Re: Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study
We read with interest the findings by Mills et al. that patients with suspected Acute Coronary Syndrome and Troponin I in the range 0.012-0.049μg/l are more likely to die or suffer recurrent myocardial infarction than those with lower levels of troponin. 1342 of 3434 identified patients met the authors exclusion criteria, suggesting that 61% of patients in their centre having Troponin tests were relatively straightforward chest pain presentations.[1] This does not reflect the use of these tests in unselected secondary care settings.
We reviewed the first complete month (November 2010) experience of the use of a high sensitivity troponin T assay in a Secondary Care hospital with an average unselected medical take of around 30 patients per day. A new diagnostic level of 0.015μg/l was introduced having previously been equivalent to 0.050 μg/l giving us a very similar population group to those identified by Mills et al. Over that 30 days 42 patients were identified with troponin levels between 0.015 and 0.049 μg/l, and not rising to meet the old diagnostic category on repeat tests. Retrospective review of the history, electrocardiograms and other investigations of these patients who were not all assessed by a cardiologist during their admission suggested the diagnosis of Acute Myocardial Infarction could be made in 13 of these patients (31%). The troponin rise was attributed to a range of other diagnoses, dominated by renal failure, dysrhythmia and sepsis, and was not limited to alternative cardiac causes of raised troponin (such as pulmonary embolus and myocarditis). In some cases the clinical documentation failed to justify any indication for a troponin assessment being requested. A group of patients, often elderly with extensive co-morbidity are seen where no clear explanation for a small troponin rise can be pinpointed, but the clinical picture is not of Acute Coronary Syndrome. This is not a new finding, and the prognostic significance has been documented before.[2] With more widespread and indiscriminate use of high sensitivity troponins in secondary care it is likely that higher numbers of these patients, for whom there is a lack of evidence on which to base management, will be identified.
Prof Timmis [3] suggests that new troponin diagnostic definitions would reclassify troponin negative acute coronary syndromes to troponin positive myocardial infarctions. In patients with a typical history and/or suggestive ECG changes this will be the case, or alternatively, the diagnosis of “troponin positive acute coronary syndrome” may be made. In this way the new assays are identifying more patients at potential cardiac risk and these patients should be offered appropriate cardioprotective medication and be considered for coronary intervention and/or functional cardiac testing. In this way the use of new troponin limits may identify patients benefitting from more aggressive investigation and management, given the adverse prognosis suggested by Mills et al. We have similarly found that this is not a small group (more than one person every 2.3 days in our hospital) and we agree fully that urgent work is needed to determine the correct approach to managing these patients.
In patients in whom the high sensitive troponin assay is negative, there will be more confidence that early discharge from A&E or the emergency admission unit will be safe and that further cardiac or non-cardiac investigation can occur as an out-patient.
1.Mills NL, Lee KK, McAllister DA, Churchhouse AM, Macleod M, Stoddart M, et al. Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study. BMJ 2012; 344: e1533.
2.Zaman MJS, Vrotsou K, Chu GS, May HM, Myint PK. A high incidental rise in cardiac troponin I carries a higher mortality risk in older patients than in those with a diagnosed acute coronary syndrome. Age and ageing. 2011;40:122-5.
3.Timmis A. New guidance for troponin assays. BMJ 2012; 344: e1736.
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Re: Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study
We read with interest the findings by Mills et al. that patients with suspected Acute Coronary Syndrome and Troponin I in the range 0.012-0.049μg/l are more likely to die or suffer recurrent myocardial infarction than those with lower levels of troponin. 1342 of 3434 identified patients met the authors exclusion criteria, suggesting that 61% of patients in their centre having Troponin tests were relatively straightforward chest pain presentations.[1] This does not reflect the use of these tests in unselected secondary care settings.
We reviewed the first complete month (November 2010) experience of the use of a high sensitivity troponin T assay in a Secondary Care hospital with an average unselected medical take of around 30 patients per day. A new diagnostic level of 0.015μg/l was introduced having previously been equivalent to 0.050 μg/l giving us a very similar population group to those identified by Mills et al. Over that 30 days 42 patients were identified with troponin levels between 0.015 and 0.049 μg/l, and not rising to meet the old diagnostic category on repeat tests. Retrospective review of the history, electrocardiograms and other investigations of these patients who were not all assessed by a cardiologist during their admission suggested the diagnosis of Acute Myocardial Infarction could be made in 13 of these patients (31%). The troponin rise was attributed to a range of other diagnoses, dominated by renal failure, dysrhythmia and sepsis, and was not limited to alternative cardiac causes of raised troponin (such as pulmonary embolus and myocarditis). In some cases the clinical documentation failed to justify any indication for a troponin assessment being requested. A group of patients, often elderly with extensive co-morbidity are seen where no clear explanation for a small troponin rise can be pinpointed, but the clinical picture is not of Acute Coronary Syndrome. This is not a new finding, and the prognostic significance has been documented before.[2] With more widespread and indiscriminate use of high sensitivity troponins in secondary care it is likely that higher numbers of these patients, for whom there is a lack of evidence on which to base management, will be identified.
Prof Timmis [3] suggests that new troponin diagnostic definitions would reclassify troponin negative acute coronary syndromes to troponin positive myocardial infarctions. In patients with a typical history and/or suggestive ECG changes this will be the case, or alternatively, the diagnosis of “troponin positive acute coronary syndrome” may be made. In this way the new assays are identifying more patients at potential cardiac risk and these patients should be offered appropriate cardioprotective medication and be considered for coronary intervention and/or functional cardiac testing. In this way the use of new troponin limits may identify patients benefitting from more aggressive investigation and management, given the adverse prognosis suggested by Mills et al. We have similarly found that this is not a small group (more than one person every 2.3 days in our hospital) and we agree fully that urgent work is needed to determine the correct approach to managing these patients.
In patients in whom the high sensitive troponin assay is negative, there will be more confidence that early discharge from A&E or the emergency admission unit will be safe and that further cardiac or non-cardiac investigation can occur as an out-patient.
1.Mills NL, Lee KK, McAllister DA, Churchhouse AM, Macleod M, Stoddart M, et al. Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study. BMJ 2012; 344: e1533.
2.Zaman MJS, Vrotsou K, Chu GS, May HM, Myint PK. A high incidental rise in cardiac troponin I carries a higher mortality risk in older patients than in those with a diagnosed acute coronary syndrome. Age and ageing. 2011;40:122-5.
3.Timmis A. New guidance for troponin assays. BMJ 2012; 344: e1736.
Competing interests: No competing interests