心肌梗塞通用定义

EXPERT CONSENSUS DOCUMENT Third universal definition of myocardial infarction Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. White: the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction Authors/Task Force Members Chairpersons: Kristian Thygesen(Denmark)*, Joseph S. Alpert, (USA)*, Harvey D. White, (New Zealand)*, Biomarker Subcommittee: Allan S. Jaffe (USA), Hugo A. Katus (Germany), Fred S. Apple (USA), Bertil Lindahl (Sweden), David A. Morrow (USA), ECG Subcommittee: Bernard R. Chaitman (USA), Peter M. Clemmensen (Denmark), Per Johanson (Sweden), Hanoch Hod (Israel), Imaging Subcommittee: Richard Underwood (UK), Jeroen J. Bax (The Netherlands), Robert O. Bonow (USA), Fausto Pinto (Portugal), Raymond J.Gibbons (USA),ClassificationSubcommittee:KeithA.Fox (UK),DanAtar (Norway), L. Kristin Newby (USA), Marcello Galvani (Italy), Christian W. Hamm (Germany), Intervention Subcommittee: Barry F. Uretsky (USA), Ph. Gabriel Steg (France),WilliamWijns (Belgium), Jean-Pierre Bassand (France), Phillippe Menasche´ (France), Jan Ravkilde (Denmark), Trials & Registries Subcommittee: E. Magnus Ohman (USA), Elliott M. Antman (USA), Lars C. Wallentin (Sweden), Paul W. Armstrong (Canada), Maarten L. Simoons (The Netherlands), Heart Failure Subcommittee: James L. Januzzi (USA), Markku S. Nieminen (Finland), Mihai Gheorghiade (USA), Gerasimos Filippatos (Greece), Epidemiology Subcommittee: Russell V. Luepker (USA), Stephen P. Fortmann (USA), Wayne D. Rosamond (USA), Dan Levy (USA), DavidWood (UK), Global Perspective Subcommittee: Sidney C. Smith (USA), Dayi Hu (China), Jose´-Luis Lopez-Sendon (Spain), Rose Marie Robertson (USA), Douglas Weaver (USA), Michal Tendera (Poland), Alfred A. Bove (USA), Alexander N. Parkhomenko (Ukraine), Elena J. Vasilieva (Russia), Shanti Mendis (Switzerland). ESC Committee for Practice Guidelines (CPG): Jeroen J. Bax, (CPG Chairperson) (Netherlands), Helmut Baumgartner (Germany), Claudio Ceconi (Italy), Veronica Dean (France), Christi Deaton (UK), Robert Fagard (Belgium), Christian Funck-Brentano (France), David Hasdai (Israel), Arno Hoes (Netherlands), Paulus Kirchhof (Germany/UK), Juhani Knuuti (Finland), Philippe Kolh (Belgium), Theresa McDonagh (UK), Cyril Moulin (France), Bogdan A. Popescu (Romania), Zˇeljko Reiner (Croatia), Udo Sechtem (Germany), Per Anton Sirnes (Norway), Michal Tendera (Poland), Adam Torbicki (Poland), Alec Vahanian (France), StephanWindecker (Switzerland). * Corresponding authors/co-chairpersons: Professor Kristian Thygesen, Department of Cardiology, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark. Tel: +45 7846-7614; fax: +45 7846-7619: E-mail: kristhyg@rm.dk. Professor Joseph S. Alpert, Department of Medicine, Univ. of Arizona College of Medicine, 1501 N. Campbell Ave., P.O. Box 245037, Tucson AZ 85724, USA, Tel: +1 520 626 2763, Fax: +1 520 626 0967, Email: jalpert@email.arizona.edu. Professor Harvey D. White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, 1030 Auckland, New Zealand. Tel: +64 9 630 9992, Fax: +64 9 630 9915, Email: harveyw@ adhb.govt.nz. & The European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart Federation 2012. For permissions please email: journals.permissions@oup.com European Heart Journal doi:10.1093/eurheartj/ehs184 European Heart Journal Advance Access published August 24, 2012 by guest on A ugust 26, 2012 http://eurheartj.oxfordjournals.org/ D ow nloaded from 医 脉 通 ww w. me dl iv e. cn Document Reviewers: Joao Morais, (CPG Review Co-ordinator) (Portugal), Carlos Aguiar (Portugal), Wael Almahmeed (United Arab Emirates), David O. Arnar (Iceland), Fabio Barili (Italy), Kenneth D. Bloch (USA), Ann F. Bolger (USA), Hans Erik Bøtker (Denmark), Biykem Bozkurt (USA), Raffaele Bugiardini (Italy), Christopher Cannon (USA), James de Lemos (USA), Franz R. Eberli (Switzerland), Edgardo Escobar (Chile), Mark Hlatky (USA), Stefan James (Sweden), Karl B. Kern (USA), David J. Moliterno (USA), Christian Mueller (Switzerland), Aleksandar N. Neskovic (Serbia), Burkert Mathias Pieske (Austria), Steven P. Schulman (USA), Robert F. Storey (UK), KathrynA.Taubert (Switzerland), PascalVranckx (Belgium),Daniel R.Wagner (Luxembourg) The disclosure forms of the authors and reviewers are available on the ESC website www.escardio.org/guidelines Table of Contents Abbreviations and acronyms . . . . . . . . . . . . . . . . . . . . . . . . 