Serum troponin estimation is widely used in the diagnosis and management of coronary syndromes, but it is possible to be misled by a positive result unless it is put carefully into clinical context. The serum troponin can be positive in pulmonary embolus and carries prognostic significance. A case report is presented and a review of the relevant literature.
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Troponin assays have had a considerable impact in the diagnosis and risk stratification of patients presenting with an acute coronary syndrome. A correctly timed troponin assay has 95%–100% sensitivity and 85%–90% specificity for myocardial damage.1–4 However, there are many other causes of a positive troponin test that should be remembered when assessing these patients in order to avoid misdiagnosis.
A 77 year old woman was admitted to hospital with an exacerbation of chronic obstructive pulmonary disease. She had a background of controlled hypertension, paroxysmal atrial fibrillation, and had been a heavy smoker for 30 years. She responded well to initial treatment with antibiotics, bronchodilators, and corticosteroids.
Five days after her admission, she deteriorated acutely with tight central chest pain and dyspnoea. On examination, she was tachycardic (rate 110, sinus rhythm), hypotensive (BP 90/50), but heart sounds were normal and the jugular venous pressure was not elevated. Her ECG showed ST segment depression and T-wave inversion antero-laterally, suggestive of myocardial ischaemia. The chest radiograph showed hyperinflated lung fields but was otherwise unremarkable; her peripheral oxygen saturations were 85%. She was treated with diamorphine, low molecular weight heparin, and aspirin. There was a small rise in creatine kinase (52 to 209 IU/l (normal range 24–195 IU/l)) and the troponin T 12 hours after the pain was significantly raised at 2.1 μg/l (normal <0.01 μg/l), consistent with significant myocardial damage. Two days later she was still limited by significant dyspnoea and hypoxia (po2 8.3 on air) and the diagnosis of pulmonary embolus was suspected. An echocardiogram was normal in particular demonstrating normal left and right ventricular dimensions and no regional wall motion abnormalities. There was no significant tricuspid regurgitation to permit an estimation of the pulmonary artery pressure. A d-dimer assay was strongly positive at 3872 ng/ml (normal <500 ng/ml) and a ventilation-perfusion scan showed multiple unmatched defects, indicating a high probability of pulmonary embolus.
An increased serum troponin concentration is found not only in acute coronary syndromes but in several other conditions: myocarditis, stroke, myocardial trauma, post-CABG, chronic renal failure, ischaemic heart failure, ischaemic arrhythmia, and pulmonary embolism.5–7 The combination of the ischaemic ECG and positive troponin test made pulmonary embolus a difficult initial diagnosis to make in this patient. Indeed, our patient met the revised joint guidelines8 for the diagnosis of myocardial infarction. Whether there was concomitant pulmonary embolus and myocardial infarction or pulmonary embolus revealing underlying myocardial ischaemia, is difficult to determine absolutely as further investigation (for example, coronary angiography) was not performed.
Typically, the ECG changes of a pulmonary embolus, if any, are those of either a sinus tachycardia or atrial fibrillation with right heart strain, though many electrocardiographic abnormalities have been reported—rhythm disturbances, axis change, ST-T changes and QT interval prolongation.9–11 However, such changes are often transient and the value of the 12-lead ECG in the diagnosis and risk stratification of suspected pulmonary embolus is limited.12 ST elevation on the ECG in pulmonary embolus is recognised but an unusual finding.13 Given the cardiovascular risk factors present in our patient, it seems probable that there was significant coronary artery disease, which was revealed by the hypoxia and acute cardiac insult of a pulmonary embolus.
A positive troponin test is an important prognostic marker in pulmonary embolus, and predicts right ventricular dilatation and an increased number of segmental perfusion defects on lung scintigraphy.14 In a series of 56 patients presenting with pulmonary embolism, 18 (32%) had an increased troponin T concentration (>0.1 μg/l) taken at 12 hours after presentation. These patients had higher risk of developing complications including in-hospital death (odds ratio 29.6:1, 95% CI 3.3 to 265.3), prolonged hypotension and cardiogenic shock (odds ratio 11.4:1, 95% CI 2.1 to 63.4), the need for iontropic support (odds ratio 37.6:1, 95% CI 5.8 to 245.6), and mechanical ventilation (odds ratio 78.8:1, 95% CI 9.5 to 653.2).15 Moreover, after adjustment, an increased troponin T value was an independent predictor of 30 day mortality in pulmonary embolus (odds ratio 15.2:1, 95% CI 1.22 to 190.4). It is suggested that troponin estimation may be used to help risk stratify patients with pulmonary embolus who warrant more aggressive treatment.
The recent Joint American and European guidelines8 on the diagnosis of myocardial infarction rely heavily upon troponin testing (box). An awareness of other conditions that cause an increased troponin concentration is needed to avoid misdiagnoses. This is particularly the case for patients with pulmonary emboli that may clinically mimic myocardial ischaemia but for which the management is completely different.
Joint European and American guidelines on the diagnosis of myocardial infarction8
A typical rise and fall in troponin or CK-MB
Plus at least one of the following:
– ischaemic symptoms
– development of pathological Q waves on the ECG
– ECG changes suggestive of ischaemia—ST elevation or ST depression
Coronary artery intervention, for example, coronary angioplasty
Simon Conroy: original idea and literature review. Imad Kamal: advice on content and style. John Cooper: advice on cardiological aspects, style, and content.
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