European Heart Journal (2023) 44, 3720–3826 ESC GUIDELINES

https://doi.org/10.1093/eurheartj/ehad191

2023 ESC Guidelines for the management

of acute coronary syndromes
Developed by the task force on the management of acute coronary
syndromes of the European Society of Cardiology (ESC)

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Authors/Task Force Members: Robert A. Byrne *†, (Chairperson) (Ireland),
Xavier Rossello ‡, (Task Force Co-ordinator) (Spain), J.J. Coughlan ‡,
(Task Force Co-ordinator) (Ireland), Emanuele Barbato (Italy), Colin Berry
(United Kingdom), Alaide Chieffo (Italy), Marc J. Claeys (Belgium),
Gheorghe-Andrei Dan (Romania), Marc R. Dweck (United Kingdom),
Mary Galbraith (United Kingdom), Martine Gilard (France),
Lynne Hinterbuchner (Austria), Ewa A. Jankowska (Poland), Peter Jüni
(United Kingdom), Takeshi Kimura (Japan), Vijay Kunadian (United Kingdom),
Margret Leosdottir (Sweden), Roberto Lorusso (Netherlands),
Roberto F.E. Pedretti (Italy), Angelos G. Rigopoulos (Greece),
Maria Rubini Gimenez (Germany), Holger Thiele (Germany),
Pascal Vranckx (Belgium), Sven Wassmann (Germany), Nanette Kass Wenger
(United States of America), Borja Ibanez *†, (Chairperson) (Spain), and ESC
Scientific Document Group
* Corresponding authors: Robert A. Byrne, Department of Cardiology and Cardiovascular Research Institute (CVRI) Dublin, Mater Private Network, Dublin, Ireland, and School of Pharmacy
and Biomolecular Sciences, RCSI University of Medicine and Health Sciences, Dublin, Ireland. Tel: +353-1-2483190, E-mail: [email protected]; and Borja Ibanez, Clinical Research
Department, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain, and Cardiology Department, IIS-Fundación Jiménez Díaz University Hospital, Madrid,
Spain, CIBERCV, ISCIII, Madrid, Spain. Tel: +3491 4531200, E-mail: [email protected]
†
The two Chairpersons contributed equally to the document and are joint corresponding authors.
‡
The two Task Force Co-ordinators contributed equally to the document.
Author/Task Force Member affiliations are listed in author information.
ESC Clinical Practice Guidelines (CPG) Committee: listed in the Appendix.
ESC subspecialty communities having participated in the development of this document:
Associations: Association of Cardiovascular Nursing & Allied Professions (ACNAP), Association for Acute CardioVascular Care (ACVC), European Association of Cardiovascular Imaging
(EACVI), European Association of Preventive Cardiology (EAPC), European Association of Percutaneous Cardiovascular Interventions (EAPCI), European Heart Rhythm Association (EHRA),
and Heart Failure Association (HFA).
Working Groups: Cardiovascular Pharmacotherapy, Cardiovascular Surgery, E-Cardiology, Myocardial and Pericardial Diseases, Thrombosis.
Patient Forum
The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC
Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a written request to Oxford
University Press, the publisher of the European Heart Journal, and the party authorized to handle such permissions on behalf of the ESC ([email protected]).
Disclaimer. The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and medical knowledge and the evidence available at the time
of their publication. The ESC is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the ESC Guidelines and any other official recommendations or
guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the
ESC Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the implementation of preventive, diagnostic or therapeutic medical strategies;
however, the ESC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each
patient’s health condition and in consultation with that patient and, where appropriate and/or necessary, the patient’s caregiver. Nor do the ESC Guidelines exempt health professionals from
taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient’s case
in light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional’s responsibility to verify the applicable rules and
regulations relating to drugs and medical devices at the time of prescription.
This article is co-published with permission in European Heart Journal and European Heart Journal - Acute Cardiovascular Care. All rights reserved. © The European Society of Cardiology
2023. The articles are identical except for stylistic differences in keeping with each journal’s style. Either citation can be used when citing this article. For permissions, please e-mail:
[email protected]
ESC Guidelines 3721

Document Reviewers: Sigrun Halvorsen, (Clinical Practice Guidelines Review Co-ordinator) (Norway),
Stefan James, (Clinical Practice Guidelines Review Co-ordinator) (Sweden), Magdy Abdelhamid (Egypt),
Victor Aboyans (France), Nina Ajmone Marsan (Netherlands), Sotiris Antoniou (United Kingdom),
Riccardo Asteggiano (Italy), Maria Bäck (Sweden), Davide Capodanno (Italy), Ruben Casado-Arroyo (Belgium),
Salvatore Cassese (Germany), Jelena Čelutkienė (Lithuania), Maja Cikes (Croatia), Jean-Philippe Collet (France),
Gregory Ducrocq (France), Volkmar Falk (Germany), Laurent Fauchier (France), Tobias Geisler (Germany), Diana
A. Gorog (United Kingdom), Lene Holmvang (Denmark), Tiny Jaarsma (Sweden), Hywel Wynne Jones (United
Kingdom), Lars Køber (Denmark), Konstantinos C. Koskinas (Switzerland), Dipak Kotecha (United Kingdom),
Konstantin A. Krychtiuk (Austria), Ulf Landmesser (Germany), George Lazaros (Greece), Basil S. Lewis (Israel),
Bertil Lindahl (Sweden), Ales Linhart (Czech Republic), Maja-Lisa Løchen (Norway), Mamas A. Mamas (United
Kingdom), John William McEvoy (Ireland), Borislava Mihaylova (United Kingdom), Richard Mindham (United
Kingdom), Christian Mueller (Switzerland), Lis Neubeck (United Kingdom), Josef Niebauer (Austria), Jens

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Cosedis Nielsen (Denmark), Alexander Niessner (Austria), Valeria Paradies (Netherlands), Agnes A. Pasquet
(Belgium), Steffen E. Petersen (United Kingdom), Eva Prescott (Denmark), Amina Rakisheva (Kazakhstan),
Bianca Rocca (Italy), Giuseppe M.C. Rosano (Italy), Leyla Elif Sade (United States of America / Türkiye),
François Schiele (France), Jolanta M. Siller-Matula (Austria), Christian Sticherling (Switzerland), Robert F. Storey
(United Kingdom), Matthias Thielmann (Germany), Christiaan Vrints (Belgium), Stephan Windecker
(Switzerland), Rune Wiseth (Norway), and Adam Witkowski (Poland)

All experts involved in the development of these guidelines have submitted declarations of interest. These have
been compiled in a report and simultaneously published in a supplementary document to the guidelines. The
report is also available on the ESC website www.escardio.org/Guidelines

See the European Heart Journal online for supplementary documents that include background information and
evidence tables.

