that test hundreds of community samples daily involving a large number of collection centres and clinical practices.
The clinical utility of troponin in an outpatient setting is best reserved for low-risk patients and may occur in two situations.
The first is when a patient has had symptoms of ACS in the preceding days but, on presentation, symptoms have resolved and the patient is clinically stable and deemed to be at low risk. The second is when the patient presents with atypical symptoms with a low likelihood of ACS, and the clinician uses troponin testing to ‘rule out’ ACS. An elevated troponin in this setting may occasionally be detected, which will subsequently allow for appropriate management and specialist referral.
Ordering a troponin test in the community setting should be done cautiously. It is not appropriate to measure serial troponin levels in the community, as the patient will not be monitored for possible worsening symptoms and potential complications. It is also not recommended to measure troponin in asymptomatic patients or to use troponin as a screening tool as the result may be problematic, with no clear management strategy, and may lead to further unnecessary investigations.
If a troponin test is ordered in an outpatient setting, it should be clearly marked as urgent and a mechanism in place for the doctor and patient to be contacted with the results. If such logistics are not in place, potential delays with follow-up of positive results may occur. The patient could potentially be in the community with an elevated troponin level without adequate follow-up and not be receiving appropriate clinical care.
If there is a lack of capacity to receive troponin results and arrange appropriate clinical follow-up when performed in the community on low-risk patients (e.g. afternoon, weekends), referral to an emergency department would be considered appropriate. It is acceptable clinical practice to promptly refer patients presenting with symptoms suggestive of ACS to hospital without first undertaking community troponin testing.
As with any request, referral for acute management should not be delayed until receipt of the troponin result, as any delay may significantly negatively impact on outcomes and result in increased morbidity and mortality.
Conclusion
Clinicians should have a high threshold for requesting troponin testing in the outpatient setting, carefully assessing and evaluating the risk before ordering. Positive troponin test results usually change the course of management, but the time frame in which the result becomes available must be balanced against the risk of delay in diagnosis and therapy.
A troponin test should not be requested unless a Clinician is confident a robust process is in place by which they can be contacted, day or night in the case of a positive result.
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