2 Definition of myocardial infarction . . . . . . . . . . . . . . . . . 3 Criteria for acute myocardial infarction . . . . . . . . . . . . . . 3 Criteria for prior myocardial infarction . . . . . . . . . . . . . . 3 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Pathological characteristics of myocardial ischaemia and infarction 4 Biomarker detection of myocardial injury with necrosis . . . . . . 4 Clinical features of myocardial ischaemia and infarction . . . . . . 5 Clinical classification of myocardial infarction . . . . . . . . . . . . . 6 Spontaneous myocardial infarction (MI type 1) . . . . . . . . . 6 Myocardial infarction secondary to an ischaemic imbalance (MI type 2) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Cardiac death due to myocardial infarction (MI type 3) . . . . 7 Myocardial infarction associated with revascularization procedures (MI types 4 and 5) . . . . . . . . . . . . . . . . . . . . 7 Electrocardiographic detection of myocardial infarction . . . . . . 7 Prior myocardial infarction . . . . . . . . . . . . . . . . . . . . . . . . . 8 Silent myocardial infarction . . . . . . . . . . . . . . . . . . . . . . . . . 9 Conditions that confound the ECG diagnosis of myocardial infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Imaging techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Radionuclide imaging . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Magnetic resonance imaging . . . . . . . . . . . . . . . . . . . . . . 10 Computed tomography . . . . . . . . . . . . . . . . . . . . . . . . . 10 Applying imaging in acute myocardial infarction . . . . . . . . . 10 Applying imaging in late presentation of myocardial infarction 10 Diagnostic criteria for myocardial infarction with PCI (MI type 4) 10 Diagnostic criteria for myocardial infarction with CABG (MI type 5) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Assessment of MI in patients undergoing other cardiac procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Myocardial infarction associated with non-cardiac procedures . . 12 Myocardial infarction in the intensive care unit . . . . . . . . . . . . 12 Recurrent myocardial infarction . . . . . . . . . . . . . . . . . . . . . . 12 Reinfarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Myocardial injury or infarction associated with heart failure . . . . 12 Application of MI in clinical trials and quality assurance programmes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Public policy implications of the adjustment of the MI definition 13 Global perspectives of the definition of myocardial infarction . . 14 Conflicts of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Abbreviations and acronyms ACCF American College of Cardiology Foundation ACS acute coronary syndrome AHA American Heart Association CAD coronary artery disease CABG coronary artery bypass grafting CKMB creatine kinase MB isoform cTn cardiac troponin CT computed tomography CV coefficient of variation ECG electrocardiogram ESC European Society of Cardiology FDG fluorodeoxyglucose h hour(s) HF heart failure LBBB left bundle branch block LV left ventricle LVH left ventricular hypertrophy MI myocardial infarction mIBG meta-iodo-benzylguanidine min minute(s) MONICA Multinational MONItoring of trends and determinants in CArdiovascular disease) MPS myocardial perfusion scintigraphy MRI magnetic resonance imaging mV millivolt(s) ng/L nanogram(s) per litre Non-Q MI non-Q wave myocardial infarction NSTEMI non-ST-elevation myocardial infarction PCI percutaneous coronary intervention PET positron emission tomography pg/mL pictogram(s) per millilitre Q wave MI Q wave myocardial infarction RBBB right bundle branch block sec second(s) SPECT single photon emission computed tomography STEMI ST elevation myocardial infarction ST–T ST-segment –T wave URL upper reference limit WHF World Heart Federation WHO World Health Organization EXPERT CONSENSUS DOCUMENTPage 2 of 17 by guest on A ugust 26, 2012 http://eurheartj.oxfordjournals.org/ D ow nloaded from 医 脉 通 ww w. me dl iv e. cn Introduction Myocardial infarction (MI) can be recognised by clinical features, in- cluding electrocardiographic (ECG) findings, elevated values of bio- chemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that distinguishes between incident