Keywords Guidelines • Acute cardiac care • Acute coronary syndrome • Antithrombotic therapy • Fibrinolysis • High-
sensitivity troponin • Invasive strategy • MINOCA • Myocardial infarction • Non-ST-elevation myocardial infarction
• Patient-centred care • Percutaneous coronary intervention • Recommendations • Reperfusion therapy •
Revascularization • Secondary prevention • ST-segment elevation myocardial infarction • Unstable angina

3.3.2. Central laboratory vs. point of care ....................................... 3739

Table of contents 3.3.3. Confounders of cardiac troponin concentration ............. 3739
1. Preamble .............................................................................................................. 3727 3.3.4. Rapid ‘rule-in’ and ‘rule-out’ algorithms ................................ 3739
2. Introduction ....................................................................................................... 3728 3.3.4.1. European Society of Cardiology 0 h/1 h and 0 h/2 h
2.1. Definitions | Acute coronary syndromes and myocardial algorithms .................................................................................................. 3740
infarction ............................................................................................................. 3730 3.3.4.1.1. Rule-out ............................................................................. 3740
2.2. Epidemiology of acute coronary syndromes .............................. 3732 3.3.4.1.2. Rule-in ................................................................................ 3740
2.3. Number and breakdown of classes of recommendations ... 3732 3.3.4.1.3. Observe ............................................................................. 3740
2.4. What is new ............................................................................................. 3733 3.3.4.2. Practical guidance on how to implement the
3. Triage and diagnosis ........................................................................................ 3735 European Society of Cardiology 0 h/1 h algorithm ................. 3742
3.1. Clinical presentation and physical examination ......................... 3735 3.3.5. Other biomarkers .......................................................................... 3742
3.1.1. Clinical presentation ...................................................................... 3735 3.4. Diagnostic tools | Non-invasive imaging ....................................... 3742
3.1.2. History taking and physical examination .............................. 3737 3.4.1. Echocardiography ........................................................................... 3742
3.2. Diagnostic tools | Electrocardiogram ............................................ 3737 3.4.2. Computed tomography ............................................................... 3742
3.2.1. Acute coronary syndrome with persistent ST-segment 3.4.3. Cardiac magnetic resonance imaging with or without
elevation (suspected ST-elevation myocardial infarction) ......... 3738 stress testing ................................................................................................. 3742
3.2.2. Acute coronary syndrome without persistent ST- 3.5. Differential diagnosis for acute chest pain .................................. 3743
segment elevation (non-ST elevation acute coronary 4. Initial measures for patients presenting with suspected acute
syndrome) ...................................................................................................... 3738 coronary syndrome | Initial treatment ........................................................ 3743
3.3. Diagnostic tools | Biomarkers ........................................................... 3739 4.1. Pre-hospital logistics of care .............................................................. 3743
3.3.1. High-sensitivity cardiac troponins ............................................ 3739 4.1.1. Time to treatment ......................................................................... 3743
3722 ESC Guidelines

4.1.2. Healthcare systems and system delays .................................. 3743 6.3.1. Shortening dual antiplatelet therapy ....................................... 3756
4.1.3. Emergency medical services ....................................................... 3743 6.3.2. De-escalation from potent P2Y12 inhibitor to
4.1.4. General practitioners .................................................................... 3744 clopidogrel ..................................................................................................... 3756
4.1.5. Organization of ST-elevation myocardial infarction 6.3.3. Summary of alternative antiplatelet strategies to reduce
treatment in networks .............................................................................. 3744 bleeding risk in the first 12 months after acute coronary
4.2. Emergency care ....................................................................................... 3744 syndrome ........................................................................................................ 3757
4.2.1. Initial diagnosis and monitoring ................................................ 3744 6.4. Long-term treatment ............................................................................ 3759
4.2.2. Acute pharmacotherapy .............................................................. 3744 6.4.1. Prolonging antithrombotic therapy beyond 12 months 3759
4.2.2.1. Oxygen ....................................................................................... 3744 6.5. Antiplatelet therapy in patients requiring oral
4.2.2.2. Nitrates ...................................................................................... 3744 anticoagulation ................................................................................................. 3760
4.2.2.3. Pain relief ................................................................................... 3744 6.5.1. Acute coronary syndrome patients requiring
4.2.2.4. Intravenous beta-blockers .................................................. 3744 anticoagulation ............................................................................................. 3760

