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The American College of Cardiology and European Society of Cardiology have redefined myocardial infarction as a rise of troponin above the laboratory reference range (99th percentile of a reference control group), in conjunction with typically ischaemic symptoms, a history of recent coronary intervention, the development of Q waves or dynamic ST-segment changes.1
Troponin concentrations are highly specific for myocardial necrosis, but disease states other than myocardial infarction can cause elevated plasma levels (table 1).2 It is our impression that there has been widespread misinterpretation of the new definition, and troponin concentrations are frequently assumed to reflect myocardial infarction without corroborative evidence from the patient’s history or electrocardiogram (ECG). We present an illustrative case of elevated troponin concentrations following minor chest trauma.
A fit 29 year old man presented to the ED with chest discomfort. He was the goalkeeper in a football match the previous day and was struck forcibly in the chest with a football. He continued the rest of the match without difficulty but subsequently developed diffuse non-radiating central chest discomfort and malaise persisting for several hours.
His past medical history was unremarkable. He used no regular medications or illicit drugs. He smoked 20 cigarettes per day but had no other risk factors for ischaemic heart disease.
On examination, there were no signs of external injury to his praecordium. Cardiovascular examination was normal with a blood pressure of 137/72. His full blood count, renal function, ECG, and chest x ray were normal with a total cholesterol of 3.79 mmol/l. Troponin I was measured 12 hours after the onset of his symptoms, and was elevated at 5.18 μg/L (reference range 0.00–0.03 μg/L). CK measured from admission was elevated at 1018 IU/L with a CK-MB fraction of 6.4%, and repeat troponin I the following day was also elevated at 4.40 μg/L. Serial ECGs were normal but a diagnosis of myocardial infraction was made and he was referred to a tertiary referral centre for future management.
On transfer, his echocardiography revealed normal valvular and ventricular function, with no pericardial effusion or abnormalities of the aortic root. He completed 9 minutes of exercise in standard Bruce Protocol without symptoms or ECG changes. Coronary angiography revealed normal coronary arteries and left ventricular function. A diagnosis of myocardial contusion was made, and after considerable difficulty resulting from the anxiety provoked by his earlier diagnosis of myocardial infarction, he was reassured and discharged.
Measurement of plasma troponin has been a major advance in the management of acute coronary syndromes, identifying a high risk subset of patients likely to benefit from an early invasive treatment strategy.3,4 These patients are now classified as having had myocardial infarctions, though many have only small areas of myocardial necrosis. The epidemiological and societal consequences of this new definition are as yet unclear. More worrying is the observed trend to use troponin measurement as the sole criterion for the diagnosis of myocardial infarction.
Myocardial infarction is the most likely cause of elevated plasma troponin in the acute setting, but levels can be raised in other conditions (table 1).2 Myocardial trauma should be considered in patients with a history of blunt chest injury and cardiac troponins have been proposed as a means to diagnose and measure degrees of myocardial contusion.5–7 In this patient, his young age, history, lack of risk factors, and normal ECGs would suggest a low likelihood of myocardial infarction. Importantly an elevated troponin level alone was insufficient to make the diagnosis of myocardial infarction.
The diagnosis of myocardial infraction has major psychological and socioeconomic implications. Elevated troponin without a typical history or ECG change should prompt consideration of alternative diagnoses.