and recurrent events. From the epidemiological point of view, the incidence of MI in a population can be used as a proxy for the prevalence of CAD in that population. The term ‘myocardial infarction’ may have major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world and it is an outcome measure in clinical trials, obser- vational studies and quality assurance programmes. These studies and programmes require a precise and consistent definition of MI. In the past, a general consensus existed for the clinical syndrome designated as MI. In studies of disease prevalence, the World Health Organization (WHO) defined MI from symptoms, ECG abnormalities and cardiac enzymes. However, the development of ever more sensitive and myocardial tissue-specific cardiac biomarkers and more sensitive imaging techniques now allows for detection of very small amounts of myocardial injury or necrosis. Additionally, the management of patients with MI has significantly improved, resulting in less myocardial injury and necro- sis, in spite of a similar clinical presentation. Moreover, it appears necessary to distinguish the various conditions which may cause MI, such as ‘spontaneous’ and ‘procedure-related’ MI. Accordingly, physicians, other healthcare providers and patients require an up-to-date definition of MI. In 2000, the First Global MI Task Force presented a new definition of MI, which implied that any necrosis in the setting of myocardial ischaemia should be labelled as MI.1 These principles were further refined by the Second Global MI Task Force, leading to the Universal Definition of Myocardial Infarction Consensus Document in 2007, which emphasized the different conditions which might lead to an MI.2 This document, endorsed by the European Society of Cardiology (ESC), the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the World Heart Federation (WHF), has been well accepted by the medical community and adopted by the WHO.3 However, the development of even more sensitive assays for markers of myocardial necrosis mandates further revision, particularly when such necrosis occurs in the setting of the critically ill, after percutaneous coronary procedures or after cardiac surgery. The Third Global MI Task Force has continued the Joint ESC/ACCF/AHA/WHF efforts by integrating these insights and new data into the current document, which now recognizes that very small amounts of myocardial injury or necrosis can be detected by biochemical markers and/or imaging. Definition of myocardial infarction Criteria for acute myocardial infarction The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis for MI: • Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following: Symptoms of ischaemia. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB). Development of pathological Q waves in the ECG. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. Identification of an intracoronary thrombus by angiography or autopsy. • Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB,but death occurred before cardiac biomarkers were obtained, or before cardiac biomarker values would be increased. • Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (>5 x 99th percentile URL) in patients with normal baseline values (≤99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial ischaemia or (ii) new ischaemic ECG changes or (iii) angiographic findings consistent with a procedural complication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required. • Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL. • Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (>10 x 99th percentile URL) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB, or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. Criteria for prior myocardial infarction Any one of the following criteria meets the diagnosis for prior MI: • Pathological Q waves with or without symptoms in the absence of non-ischaemic causes. • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non-ischaemic cause. • Pathological findings of a prior MI. EXPERT CONSENSUS DOCUMENT Page 3 of 17 by guest on A ugust 26, 2012 http://eurheartj.oxfordjournals.org/ D ow nloaded from 医 脉 通 ww w. me dl iv e. cn Pathological characteristics of myocardial ischaemia and infarction MI is defined in pathology as myocardial cell death due to pro- longed ischaemia. After