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5. Acute-phase management of patients with acute coronary 6.5.2. Patients requiring vitamin K antagonists or undergoing
syndrome .................................................................................................................. 3745 coronary artery bypass surgery ............................................................ 3762
5.1. Selection of invasive strategy and reperfusion therapy ......... 3745 6.6. Antithrombotic therapy as an adjunct to fibrinolysis ............. 3762
5.2. Acute coronary syndrome managed with invasive strategy 3745 6.7. Antithrombotic therapy in patients not undergoing
5.2.1. Primary percutaneous coronary intervention strategy for reperfusion ......................................................................................................... 3762
ST-elevation myocardial infarction ...................................................... 3745 7. Acute coronary syndrome with unstable presentation .................. 3762
5.2.1.1. Invasive strategy in ST-elevation myocardial infarction 7.1. Out-of-hospital cardiac arrest in acute coronary syndrome 3763
late presenters ......................................................................................... 3747 7.1.1. Systems of care ................................................................................ 3763
5.2.2. Immediate invasive strategy for non-ST elevation acute 7.2. Cardiogenic shock complicating acute coronary syndrome 3763
coronary syndrome .................................................................................... 3747 8. Management of acute coronary syndrome during hospitalization 3764
5.2.3. Routine vs. selective invasive strategy .................................... 3747 8.1. Coronary care unit/intensive cardiac care unit ......................... 3764
5.2.3.1. Early vs. delayed invasive strategy for non-ST 8.1.1. Monitoring ......................................................................................... 3764
elevation acute coronary syndrome .............................................. 3747 8.1.2. Ambulation ........................................................................................ 3764
5.2.4. Summary of invasive strategies for patients with non-ST 8.1.3. Length of stay in the intensive cardiac care unit ............... 3765
elevation acute coronary syndrome ................................................... 3747 8.2. In-hospital care ........................................................................................ 3765
5.3. Fibrinolysis and pharmaco-invasive strategy in patients with 8.2.1. Length of hospital stay ................................................................. 3765
ST-elevation myocardial infarction .......................................................... 3749 8.2.2. Risk assessment ............................................................................... 3765
5.3.1. Benefit and indication of fibrinolysis ....................................... 3749 8.2.2.1. Clinical risk assessment ........................................................ 3765
5.3.1.1. Pre-hospital fibrinolysis ........................................................ 3749 8.2.2.2. Imaging risk assessment ....................................................... 3765
5.3.1.2. Angiography and percutaneous coronary 8.2.2.3. Biomarkers for risk assessment ....................................... 3765
intervention after fibrinolysis (pharmaco-invasive strategy) 3749 8.2.2.4. Bleeding risk assessment ..................................................... 3765
5.3.1.2.1. Comparison of fibrinolytic agents .......................... 3749 8.2.2.5. Integrating ischaemic and bleeding risks ....................... 3765
5.3.1.2.2. Hazards of fibrinolysis and contraindications .... 3749 9. Technical aspects of invasive strategies .................................................. 3766
5.4. Patients not undergoing reperfusion ............................................. 3749 9.1. Percutaneous coronary intervention ............................................. 3766
5.4.1. Patients who are not candidates for invasive coronary 9.1.1. Vascular access ................................................................................ 3766
angiography .................................................................................................... 3749 9.1.2. Intravascular imaging/physiology of the infarct-related
5.4.2. Patients with coronary artery disease not amenable to artery ................................................................................................................ 3766
revascularization .......................................................................................... 3749 9.1.2.1. Intravascular imaging ............................................................. 3766
6. Antithrombotic therapy ................................................................................ 3750 9.1.2.2. Intravascular physiology ....................................................... 3767
6.1. Antiplatelet therapy in the acute phase ....................................... 3752 9.1.3. Timing of revascularization with percutaneous coronary
6.1.1. Oral antiplatelet therapy ............................................................. 3752 intervention ................................................................................................... 3767
6.1.2. Timing of loading dose of oral antiplatelet therapy ......... 3753 9.1.4. Balloons and stents ........................................................................ 3768
6.1.2.1. Pre-treatment in patients with suspected ST- 9.1.5. Embolic protection and microvascular salvage strategies 3768
elevation myocardial infarction ........................................................ 3753 9.1.5.1. Thrombus aspiration ............................................................ 3768
6.1.2.2. Pre-treatment in patients with non-ST-elevation 9.1.5.2. Interventions to protect the microcirculation .......... 3768
acute coronary syndrome .................................................................. 3753 9.2. Coronary artery bypass grafting ...................................................... 3768
6.1.2.3. Summary of pre-treatment strategies ........................... 3753 9.2.1. Indication and timing of coronary artery bypass grafting in
6.1.3. Intravenous antiplatelet drugs ................................................... 3753 acute coronary syndrome patients ..................................................... 3768
6.2. Anticoagulant treatment in the acute phase .............................. 3754 9.2.2. Technical considerations specific to acute coronary
6.2.1. Anticoagulation in patients with ST-elevation myocardial syndrome patients ...................................................................................... 3768
infarction undergoing primary percutaneous coronary 9.3. Spontaneous coronary artery dissection ..................................... 3768
intervention ................................................................................................... 3754 9.3.1. Intravascular imaging ..................................................................... 3769
6.2.2. Anticoagulation in patients with non-ST-elevation acute 9.3.2. Revascularization ............................................................................. 3769
coronary syndrome undergoing angiography and percutaneous 10. Management of patients with multivessel disease ........................... 3769
coronary intervention if indicated ....................................................... 3754 10.1. Management of multivessel disease in acute coronary
6.3. Maintenance antithrombotic therapy after revascularization 3755 syndrome complicated by cardiogenic shock ..................................... 3769
ESC Guidelines 3723

10.2. Patients with multivessel coronary artery disease 13.3.8. Vaccination ...................................................................................... 3787
undergoing primary percutaneous coronary intervention ............ 3770 13.3.9. Anti-inflammatory drugs ........................................................... 3787
10.3. Timing of non-infarct-related artery revascularization in 13.3.10. Hormone replacement therapy .......................................... 3787
acute coronary syndrome ........................................................................... 3771 14. Patient perspectives ..................................................................................... 3788
10.3.1. Patients presenting with ST-elevation myocardial 14.1. Patient-centred care ........................................................................... 3788
infarction and multivessel coronary artery disease ...................... 3771 14.2. Shared decision-making ..................................................................... 3789
10.3.2. Patients presenting with non-ST-elevation acute 14.3. Informed consent ................................................................................ 3789
coronary syndrome and multivessel coronary artery disease . 3771 14.4. Research participation and consent in the acute setting .... 3790
10.4. Evaluation of non-infarct-related artery stenosis severity 14.5. Patient satisfaction and expectations .......................................... 3790
(angiography vs. physiology) ....................................................................... 3771 14.6. Patient-reported outcome measures and patient-reported
10.5. Hybrid revascularization ................................................................... 3772 experience measures ..................................................................................... 3791
11. Myocardial infarction with non-obstructive coronary arteries . 3772 14.7. Preparation for discharge ................................................................. 3791

