doi: 10.1111/j.1742 6723.2009.01225.x

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  • 8/14/2019 Doi: 10.1111/j.1742 6723.2009.01225.x

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  • 8/14/2019 Doi: 10.1111/j.1742 6723.2009.01225.x

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    indicating ACS might result in inappropriate investiga-tions or treatment, at risk to the patient and cost tohealth services. Perhaps of more concern, it could alsoresult in a delay to appropriate treatment for thepatients condition.

    What is required is appropriate clinical assessment,serial biomarker assays (if indicated) and a manage-ment plan tailored to the patients condition. Thestudys results cannot tell us one way or the otherwhether appropriate assessments were made in thecases in question, or had the patients been admittedwhether a different outcome might have occurred. Asignicant proportion of troponin-positive patients, par-ticularly those with chronic troponin elevations, mightbe quite appropriately managed in the community. Thisdoes not underplay their mortality risk. Rather, itaccepts that these patients have chronic illnesses requir-ing long-term supervision. The study also does not tellus what proportion of patients chose to leave hospitalagainst medical advice.

    Studies such as this are powerful tools to alert clini-cians to potential problems in systems of care. Their

    weakness is the inability to provide data about the con-tributing factors to the outcome found. They are a start-ing point. The hypotheses they raise, in this case thatthere is preventable mortality associated with a positivetroponin level in patients discharged from the ED,require detailed analysis at the case level to conrm orrefute the hypothesis, and to identify improvements tosystems of care. We need to understand why if we aregoing to x it.

    The troponin story, particularly from the emergencymedicine perspective, is far from over. Debate continuesabout the signicance and management of troponinlevels in the one to ve times upper limit of normal zone.The use of troponin for risk stratication of conditionsother than ACS is also under active exploration. Timingof serial troponin assays is in ux as more sensitivetests become more widely available. And research con-tinues to identify even better biomarkers for identica-tion of ACS. Watch this space!

    References

    1. Fleming SM, Daly KM. Cardiac troponins in suspected acutecoronary syndrome: a meta-analysis of published trials. Cardiol-

    ogy 2001; 95 : 6673.2. Jeremias A, Gibson CM. Narrative review: alternative causes for

    elevated cardiac troponin levels when acute coronary syndromesare excluded. Ann. Intern. Med. 2005; 142 : 78691.

    3. Burness CE, Beacock D, Channer KS. Pitfalls and problems of relying on serum troponin. QJM. 2005; 98 : 36571.

    4. Eggers KM, Oldgren J, Nordenskjold A, Lindahl D. Diagnosticvalue of serial measurement of cardiac markers in patients withchest pain: Limited value of adding myoglobin to troponin I forexclusion of myocardial infarction. Am. Heart. J. 2004; 148 :57481.

    5. Hill SA, Devereaux PJ, Grifth L et al. Can TnI I measurementpredict short-term serious cardiac outcomes in patients present-ing to the emergency department with possible acute coronarysyndrome? CJEM. 2004; 6 : 2230.

    6. Roe MT, Peterson ED, Li Y et al. Relationship between riskstratication by cardiac troponin level and adherence to guide-lines for nonST-segment elevation acute coronary syndromes. Arch. Intern. Med. 2005; 165 : 18706.

    7. Lee HM, Kerr D, Oh Ici D, Kelly AM. Clinical signicance of initial troponin i in the intermediate band in emergency depart-ment chest pain patients: a pilot study. Emerg. Med. J. in press.

    8. Flindell JA, Finn JC, Gibson NP, Jacobs IG. Short-term risk of adverse outcome is signicantly higher in patients returning anabnormal troponin result when tested in the emergency depart-ment. Emerg. Med. Australas. 2009; 21 : 46571.

    Table 1. Non-ACS causes of troponin elevations 2,3

    Acute rheumatic fever

    Cardiac contusionCardiac inltrative disordersCardiac transplantationChemotherapyChronic renal insufciencyCongestive cardiac failureCoronary vasospasmDirect current cardioversionEmphysema (COAD)Envenomation (e.g. jellysh, scorpion)Heterophile antibodyHypotensionHypovolaemiaIdiopathicIngestion of sympathomimetic agentsIntracranial haemorrhage or strokeLeft ventricular hypertrophyMyocarditis/pericarditisPhysical exertionPolymyositis/dermatomyositisPulmonary embolismPulmonary hypertensionSepsis/ systemic inammatory response syndromeSeropositive rheumatoid arthritisSupraventricular tachycardia/atrial brillation

    ACS, acute coronary syndrome; COAD, chronic obstructiveairways disease.

    A-M Kelly

    434 2009 The Author Journal compilation 2009 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine