Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Innovation fails to address the issue of mild troponinemia
- Malvinder S. Parmar (3 February 2009)
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The diagnostic precision of troponin in clinical research: a problem solved by a panel?
- Madeleine HE Bruins Slot (10 February 2009)
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Clinical classification
- Malvinder S. Parmar (12 February 2009)
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One for the editor
- Rosanne E Murray (13 February 2009)
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Troponin: Time for interpretation
- Jaimini Cegla, Gurjinder M. Nijher (22 February 2009)
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Malvinder S. Parmar, Associate Professor, Northern Ontario School of Medicine Timmins & District Hospital, Timmins, ON, Canada P4N 8P2
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I find the use of term ‘bold innovation’ in the new definition of myocardial infarction somewhat amusing, when the classification fails to address the main issue of over-diagnosis of myocardial infarction (1). The definition or classification fails to address the issue of ‘mild troponinemia’ [slight elevation in troponin I or T levels that is often seen in clinical practice, especially in patients with multiple co-morbid conditions, like diabetes, heart or kidney failure who often present with dyspnea, infectious process like pneumonia or exacerbation of chronic obstructive pulmonary disease, or atypical symptoms](2). These patients, no doubt, are at increased risk for cardiovascular mortality (3). However, these episodes, in true sense, do not fulfill the definition of acute myocardial infarction but often such patients are given a diagnosis of “non-ST elevation myocardial infarction (NSTEMI)” at the time of discharge that likely is responsible for the increase in the incidence of myocardial infarction since 2000. Such patients are often told that they had a “small heart attack” and some of the patients may have had the so called “small heart attacks” many times and appear to outlive cats, as cats are said to have nine-lives. A sudden death is a death that may be secondary to myocardial infarction but there are other causes of sudden death that shouldn’t be undermined. Labeling all cases of sudden death or cardiac arrest as type 3 myocardial infarction would undermine the importance of other treatable causes – like arrhythmia, pulmonary embolism, hyperkalemia etc., where establishing a correct diagnosis is important to tailor appropriate therapy and advocate preventive strategies. Labeling sudden death as type 3 myocardial infarction is no consolation or relief to the deceased’s family. It doesn’t make sense clinically to divide peri-procedural myocardial infarction following cardiac procedures (like percutaneous coronary intervention (PCI) and coronary artery bypass surgery) into two types – Type 4 and type 5. This is redundant and the classification still misses addressing the mild troponinemia seen with other cardiac procedures, such as defibrillation and electrical cardioversion. I could understand if type 4 was related to cardiac procedures and type 5 associated with non-cardiac procedures or surgeries, for research purposes. The current classification may be helpful to the researcher but doesn’t help the clinician or the patient. Issues concerning ‘mild troponinemia’ require attention to properly call a true myocardial infarct as “myocardial infarct” and how to address others remains to be clarified and I strongly feel that a new term “mild troponinemia of clinical significance (MTCG)” should be coined to address this issue, akin to monoclonal gammopathy of unknown significance (MGUS) in patients with paraproteinemic disorders who doesn’t fulfill the criteria of multiple myeloma but has abnormal monoclonal bands. Labeling patients with MTCG would clearly define such patients with borderline or mild elevations in troponin levels, who don’t fulfill the criteria for myocardial infarction, but who are still at increased risk (2) compared to normal population and this classification would then correctly determine the correct incidence of myocardial infarction that likely is exaggerated by the current criteria (1) around the world. I strongly feel that these issues should be addressed before implementing the new ‘Clinical’ classification that doesn’t help the clinician at all, in present form. References: 1. Hagen TP, Reikvam A. [Marked increase of the number of myocardial infarctions following introduction of the new diagnostic criteria]. Tidsskr Nor Laegeforen. 2003 Nov 6;123(21):3041-3. PMID: 14618172 2. De Gennaro L, Brunetti ND, Cuculo A, Pellegrino PL, Izzo P, Roma F, Di Biase M. Increased troponin levels in nonischemic cardiac conditions and noncardiac diseases. J Interv Cardiol. 2008 Apr;21(2):129-39. Epub 2008 Jan 28 PMID: 18248355 3. Eggers KM, Lagerqvist B, Venge P, Wallentin L, Lindahl B. Persistent cardiac troponin I elevation in stabilized patients after an episode of acute coronary syndrome predicts long-term mortality. Circulation. 2007 Oct 23;116(17):1907-14. Epub 2007 Oct 1. PMID: 17909103 Competing interests: None declared |
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Madeleine HE Bruins Slot, Researcher - general practitioner in training Julius Center, UMC Utrecht, PO Box 85500, 3508 GA Utrecht