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12. Special situations ............................................................................................ 3775 15. Key messages .................................................................................................. 3791
12.1. Type 2 myocardial infarction and acute myocardial injury 3775 16. Gaps in evidence ............................................................................................ 3793
12.2. Complications ....................................................................................... 3775 17. Sex differences ............................................................................................... 3795
12.2.1. Heart failure ................................................................................... 3775 18. ‘What to do’ and ‘What not to do’ messages from the
12.2.2. Mechanical complications ......................................................... 3776 Guidelines ................................................................................................................. 3796
12.2.3. Left ventricular thrombus ......................................................... 3776 19. Quality indicators .......................................................................................... 3801
12.2.4. Post-acute coronary syndrome pericarditis ..................... 3776 20. Supplementary data ...................................................................................... 3801
12.2.5. Arrhythmias .................................................................................... 3776 21. Data availability statement ......................................................................... 3801
12.2.5.1. Atrial fibrillation .................................................................... 3776 22. Author information ...................................................................................... 3801
12.2.5.2. Ventricular arrhythmias .................................................... 3777 23. Appendix ........................................................................................................... 3801
12.2.6. Bleeding ............................................................................................ 3777 24. References ........................................................................................................ 3802
12.2.6.1. Management of bleeding .................................................. 3777
12.3. Comorbid conditions ......................................................................... 3778
12.3.1. Patients at high bleeding risk and with blood disorders
(anaemia and thrombocytopaenia) ..................................................... 3778
Tables of Recommendations
12.3.2. Chronic kidney disease .............................................................. 3779 Recommendation Table 1 — Recommendations for clinical and
12.3.3. Diabetes mellitus .......................................................................... 3779 diagnostic tools for patients with suspected acute coronary
12.3.4. Older adults with frailty and multimorbidity ................... 3779 syndrome .................................................................................................................. 3738
12.3.4.1. The older person ................................................................. 3779 Recommendation Table 2 — Recommendations for non-invasive
12.3.4.2. Frailty and multimorbidity ................................................ 3779 imaging in the initial assessment of patients with suspected acute
12.3.5. Pregnancy ........................................................................................ 3780 coronary syndrome .............................................................................................. 3742
12.3.6. Drug abuse ...................................................................................... 3780 Recommendation Table 3 — Recommendations for the initial
management of patients with acute coronary syndrome ................... 3745
12.3.7. Patients with cancer .................................................................... 3780
Recommendation Table 4 — Recommendations for reperfusion
12.3.8. Coronavirus disease (COVID-19) ........................................ 3780
therapy and timing of invasive strategy ....................................................... 3750
13. Long-term treatment ................................................................................... 3781
Recommendation Table 5 — Recommendations for antiplatelet and
13.1. Cardiac rehabilitation ......................................................................... 3783
anticoagulant therapy in acute coronary syndrome .............................. 3758
13.1.1. Comprehensive cardiac rehabilitation ................................. 3783
Recommendation Table 6 — Recommendations for
13.1.2. Digital health .................................................................................. 3783
alternative antithrombotic therapy regimens ........................................... 3759
13.1.3. Adherence and persistence ..................................................... 3783 Recommendation Table 7 — Recommendations for fibrinolytic
13.2. Lifestyle management ......................................................................... 3783 therapy ....................................................................................................................... 3762
13.2.1. Tobacco ........................................................................................... 3783 Recommendation Table 8 — Recommendations for cardiac arrest
13.2.2. Nutrition and alcohol ................................................................. 3783 and out-of-hospital cardiac arrest ................................................................. 3763
13.2.3. Physical activity and exercise .................................................. 3784 Recommendation Table 9 — Recommendations for cardiogenic
13.2.4. Psychological considerations ................................................... 3784 shock .......................................................................................................................... 3764
13.2.5. Resumption of activities ............................................................ 3784 Recommendation Table 10 — Recommendations for in-hospital
13.3. Pharmacological treatment .............................................................. 3784 management ............................................................................................................ 3766
13.3.1. Antithrombotic therapy ............................................................ 3784 Recommendation Table 11 — Recommendations for technical
13.3.2. Lipid-lowering therapy ............................................................... 3784 aspects of invasive strategies ............................................................................ 3769
13.3.3. Beta-blockers ................................................................................. 3785 Recommendation Table 12 — Recommendations for management
13.3.4. Nitrates and calcium channel blockers ............................... 3786 of patients with multivessel disease .............................................................. 3772
13.3.5. Renin–angiotensin–aldosterone system inhibitors ......... 3786 Recommendation Table 13 — Recommendations for myocardial
13.3.6. Medications for diabetes ........................................................... 3786 infarction with non-obstructive coronary arteries ................................. 3775
13.3.6.1. Sodium–glucose co-transporter 2 inhibitors ........... 3786 Recommendation Table 14 — Recommendations for acute
13.3.6.2. Glucagon-like peptide-1 receptor agonists .............. 3787 coronary syndrome complications ................................................................ 3777
13.3.7. Proton pump inhibitors ............................................................. 3787 Recommendation Table 15 — Recommendations for acute
coronary syndrome comorbid conditions ................................................. 3781
3724 ESC Guidelines

Recommendation Table 16 — Recommendations for long-term Figure 17 Long-term management after acute coronary syndrome 3782
management ............................................................................................................ 3787 Figure 18 Lipid-lowering therapy in ACS patients .................................. 3785
Recommendation Table 17 — Recommendations for patient Figure 19 A person-centred approach to the ACS journey .............. 3789
perspectives in acute coronary syndrome care ....................................... 3791 Figure 20 Acute coronary syndrome patient expectations ................ 3790

List of tables
Table 1 Classes of recommendations .......................................................... 3728
Abbreviations and acronyms
Table 2 Levels of evidence ................................................................................ 3728 AβYSS Beta Blocker Interruption After
Table 3 Definitions of terms related to invasive strategy and Uncomplicated Myocardial Infarction
reperfusion therapy commonly used in this document ....................... 3731 ACCOAST A Comparison of Prasugrel at the Time of
Table 4 New recommendations .................................................................... 3733 Percutaneous Coronary Intervention or as
Table 5 Revised recommendations ............................................................... 3734 Pretreatment at the Time of Diagnosis in

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Table 6 Dose regimen of antiplatelet and anticoagulant drugs in Patients with Non-ST Elevation Myocardial
acute coronary syndrome patients ............................................................... 3751 Infarction
Table 7 Suggested strategies to reduce bleeding risk related to ACE Angiotensin-converting enzyme
percutaneous coronary intervention ............................................................ 3760 ACS Acute coronary syndrome
Table 8 Gaps in evidence .................................................................................. 3793 AF Atrial fibrillation
Table 9 ‘What to do’ and ‘What not to do’ ............................................. 3796 AFIRE Atrial Fibrillation and Ischemic Events With
Rivaroxaban in Patients With Stable Coronary
Artery Disease
List of figures AMI Acute myocardial infarction
Figure 1 Central illustration .............................................................................. 3729 ARB Angiotensin receptor blocker
Figure 2 The spectrum of clinical presentations, electrocardiographic ARC-HBR Academic Research Consortium for High
findings, and high-sensitivity cardiac troponin levels in patients with Bleeding Risk
acute coronary syndrome ................................................................................. 3730 ARNI Angiotensin receptor/neprilysin inhibitor
Figure 3 Classification of patients presenting with suspected acute ASCVD Atherosclerotic cardiovascular disease
coronary syndrome: from a working to a final diagnosis .................... 3732 ASSENT 3 ASsessment of the Safety and Efficacy of a New
Figure 4 An overview of the initial triage, management and Thrombolytic 3
investigation of patients who present with signs and symptoms ATLANTIC Administration of Ticagrelor in the Cath Lab or
potentially consistent with acute coronary syndrome ......................... 3736 in the Ambulance for New ST Elevation
Figure 5 The A.C.S. assessment for the initial evaluation of patients Myocardial Infarction to Open the Coronary
with suspected acute coronary syndrome ................................................. 3737 Artery
Figure 6 The 0 h/1 h or 0 h/2 h rule-out and rule-in algorithms using AUGUSTUS An Open-Label, 2 × 2 Factorial, Randomized
high-sensitivity cardiac troponin assays in patients presenting to the Controlled, Clinical Trial to Evaluate the Safety
emergency department with suspected NSTEMI and without an of Apixaban Versus Vitamin K Antagonist and
indication for immediate invasive angiography ......................................... 3741 Aspirin Versus Aspirin Placebo in Patients With
Figure 7 Modes of presentation and pathways to invasive Atrial Fibrillation and Acute Coronary
management and myocardial revascularization in patients presenting Syndrome or Percutaneous Coronary
with STEMI .............................................................................................................. 3746 Intervention
Figure 8 Selection of invasive strategy and reperfusion therapy in AV Atrioventricular
patients presenting with NSTE-ACS ............................................................ 3748 BARC Bleeding Academic Research Consortium
Figure 9 Antithrombotic treatments in acute coronary syndrome: b.i.d. Bis in die (twice a day)
pharmacological targets ...................................................................................... 3752 BBB Bundle branch block
Figure 10 Recommended default antithrombotic therapy regimens BEACON Better Evaluation of Acute Chest Pain with
in acute coronary syndrome patients without an indication for oral Coronary Computed Tomography Angiography
anticoagulation ....................................................................................................... 3755 BETAMI BEtablocker Treatment After Acute
Figure 11 Alternative antiplatelet strategies to reduce bleeding risk in Myocardial Infarction in Patients Without
the first 12 months after an ACS .................................................................. 3757 Reduced Left Ventricular Systolic Function
Figure 12 Antithrombotic regimens in patients with acute coronary BMS Bare metal stent
syndrome and an indication for oral anticoagulation ................................ 3761 BNP Brain natriuretic peptide
Figure 13 A practical algorithm to guide intravascular imaging in CABG Coronary artery bypass grafting
acute coronary syndrome patients ............................................................... 3767 CAD Coronary artery disease
Figure 14 Algorithm for the management of acute coronary CAPITAL-RCT Carvedilol Post-Intervention Long-Term
syndrome patients with multivessel coronary artery disease ............ 3770 Administration in Large-scale Randomized
Figure 15 Underlying causes for patients with a working diagnosis of Controlled Trial
myocardial infarction with non-obstructive coronary arteries ......... 3773 CAPRICORN CArvedilol Post-infaRct survIval COntRolled
Figure 16 Evaluation of patients with a working diagnosis of evaluatioN
MINOCA .................................................................................................................. 3774 CCS Chronic coronary syndrome
ESC Guidelines 3725

CCTA Coronary computed tomography angiography ESC European Society of Cardiology

CCU Coronary care unit EXAMINATION Everolimus-Eluting Stents Versus Bare-Metal
CHA2DS2-VASc Congestive heart failure, Hypertension, Age, Stents in ST Segment Elevation Myocardial
Diabetes, Stroke or TIA-Vascular disease Infarction
CHAMPION PCI Cangrelor versus Standard Therapy to ExTRACT-TIMI 25 Enoxaparin and Thrombolysis Reperfusion for
Achieve Optimal Management of Platelet Acute myocardial infarction Treatment
Inhibition Thrombolysis In Myocardial Infarction—Study 25
CHAMPION A Clinical Trial Comparing Cangrelor to FAME Fractional Flow Reserve versus Angiography
PHOENIX Clopidogrel Standard Therapy in Subjects for Multivessel Evaluation
Who Require Percutaneous Coronary FAMOUS-NSTEMI Fractional flow reserve (FFR) versus
Intervention angiography in guiding management to
CHAMPION Cangrelor Versus Standard Therapy to optimise outcomes in non-ST segment
PLATFORM Achieve Optimal Management of Platelet elevation myocardial infarction

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Inhibition FAST-MI French Registry of Acute ST-elevation and
CKD Chronic kidney disease non-ST-elevation Myocardial Infarction
CMR Cardiac magnetic resonance FFR Fractional flow reserve
CI Confidence interval FLOWER-MI Flow Evaluation to Guide Revascularization in
COACT Coronary Angiography after Cardiac Arrest Multivessel ST-Elevation Myocardial Infarction
COLCOT Colchicine Cardiovascular Outcomes Trial FMC First medical contact
COMFORTABLE- Comparison of Biolimus Eluted From an Erodible GLP-1RA Glucagon-like peptide-1 receptor agonist
AMI Stent Coating With Bare Metal Stents in Acute GP Glycoprotein
ST-Elevation Myocardial Infarction GRACE Global Registry of Acute Coronary Events
COMPARE-ACUTE Comparison Between FFR Guided HBR High bleeding risk
Revascularization Versus Conventional HCR Hybrid coronary revascularization
Strategy in Acute STEMI Patients With MVD HF Heart failure
COMPASS Cardiovascular Outcomes for People Using HFrEF Heart failure with reduced ejection fraction
Anticoagulation Strategies HOST-REDUCE-P­ Harmonizing Optimal Strategy for Treatment
COMPLETE Complete vs. Culprit-only Revascularization to OLYTECH-ACS of Coronary Artery Diseases Trial—
Treat Multivessel Disease After Early PCI for Comparison of REDUCTION of PrasugrEl
STEMI Dose & POLYmer TECHnology in ACS
COVID-19 Coronavirus disease 2019 Patients
CR Cardiac rehabilitation HR Hazard ratio
CRT Cardiac resynchronization therapy— HR-QoL Health-related quality of life
defibrillator/pacemaker hs-cTn High-sensitivity cardiac troponin
CS Cardiogenic shock IABP Intra-aortic balloon counter pulsation/pumping
CT Computed tomography IABP-SHOCK II Intraaortic Balloon Pump in Cardiogenic Shock II
CV Cardiovascular ICA Invasive coronary angiography
CVD Cardiovascular disease ICCU Intensive cardiac care unit
CvLPRIT Complete versus Lesion-only Primary PCI Trial ICD Implantable cardioverter defibrillator
cTn Cardiac troponin ICU Intensive care unit
CULPRIT-SHOCK Culprit Lesion Only PCI versus Multivessel PCI IMPROVE-IT Improved Reduction of Outcomes: Vytorin
in Cardiogenic Shock Efficacy International Trial
DANAMI-3– Third Danish Study of Optimal Acute INR International normalized ratio
PRIMULTI Treatment of Patients with ST-Segment IRA Infarct-related artery
Elevation Myocardial Infarction—Primary PCI ISAR-REACT 5 Intracoronary stenting and Antithrombotic
in Multivessel Disease regimen Rapid Early Action for Coronary
DANBLOCK Danish Trial of Beta Blocker Treatment After Treatment
Myocardial Infarction Without Reduced ISIS-4 Fourth International Study of Infarct Survival
Ejection Fraction i.v. Intravenous
DAPT Dual antiplatelet therapy IVUS Intravascular ultrasound
DAT Dual antithrombotic therapy LAD Left anterior descending
DCB Drug-coated balloon LBBB Left bundle branch block
DES Drug-eluting stent(s) LD Loading dose
DM Diabetes mellitus LDL-C Low-density lipoprotein-cholesterol
ECG Electrocardiography/gram LIMA Left internal mammary artery
ECMO Extracorporeal membrane oxygenation LMWH Low-molecular-weight heparin
eGFR Estimated glomerular filtration rate LoDoCo2 Low-dose Colchicine trial-2
ED Emergency department LV Left ventricular(cle)
EMS Emergency medical service(s) LVAD Left ventricular assist device
EPHESUS Eplerenone Post-AMI Heart failure Efficacy and LVEF Left ventricular ejection fraction
SUrvival Study MACE Major adverse cardiovascular events
3726 ESC Guidelines

MASTER DAPT Management of High Bleeding Risk Patients PPI Proton pump inhibitor
Post Bioresorbable Polymer Coated Stent PPV Positive predictive value
Implantation With an Abbreviated Versus PRAMI Preventive Angioplasty in Myocardial Infarction
Prolonged DAPT Regimen PREM Patient-reported experience measure
MATRIX Minimizing Adverse Haemorrhagic Events by PROM Patient-reported outcome measure
Transradial Access Site and Systemic QI Quality indicator
Implementation of angioX RAAS Renin–angiotensin–aldosterone system
MCS Mechanical circulatory support RAPID-CTCA Rapid Assessment of Potential Ischaemic heart
MD Maintenance dose Disease with CTCA
MI Myocardial infarction RCT Randomized controlled trial
MINOCA Myocardial infarction with non-obstructive REALITY Restrictive and Liberal Transfusion
coronary arteries Strategies in Patients With Acute Myocardial
MRA Mineralocorticoid receptor antagonist Infarction

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MVD Multivessel disease REBOOT-CNIC TREatment With Beta-blockers After
MVO Microvascular obstruction myOcardial Infarction withOut Reduced
NOAC Non-vitamin K antagonist oral anticoagulant Ejection fracTion
NORSTENT Norwegian Coronary Stent Trial REDUCE-SWEDE­ Evaluation of Decreased Usage of Betablockers
NPV Negative predictive value HEART After Myocardial Infarction in the
NRT Nicotine replacement therapy SWEDEHEART Registry
NSTE Non-ST elevation REMINDER Double-Blind, Randomized,
NSTE-ACS Non-ST elevation acute coronary syndrome Placebo-Controlled Trial Evaluating The Safety
NSTEMI Non-ST-elevation myocardial infarction And Efficacy Of Early Treatment With
NT-pro BNP N-terminal pro B-type natriuretic peptide Eplerenone In Patients With Acute Myocardial
NYHA New York Heart Association Infarction
o.d. Once a day REVELATION REVascularization With PaclitaxEL-Coated
OAC Oral anticoagulant/ation Balloon Angioplasty Versus Drug-Eluting
OASIS-5 Fifth Organization to Assess Strategies in Acute Stenting in Acute Myocardial InfarcTION
Ischemic Syndromes RIVAL RadIal Vs femorAL access for coronary
OASIS-6 The Safety and Efficacy of Fondaparinux Versus intervention
Control Therapy in Patients With ST Segment ROMICAT II Multicenter Study to Rule Out Myocardial
Elevation Acute Myocardial Infarction Infarction by Cardiac Computed Tomography
OAT Occluded Artery Trial ROSC Return of spontaneous circulation
OCT Optical coherence tomography RR Relative risk
ODYSSEY Evaluation of Cardiovascular Outcomes After RV Right ventricular
OUTCOMES an Acute Coronary Syndrome During SAPT Single antiplatelet therapy
Treatment With Alirocumab SBP Systolic blood pressure
OHCA Out-of-hospital cardiac arrest s.c. Subcutaneous
OR Odds ratio SCAD Spontaneous coronary artery dissection
PARADISE-MI Prospective ARNI vs ACE Inhibitor Trial to SHOCK Should We Emergently Revascularize
Determine Superiority in Reducing Heart Occluded Coronaries for Cardiogenic Shock
Failure Events After MI SGLT2 Sodium–glucose co-transporter 2
PCI Percutaneous coronary intervention SMART-DECISION Long-term Beta-blocker Therapy After Acute
PCSK9 Proprotein convertase subtilisin/kexin type 9 Myocardial Infarction
PE Pulmonary embolism SPECT Single-photon emission computerized
PEGASUS-TIMI 54 PrEvention with TicaGrelor of SecondAry tomography
Thrombotic Events in High-RiSk Patients with STE ST elevation
Prior AcUte Coronary Syndrome— STEMI ST-elevation myocardial infarction
Thrombolysis In Myocardial Infarction STOPDAPT-2-ACS ShorT and OPtimal Duration of Dual
PEPCAD NSTEMI Bare Metal Stent Versus Drug Coated Balloon AntiPlatelet Therapy-2 Study for the Patients
With Provisional Stenting in Non-ST-Elevation With ACS
Myocardial Infarction STREAM Strategic Reperfusion Early After Myocardial
PLATO PLATelet inhibition and patient Outcomes Infarction
POC Point of care SWEDEHEART Swedish Web-System for Enhancement and
POPular Genetics Cost-effectiveness of CYP2C19 Genotype Development of Evidence-Based Care in Heart
Guided Treatment With Antiplatelet Drugs in Disease Evaluated According to
Patients With ST-segment-elevation Myocardial Recommended Therapies
Infarction Undergoing Immediate PCI With TALOS-AMI TicAgrelor Versus CLOpidogrel in Stabilized
Stent Implantation: Optimization of Treatment Patients With Acute Myocardial Infarction
PPCI Primary percutaneous coronary intervention TAT Triple antithrombotic therapy
ESC Guidelines 3727

TICO Ticagrelor Monotherapy After 3 Months in the The Members of this Task Force were selected by the ESC to
Patients Treated With New Generation represent professionals involved with the medical care of patients
Sirolimus Stent for Acute Coronary Syndrome with this pathology. The selection procedure aimed to include
TIMI Thrombolysis In Myocardial Infarction members from across the whole of the ESC region and from rele­
TLR Target lesion revascularization vant ESC Subspecialty Communities. Consideration was given to
TOMAHAWK Immediate Unselected Coronary Angiography diversity and inclusion, notably with respect to gender and country
Versus Delayed Triage in Survivors of of origin. The Task Force performed a critical evaluation of diag­
Out-of-hospital Cardiac Arrest Without nostic and therapeutic approaches, including assessment of the
ST-segment Elevation risk-benefit ratio. The strength of every recommendation and the
TOPIC Timing of Platelet Inhibition After Acute level of evidence supporting them were weighed and scored ac­
Coronary Syndrome cording to predefined scales as outlined below. The Task Force fol­
TOTAL Trial of routine aspiration ThrOmbecTomy lowed ESC voting procedures, and all approved recommendations
with PCI vs. PCI ALone in patients with STEMI were subject to a vote and achieved at least 75% agreement among

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TRITON-TIMI 38 TRial to Assess Improvement in Therapeutic voting members.
Outcomes by Optimizing Platelet InhibitioN The experts of the writing and reviewing panels provided declaration
with Prasugrel Thrombolysis In Myocardial of interest forms for all relationships that might be perceived as real or
Infarction 38 potential sources of conflicts of interest. Their declarations of interest
TROPICAL-ACS Testing Responsiveness to Platelet Inhibition were reviewed according to the ESC declaration of interest rules and
on Chronic Antiplatelet Treatment For Acute can be found on the ESC website (http://www.escardio.org/
Coronary Syndromes Guidelines) and have been compiled in a report published in a supple­
TTE Transthoracic echocardiography mentary document with the guidelines. The Task Force received its en­
TWILIGHT Ticagrelor With Aspirin or Alone in High-Risk tire financial support from the ESC without any involvement from the
Patients After Coronary Intervention healthcare industry.
UA Unstable angina The ESC Clinical Practice Guidelines (CPG) Committee supervises
UFH Unfractionated heparin and co-ordinates the preparation of new guidelines and is responsible
VA-ECMO Veno-arterial extracorporeal membrane for the approval process. ESC Guidelines undergo extensive review
oxygenation by the CPG Committee and external experts, including members
VALIANT VALsartan In Acute myocardial iNfarcTion from across the whole of the ESC region and from relevant ESC
VF Ventricular fibrillation Subspecialty Communities and National Cardiac Societies. After appro­
VKA Vitamin K antagonist priate revisions, the guidelines are signed off by all the experts involved
VT Ventricular tachycardia in the Task Force. The finalized document is signed off by the CPG
Committee for publication in the European Heart Journal. The guidelines
were developed after careful consideration of the scientific and medical
knowledge and the evidence available at the time of their writing. Tables
1. Preamble of evidence summarizing the findings of studies informing development
Guidelines evaluate and summarize available evidence with the aim of as­ of the guidelines are included. The ESC warns readers that the technical
sisting health professionals in proposing the best diagnostic or therapeut­ language may be misinterpreted and declines any responsibility in this
ic approach for an individual patient with a given condition. Guidelines are respect.
intended for use by health professionals and the European Society of Off-label use of medication may be presented in this guideline if a
Cardiology (ESC) makes its Guidelines freely available. sufficient level of evidence shows that it can be considered medically ap­
ESC Guidelines do not override the individual responsibility of health propriate for a given condition. However, the final decisions concerning
professionals to make appropriate and accurate decisions in consider­ an individual patient must be made by the responsible health profes­
ation of each patient’s health condition and in consultation with that pa­ sional giving special consideration to:
tient or the patient’s caregiver where appropriate and/or necessary. It is
also the health professional’s responsibility to verify the rules and reg­ • The specific situation of the patient. Unless otherwise provided for
ulations applicable in each country to drugs and devices at the time of by national regulations, off-label use of medication should be limited
prescription, and, where appropriate, to respect the ethical rules of to situations where it is in the patient’s interest with regard to the
their profession. quality, safety, and efficacy of care, and only after the patient has
ESC Guidelines represent the official position of the ESC on a given been informed and has provided consent.
topic and are regularly updated. ESC Policies and Procedures for for­ • Country-specific health regulations, indications by governmental
mulating and issuing ESC Guidelines can be found on the ESC website drug regulatory agencies, and the ethical rules to which health profes­
(https://www.escardio.org/Guidelines). sionals are subject, where applicable.
3728 ESC Guidelines

Table 1 Classes of recommendations

Definition Wording to use

Classes of recommendations

Class I Evidence and/or general agreement Is recommended or is indicated

that a given treatment or procedure is
beneficial, useful, effective.

Class II Conflicting evidence and/or a divergence of opinion about the usefulness/

efficacy of the given treatment or procedure.

