Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction

there is greater imprecision for troponin assays than at higher ranges. 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. –3 Patients who suffer sudden cardiac death with ECG changes suggestive of ischaemia often have acute coronary events at autopsy. This can be hard to detect because necrosis of myocardial cells requires at least 2–4 h or longer. 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. –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’. 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. 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. –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 1. 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. 2. 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. 3. 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. 4. 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. 5. 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. 6. Apple FS, Jesse RL, Newby LK, Wu AHB, Christenson RH, Cannon CP, Francis G, Morrow DA, Ravkilde J, Storrow AB, Tang W; IFCC Committee on Standardization of Markers of Cardiac Damage, Jaffe AS, Mair J, Ordonez-Llanos J, Pagani F, Panteghini M, Tate J; National Academy of Clinical Biochemistry. 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. 7. 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. 8. 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.