The Universal Definition of Myocardial Infarction

HomeCirculationVol. 141, No. 18The Universal Definition of Myocardial Infarction Free AccessArticle CommentaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessArticle CommentaryPDF/EPUBThe Universal Definition of Myocardial InfarctionPresent and Future Yader Sandoval, MD, Kristian Thygesen, MD, DSc and Allan S. Jaffe, MD Yader SandovalYader Sandoval Departments of Cardiovascular Diseases (S.Y., A.S.J.), Mayo Clinic, Rochester, MN. , Kristian ThygesenKristian Thygesen Department of Cardiology, Aarhus University Hospital, Denmark (K.T.). and Allan S. JaffeAllan S. Jaffe Allan S. Jaffe, MD, Department of Cardiovascular Diseases, Gonda 5, Mayo Clinic, 200 First St SW, Rochester, MN 55905. Email E-mail Address: [email protected] https://orcid.org/0000-0003-1183-3959 Departments of Cardiovascular Diseases (S.Y., A.S.J.), Mayo Clinic, Rochester, MN. Laboratory Medicine and Pathology (A.S.J.), Mayo Clinic, Rochester, MN. Originally published4 May 2020https://doi.org/10.1161/CIRCULATIONAHA.120.045708Circulation. 2020;141:1434–1436Acute myocardial infarction (MI) historically is defined as a clinical syndrome that meets a certain set of criteria, usually a combination of symptoms, electrocardiographic changes, and cardiac biomarkers in the proper clinical context. These criteria have evolved and have been interdigitated with noninvasive and invasive diagnostic imaging and biomarkers. Before 2000, clinicians used a variety of MI definitions. To provide consistency, the Task Force for the Universal Definition of Myocardial Infarction (UDMI) developed international, collaborative, multidisciplinary, consensus definitions to facilitate standardization and a clear nomenclature based on pathophysiology.1 Although 2 of the authors of the present article were involved in those efforts, our advocacy now reflects our individual concerns with the suggestions made to change the UDMI rather than a feeling that the document cannot be improved. Accordingly, we provide clarification about issues recently raised concerning the UDMI.2The UDMI document provides clinical definitions. It is neither a clinical practice guideline nor a clinical decision pathway. Three elements are key. First, it is a pathophysiologic-based scheme. It predicates the diagnosis of acute MI as a clinical syndrome based on common signs and symptoms of acute myocardial ischemia. Finally, recognizing the variability in diagnostic resource availability across the globe, it endorses a definition based on criteria that can be implemented widely.Proposals have been made to modify the UDMI to emphasize the presence or absence of acute coronary obstruction.2 In comparison with the UDMI recommendations,1 which favor the diagnosis of acute MI as a clinical syndrome, such proposals dichotomize patients with or without acute coronary obstruction and advocate the preeminent use of coronary angiography to determine MI subtypes. Significant problems exist with relying on coronary angiography as the gate keeper. Foremost, it is not routinely available in all hospitals, constraining the ability to diagnose and treat MI, and its broader use among patients with a lower pretest probability for atherothrombosis could lead to more invasive diagnostic procedures and coronary interventions with inherent procedural risks that may not be justified, especially in those with possible type 2 MIs who have comorbidities that increase such risks. Even when available, angiographically complex atherosclerotic lesions and even plaque disruption occur in patients with stable coronary artery disease with intracoronary imaging,3 which makes unclear what angiographic criteria might be used to define diagnoses. The ACT-2 trial (Appropriateness of Coronary Investigation in Myocardial Injury and Type 2 Myocardial Infarction; URL: https//www.anzctr.org.au; Unique identifier: ACTRN1261800378224) should provide insights into the broader use of coronary angiography,4 but pending more data, its routine use to determine MI subtypes should not be advised.Some researchers have advocated that conditions leading to acute coronary obstruction other than atherothrombosis, such as coronary embolism, spasm, microvascular dysfunction, or spontaneous coronary artery dissection, should be classified as type 1 MI events because their diagnosis requires coronary angiography.2 These conditions, however, are not related to acute atherothrombotic plaque disruption. The therapeutic approach to type 1 MI presently emphasizes therapies targeting acute atherothrombosis, whereas the diagnoses of spontaneous coronary artery dissection, embolism, spasm, or microvascular dysfunction require individualized diagnostic and treatment approaches, which are often difficult to deploy, and very different than the approaches advocated for patients with acute atherosclerotic plaque disruption. The fact that coronary angiography may be useful for diagnosis should not mean that it is necessary to establish an MI diagnosis or MI subtypes. We favor the present UDMI model and are against subdividing type 1 MI, a homogeneous entity, into a heterogeneous entity of various mechanisms and disease subtypes.Misunderstandings exist about how the UDMI relates to other terms used in clinical practice and research. Clinical practice guidelines have long used the term acute coronary syndrome to define patients presenting with symptoms and signs of myocardial ischemia, whether attributable to non–ST-segment–elevation MI and ST-segment–elevation MI or unstable angina. When used in this manner, the term does not equate to acute atherothrombosis. It is appropriate to use the term initially in undifferentiated patients to identify those in whom additional diagnostic approaches and therapies for myocardial ischemia are needed. Once a more precise diagnosis is confirmed, however, the term acute coronary syndrome is broad and ambiguous. We suggest at that point that the specific MI subtypes that elaborate on pathophysiology should be used. The Figure illustrates our concept of the relationship between this nomenclature and MI subtypes.Download figureDownload PowerPointFigure. Application of universal definition of myocardial infarction (MI) and relationship to other nomenclature/classification schemes. Acute coronary syndrome (ACS) is a term that can be used when patients with possible acute ischemic heart disease present. However, once a more specific diagnosis is made, the more specific term should be used. Type 1 MI is a homogeneous condition that relates to acute atherothrombotic coronary artery disease for which standardized, evidence-based management guidelines should be used. Type 2 MI is a heterogeneous syndrome, which can be a primary or secondary illness, and is caused by either acute nonatherothrombotic coronary artery disease or other acute noncoronary trigger/illness. The term myocardial infarction with no obstructive coronary artery disease (MINOCA), and the ECG terminology (ST-segment–elevation myocardial infarction [STEMI]/non–ST-segment–elevation myocardial infarction[NSTEMI]), as well, apply for both type 1 and 2 MIs. CAD indicates coronary artery disease; and CPG, Clinical Practice Guidelines.New terms, such as MI with no obstructive coronary artery disease (MINOCA), are increasingly used as a working diagnosis to raise awareness that the absence of obstructive disease (≤50% in major epicardial vessels) should not lead to the false reassurance that MI has not occurred when other clinical criteria are met. MINOCA does not have a solitary pathophysiology. MINOCA can potentially occur because of acute atherothrombotic (type 1 MI) or nonatherothrombotic (type 2 MI) etiologies. The proposal cited claims that the suggested classification would eliminate the need for the MINOCA term because spontaneous coronary artery dissection, embolism, and macrovascular and microvascular obstruction would all fit the construct.2 However, given their proposed requisite for acute coronary obstruction to define type 1 MI, this would lead to all MINOCAs being categorized as type 2 MI. In addition, this proposal that requires acute coronary obstruction to define type 1 MI may disfavor certain patient subsets, like women, whose MIs often are attributable to nonobstructive mechanisms.We share the idea that MI diagnostic and management pathways are needed and have proposed such algorithms.5 Our advocacy for the present classification system does not prevent the tabulation of the data necessary for patient management; it simply suggests that the present system is a better universal standard. It is also clear that, for type 2 MI, more data are needed on the management and prognosis of the distinct type 2 MI phenotypes, including distinguishing those that occur from