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Biomarkers have become the cornerstone in the diagnosis of myocardial infarction (1). The use of different laboratory assays with a different diagnostic precision for the measurement of troponin I or T remains problematic however, as is addressed by Atar. We encountered a similar problem in our diagnostic study on the added value of heart-type fatty acid binding protein (H-FABP) and this is our solution. The design of our study has been published previously (2). In short: in several general practices in the Netherlands the indextest (a bedside H -FABP test) is performed by the general practitioner (GP). Subsequently, in all patients an ECG is recorded and troponin levels are measured. Due to the multicenter design of our study, the troponin measurements are performed in different hospitals and one GP laboratory, using different laboratory assays. We tackled this problem by using an expert panel consisting of two cardiologists and one GP to establish the final diagnosis of myocardial infarction (“gold standard”). The panel is provided with all available patient information (including one month of follow-up for any renewed cardiac events). In this way, the results of troponin measurements can be placed into perspective. Even “mild troponinemia” (see rapid response Parmar 3 February 2009) in our study is labeled correctly, as other etiologies for a rise in troponin (other than myocardial ischemia) will be detected. In clinical studies on myocardial infarction the use of outcome panel meetings to establish the diagnosis may help solve the problem of differences in diagnostic precision in troponin measurements. It will also provide a more detailed explanation for elevations of troponin in the absence of myocardial ischemia. (1) Bassand JP, Hamm CW, Ardissino D, Boersma E, Budaj A, Fernandez- Aviles F et al. Guidelines for the diagnosis and treatment of non-ST- segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology. Eur Heart J 2007; 28(13):1598-1660. (2) Bruins Slot MH, van der Heijden GJ, Rutten FH, van der Spoel OP, Mast EG, Bredero AC et al. Heart-type Fatty acid-binding protein in Acute Myocardial infarction Evaluation (FAME): background and design of a diagnostic study in primary care. BMC Cardiovasc Disord 2008; 8:8. Competing interests: None declared |
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Malvinder S. Parmar, Associate Professor, Northern Ontario School of Medicine Timmins & District Hospital, Timmins, ON, Canada P4N 8P2
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As a follow-up to my previous rapid response [3 February 2009], I think we should modify the current propsed definition, that is not, in its present form, is clinically applicable in daily practice. I propose the following classification,
1. ST elevation myocardial infarction (STEMI) - where there is classic ST elevation. 2. Non-ST elevation myocardial infarction (NSTEMI) - where patient has clinical and bicohemical parameters consistent with MI, but without ST elevation, as name implies 3. Mild Troponinemia of indeterminate origin and significance (MTIOS) or Undetermined origin and significance (MTUOS) - This is the group that likely has increased the incidence of acute myocardial infarction since 2000, when a diagnosis of "NSTEMI" is given to many patients who in true sense has no clear evidence of MI. This group needs to be identified as a separate group and further study is required about the long-term prognostic implications of this group. Competing interests: None declared |
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Rosanne E Murray, SPR Neurology Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE46BE
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Surely this editorial deserved higher visibility within the journal in order to effectively disseminate information most doctors will need to know. It seems more worthy of a mention on the title page than the recurring pharma relations debate. Competing interests: None declared |
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Jaimini Cegla, Specialist Registrar in Chemical Pathology (Metabolic Medicine) Imperial College Healthcare NHS Trust, Hammersmith Hospital, Du Cane Rd, London, W12 0HS, Gurjinder M. Nijher
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Troponin has taken centre stage in the diagnosis of myocardial infarction. However, with this, clinical judgment and ECG interpretation appear to have moved to the wings. As a cardiology SHO, I well remember the frustration of having to review vast numbers of nonagenerians with chronic renal failure and surprise, surprise, a mildly elevated troponin result. Now as a Chemical Pathology SpR, troponin still taunts me. For instance yesterday, we had 15 requests to the lab for a troponin. Of these, 3 came without any clinical details, 7 with chest pain, 3 ‘unwell’, 1 collapse ?cause and 1 clinician thought that ‘emergency laparotomy’ was an indication for requesting troponin. There was no information regarding timing of the clinical event with regards to timing of troponin sample. The most recent guidelines for the definition of myocardial infarction do indeed give strict laboratory criteria as to what constitutes a raised level; however, the clinical criteria are still integral to the definition (Ref 1): -Troponin above the 99th percentile of the upper reference limit together with evidence of myocardial ischaemia with at least one of the following: -Symptoms of ischaemia -ECG changes indicative of new ischaemia -Development of pathological Q waves on the ECG -Imaging evidence of new myocardial damage One of the main difficulties is that many clinicians do not understand that all assays come with their own challenges. Measurements are not absolute but dependent on error of measurement, as always, and some assays are more variable than others – plasma troponin. It has been recommended that at the 99th centile, troponin assays should have an analytical coefficient of variation of less than 10%. Coefficient of variation is the standard deviation of a particular test divided by the mean. It gives us an idea of how much a result would differ from one run to another. Many commercially available assays do not achieve this coefficient of variation and therefore their reliability for the diagnosis of myocardial infarction comes into question. Even more concerning are the number of point of care assays available which are not managed by biochemistry departments and thus are not subjected to regular quality control assessments. Chemical pathologists need to work hand in hand with cardiologists to overcome these challenges. Furthermore, we need to become much more involved in teaching laboratory medicine to our medical students if we are to expect our future clinicians to understand the tests that they are requesting. References 1. Thygesen K, Albert JS, White HD, on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J 2007;28:2525-38 Competing interests: None declared |
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