European Heart Journal Advance Access originally published online on March 17, 2008
European Heart Journal 2008 29(9):1209-1210; doi:10.1093/eurheartj/ehn131
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The universal definition of myocardial infarction: some issues and concerns: reply
Department of Medicine and Cardiology
Aarhus University Hospital
Tage Hansens gade 2
DK-8000 Aarhus C
Denmark
Email: kristian.thygesen{at}as.aaa.dk
University of Arizona College of Medicine
Tucson, AZ
USA
Mayo Clinic
Rochester, MN
USA
Auckland City Hospital
Auckland
New Zealand
We are pleased to increase the educational impact of the new universal definition of myocardial infarction (MI)1–3 by responding to Lanza, who wonders why consistency was not the only criteria we used. The obvious response is that some important scientific information is unknown; there are data in some areas that suggest different approaches and strongly held convictions in others that needed to be balanced against blind obedience to consistency.
The diagnosis of spontaneous MI remains unchanged from our previous document in the year 2000,4,5 mandating a rise and/or fall of troponin values with at least one value above the 99th percentile of the upper reference limit together with evidence of myocardial ischaemia.1–5 However, the diagnosis of PCI-related MI has changed somewhat from the original document.1–5 The reasons for mandating a normal baseline value and how to proceed when that value is elevated but stable are described in the document.1–3 The criterion employed when the baseline sample is at or below the 99th percentile is a compromise solution developed to accommodate the interventional community and the clinical trials groups who pointed to a vast literature on the use of three-fold increases to optimize prognostic accuracy. At first glance, such criteria may seem different from those proposed for spontaneous MI, but they are far closer if one includes the need to develop criteria to define the rise and/or fall. At the lower range of measurement such as the 99th percentile, there is greater imprecision for troponin assays than at higher ranges.6 Furthermore, at the lower level of measurement of troponin, a large percentage change (three standard deviations of the variability) is required for to be sure that the values are analytically different. If one also appreciates that values usually are reported to 100ths and thus the need for rounding, it becomes clear that it is necessary to show a very substantial increment of change for the analytical difference. For some assays as for the troponin T assay, that is a value fully three-fold higher than the 99th percentile range. For other assays, it may not be quite that high.
It is a different scenario when considering CABG-related MI. Obligatory myocardial necrosis always occurs during CABG. Some of this injury may be mechanical, some is due to hypothermia, and some may be the result of ischaemia. There is no way of distinguishing the impact of these various causes. Accordingly, we set criteria on the basis of prognostic data that could accommodate all the types of surgery and suggested the need for additional criteria to ascertain that the myocardial injury was ischaemic.1–3
Patients who suffer sudden cardiac death with ECG changes suggestive of ischaemia often have acute coronary events at autopsy.7 This can be hard to detect because necrosis of myocardial cells requires at least 2–4 h or longer.1–3 Some of these individuals may die before blood samples for biomarkers can be obtained, or before cardiac biomarkers have risen to detectable levels. As a consequence of the scientific debate about this matter after the 2000 document, the Task Force discussed this issue in-depth and agreed that a classification of MI type 3 could be made being without biochemical evidence of myocardial necrosis if new ECG changes or evidence of fresh thrombus by angiography and/or autopsy is present.1–3
We agree that the distinction between MIs type 1 and type 2 is sometimes difficult. That is stated as ‘on occasion, patients may manifest more than one type of MI simultaneously or sequentially’.1–3 However, we consider this classification useful given the potential differences in management. There are circumstances such as peri-operative MI where most are MI type 2.8
We believe that these considerations move all the criteria of the 2007 redefinition into reasonable alignment, and that the resultant document is scientifically accurate, and clinically useful.1–3 Use of the universal definition of MI will have a major impact on the accuracy and use of clinical data from patients with MI.
References
- Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF. Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J (2007) 28:2525–2538.
[Free Full Text] - Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF. Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. J Am Coll Cardiol (2007) 50:2173–2195.
[Free Full Text] - Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF. Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Circulation (2007) 116:2634–2653.
[Free Full Text] - The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. Eur Heart J (2000) 21:1502–1513.
[Abstract/Free Full Text] - The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol (2000) 36:959–969.
[Free Full Text] - Jaffe AS, Mair J, Ordonez-Llanos J, Pagani F, Panteghini M, Tate J, IFCC Committee on Standardization of Markers of Cardiac Damage. National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage Laboratory Medicine Practice Guidelines: analytical issues for biochemical markers of acute coronary syndromes. Clin Chem (2007) 53:547–551. National Academy of Clinical Biochemistry.
[Free Full Text] - Farb A, Tang AL, Burke AP, Sessums L, Liang Y, Virmani R. Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction. Circulation (1995) 92:1701–1709.
[Abstract/Free Full Text] - Landesberg G, Mosseri M, Zahger D, Wolf Y, Perouansky M, Anner H, Drenger B, Hasin Y, Berlatzsky Y, Weissman C. Myocardial infarction after vascular surgery: the role of prolonged, stress-induced, ST depression-type ischemia. J Am Coll Cardiol (2001) 37:1839–1845.
[Abstract/Free Full Text]
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