the onset of myocardial ischaemia, histo- logical cell death is not immediate, but takes a finite period of time to develop—as little as 20 min, or less in some animal models.4 It takes several hours before myocardial necrosis can be identified by macroscopic or microscopic post-mortem exam- ination. Complete necrosis of myocardial cells at risk requires at least 2–4 h, or longer, depending on the presence of collateral cir- culation to the ischaemic zone, persistent or intermittent coronary arterial occlusion, the sensitivity of the myocytes to ischaemia, pre- conditioning, and individual demand for oxygen and nutrients.2 The entire process leading to a healed infarction usually takes at least 5–6 weeks. Reperfusion may alter the macroscopic and micro- scopic appearance. Biomarker detection of myocardial injury with necrosis Myocardial injury is detected when blood levels of sensitive and specific biomarkers such as cTn or the MB fraction of creatine kinase (CKMB) are increased.2 Cardiac troponin I and T are com- ponents of the contractile apparatus of myocardial cells and are expressed almost exclusively in the heart. Although elevations of these biomarkers in the blood reflect injury leading to necrosis of myocardial cells, they do not indicate the underlying mechan- ism.5 Various possibilities have been suggested for release of struc- tural proteins from the myocardium, including normal turnover of myocardial cells, apoptosis, cellular release of troponin degradation products, increased cellular wall permeability, formation and release of membranous blebs, and myocyte necrosis.6 Regardless of the pathobiology, myocardial necrosis due to myocardial ischae- mia is designated as MI. Also, histological evidence of myocardial injury with necrosis may be detectable in clinical conditions associated with predomin- antly non-ischaemic myocardial injury. Small amounts of myocar- dial injury with necrosis may be detected, which are associated with heart failure (HF), renal failure, myocarditis, arrhythmias, pul- monary embolism or otherwise uneventful percutaneous or surgi- cal coronary procedures. These should not be labelled as MI or a complication of the procedures, but rather as myocardial injury, as illustrated in Figure 1. It is recognized that the complexity of clinical circumstances may sometimes render it difficult to determine where individual cases may lie within the ovals of Figure 1. In this setting, it is important to distinguish acute causes of cTn elevation, which require a rise and/or fall of cTn values, from chronic Figure 1 This illustration shows various clinical entities: for example, renal failure, heart failure, tachy- or bradyarrhythmia, cardiac or non- cardiac procedures that can be associated with myocardial injury with cell death marked by cardiac troponin elevation. However, these entities can also be associated with myocardial infarction in case of clinical evidence of acute myocardial ischaemia with rise and/or fall of cardiac troponin. EXPERT CONSENSUS DOCUMENTPage 4 of 17 by guest on A ugust 26, 2012 http://eurheartj.oxfordjournals.org/ D ow nloaded from 医 脉 通 ww w. me dl iv e. cn elevations that tend not to change acutely. A list of such clinical cir- cumstances associated with elevated values of cTn is presented in Table 1. The multifactorial contributions resulting in the myocardial injury should be described in the patient record. The preferred biomarker—overall and for each specific category of MI—is cTn (I or T), which has high myocardial tissue specificity as well as high clinical sensitivity. Detection of a rise and/or fall of the measurements is essential to the diagnosis of acute MI.7 An increased cTn concentration is defined as a value exceeding the 99th percentile of a normal reference population [upper reference limit (URL)]. This discriminatory 99th percentile is designated as the decision level for the diagnosis of MI and must be determined for each specific assay with appropriate quality control in each laboratory.8,9 The values for the 99th percentile URL defined by manufacturers, including those for many of the high-sensitivity assays in development, can be found in the package inserts for the assays or in recent publications.10,11,12 Values should be presented as nanograms per litre (ng/L) or picograms per millilitre (pg/mL) to mak