coronary and noncoronary causes.5 Given the adverse prognosis of patients who have type 2 MI, we especially urge trials to develop treatment pathways. This would be far more effective than altering a well-established system of definitions that are based on pathophysiologic mechanisms.DisclosuresDr Sandoval has served on an advisory board/speaker for Abbott Diagnostics and an advisory board for Roche Diagnostics, all without personal financial compensation. Dr Jaffe has consulted or is presently consulting for most of the major diagnostic companies, including Beckman, Abbott, Siemens, ET Healthcare, Roche, Quidel, Brava, and Sphingotec. He also consults for Blade and Novartis. Dr Thygesen reports no conflict.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.https://www.ahajournals.org/journal/circAllan S. Jaffe, MD, Department of Cardiovascular Diseases, Gonda 5, Mayo Clinic, 200 First St SW, Rochester, MN 55905. Email jaffe.[email protected]eduReferences1. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infarction (2018).Circulation. 2018; 138:e618–e651. doi: 10.1161/CIR.0000000000000617LinkGoogle Scholar2. de Lemos JA, Newby LK, Mills NL. A proposal for modest revision of the definition of type 1 and type 2 myocardial infarction.Circulation. 2019; 140:1773–1775. doi: 10.1161/CIRCULATIONAHA.119.042157LinkGoogle Scholar3. Maehara A, Mintz GS, Bui AB, Walter OR, Castagna MT, Canos D, Pichard AD, Satler LF, Waksman R, Suddath WO, et al. Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound.J Am Coll Cardiol. 2002; 40:904–910. doi: 10.1016/s0735-1097(02)02047-8CrossrefMedlineGoogle Scholar4. Lambrakis K, French JK, Scott IA, Briffa T, Brieger D, Farkouh ME, White H, Chuang AM, Tiver K, Quinn S, et al. The appropriateness of coronary investigation in myocardial injury and type 2 myocardial infarction (ACT-2): a randomized trial design.Am Heart J. 2019; 208:11–20. doi: 10.1016/j.ahj.2018.09.016CrossrefMedlineGoogle Scholar5. Sandoval Y, Jaffe AS. Type 2 myocardial infarction: JACC Review Topic of the Week.J Am Coll Cardiol. 2019; 73:1846–1860. doi: 10.1016/j.jacc.2019.02.018CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByNtsekhe M and Baker J (2023) Cardiovascular Disease Among Persons Living With HIV: New Insights Into Pathogenesis and Clinical Manifestations in a Global Context, Circulation, 147:1, (83-100), Online publication date: 3-Jan-2023. Ferencik M, Mayrhofer T, Lu M, Bittner D, Emami H, Puchner S, Meyersohn N, Ivanov A, Adami E, Voora D, Ginsburg G, Januzzi J, Douglas P and Hoffmann U (2022) Coronary Atherosclerosis, Cardiac Troponin, and Interleukin-6 in Patients With Chest Pain, JACC: Cardiovascular Imaging, 10.1016/j.jcmg.2022.03.016, 15:8, (1427-1438), Online publication date: 1-Aug-2022. Patlolla S, Kanwar A, Cheungpasitporn W, Doshi R, Stulak J, Holmes D, Bell M, Singh M and Vallabhajosyula S (2021) Temporal Trends, Clinical Characteristics, and Outcomes of Emergent Coronary Artery Bypass Grafting for Acute Myocardial Infarction in the United States, Journal of the American Heart Association, 10:15, Online publication date: 3-Aug-2021. Lindahl B, Ljung L, Herlitz J, Alfredsson J, Erlinge D, Kellerth T, Omerovic E, Ravn‐Fischer A, Sparv D, Yndigegn T, Svensson P, Östlund O, Jernberg T, James S and Hofmann R (2021) Poor long‐term prognosis in patients admitted with strong suspicion of acute myocardial infarction but discharged with another diagnosis, Journal of Internal Medicine, 10.1111/joim.13272, 290:2, (359-372), Online publication date: 1-Aug-2021. Zhao Z, Sun W, Guo Z, Liu B, Yu H, Zhang J and Chen S (2021) Long Noncoding RNAs in Myocardial Ischemia-Reperfusion Injury, Oxidative Medicine and Cellular Longevity, 10.1155/2021/8889123, 2021, (1-15), Online publication date: 5-Apr-2021. Tsukui T, Sakakura K, Taniguchi Y, Yamamoto K, Seguchi M, Jinnouchi H, Wada H, Fujita H and Santulli G (2020) Factors associated with poor clinical outcomes of ST-elevation myocardial infarction in patients with door-to-balloon time <90 minutes, PLOS ONE, 10.1371/journal.pone.0241251, 15:10, (e0241251) May 5, 2020Vol 141, Issue 18 Advertisement Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.120.045708PMID: 32364775 Originally publishedMay 4, 2020 Keywordscoronary angiographymyocardial infarctionacute coronary syndromeclinical decision-makingmyocardial ischemiaPDF download Advertisement SubjectsMyocardial Infarction