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Class IIa Weight of evidence/opinion is in Should be considered
favour of usefulness/efficacy.

Class IIb Usefulness/efficacy is less well May be considered

established by evidence/opinion.

Class III Evidence or general agreement that the Is not recommended

given treatment or procedure is not

©ESC 2023
useful/effective, and in some cases

© ESC 2023
may be harmful.

Table 2 Levels of evidence

Level of Data derived from multiple randomized clinical trials

evidence A or meta-analyses.

Level of Data derived from a single randomized clinical trial

evidence B or large non-randomized studies.

Level of Consensus of opinion of the experts and/or small studies,

evidence C retrospective studies, registries.
©ESC 2023

© ESC 2023

2. Introduction
The major aspects of the management of patients with acute coronary
syndromes described in this European Society of Cardiology (ESC)
Guideline are summarized in Figure 1.
ESC Guidelines 3729

ACS encompasses a spectrum

Unstable angina NSTEMI STEMI

1 Think ‘A.C.S.’ at initial assessment

Abnormal Clinical Stable

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ECG? context? patient?

2 Think invasive management

STEMI Very high-risk NSTE-ACS High-risk NSTE-ACS

OR

Primary PCI Fibrinolysis Immediate angiography ± PCI Early (<24 h) angiography

(If timely primary PCI not feasible) should be considered

3 Think antithrombotic therapy

Antiplatelet therapy AND Anticoagulant therapy

+ OR OR OR

Aspirin P2Y12 inhibitor UFH LMWH Bivalirudin Fondaparinux

4 Think revascularization
Based on clinical status, co-morbidities, Aim for complete Consider adjunctive tests
and disease complexity revascularization to guide revascularization

OR

PCI CABG Intravascular imaging Intravascular physiology

5 Think secondary prevention

Antithrombotic Lipid lowering Smoking Cardiac Risk factor Psychosocial

therapy therapy cessation rehabilitation management considerations

Figure 1 Central illustration. ACS, acute coronary syndrome; CABG, coronary artery bypass grafting; ECG, electrocardiogram; LMWH, low molecular-
weight heparin; NSTE-ACS, non-ST-elevation acute coronary syndrome; PCI, percutaneous coronary intervention; PPCI, primary percutaneous coronary
intervention; STEMI, ST-elevation myocardial infarction; UFH, unfractionated heparin. Patients with acute coronary syndrome (ACS) can initially present with
a wide variety of clinical signs and symptoms and it is important that there is a high degree of awareness of this amongst both the general public and healthcare
providers. If ACS is suspected, think ‘A.C.S.’ for the initial triage and assessment. This involves performing an electrocardiogram (ECG) to assess for
Abnormalities or evidence of ischaemia, taking a targeted clinical history to assess the clinical Context of the presentation, and carrying out a targeted clinical
examination to assess for clinical and haemodynamic Stability. Based on the initial assessment, the healthcare provider can decide whether immediate invasive
management is required. Patients with ST-elevation myocardial infarction (STEMI) require primary percutaneous coronary intervention (PPCI) (or fibrinoly­
sis if PPCI within 120 min is not feasible); patients with non-ST-elevation ACS (NSTE-ACS) with very high-risk features require immediate angiography ± PCI
if indicated; patients with NSTE-ACS and high-risk features should undergo inpatient angiography (angiography within 24 h should be considered). A com­
bination of antiplatelet and anticoagulant therapy is indicated acutely for patients with ACS. The majority of patients with ACS will eventually undergo re­
vascularization, most commonly with PCI. Once the final diagnosis of ACS has been established, it is important to implement measures to prevent recurrent
events and to optimize cardiovascular risk. This consists of medical therapy, lifestyle changes and cardiac rehabilitation, as well as consideration of psycho­
social factors.
3730 ESC Guidelines

2.1. Definitions | Acute coronary myocardial infarction (MI) is associated with cTn release and is
syndromes and myocardial infarction made based on the fourth universal definition of MI.1 UA is defined
as myocardial ischaemia at rest or on minimal exertion in the ab­
Acute coronary syndromes (ACS) encompass a spectrum of condi­ sence of acute cardiomyocyte injury/necrosis. It is characterized by
tions that include patients presenting with recent changes in clinical specific clinical findings of prolonged (>20 min) angina at rest; new
symptoms or signs, with or without changes on 12-lead electrocardio­ onset of severe angina; angina that is increasing in frequency, longer
gram (ECG) and with or without acute elevations in cardiac tropo­ in duration, or lower in threshold; or angina that occurs after a re­
nin (cTn) concentrations (Figure 2). Patients presenting with cent episode of MI. ACS are associated with a broad range of clinical
suspected ACS may eventually receive a diagnosis of acute myocar­ presentations, from patients who are symptom free at presentation
dial infarction (AMI) or unstable angina (UA). The diagnosis of to patients with ongoing chest discomfort/symptoms and patients

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The ACS spectrum

Oligo/ Increasing chest Persistent chest Cardiogenic shock/ Cardiac

asymptomatic pain/symptoms pain/symptoms acute heart failure arrest
Clinical
presentation

Normal ST segment ST segment Malignant

depression elevation arrhythmia
ECG
findings

Working
NSTE-ACS STEMI
diagnosis

Non-elevated Rise and fall

hs-cTn
levels

Final Unstable
NSTEMI STEMI
diagnosis angina

Figure 2 The spectrum of clinical presentations, electrocardiographic findings, and high-sensitivity cardiac troponin levels in patients with acute coronary
syndrome. ACS, acute coronary syndrome; ECG, electrocardiogram; hs-cTn, high-sensitivity cardiac troponin; NSTE-ACS, non-ST-elevation acute coronary
syndrome; NSTEMI, non-ST-elevation myocardial infarction; STEMI, ST-elevation myocardial infarction.
ESC Guidelines 3731

with cardiac arrest, electrical/haemodynamic instability, or cardio­ Table 3 Definitions of terms related to invasive strat­
genic shock (CS) (Figure 2). egy and reperfusion therapy commonly used in this
Patients presenting with suspected ACS are typically classified based document
on ECG at presentation for the purposes of initial management. After
Term Definition
this, patients can be further classified based on the presence or absence
of cardiac troponin elevation (once these results are available), as de­ First medical contact (FMC) The time point when the patient is initially
monstrated in Figures 2 and 3. These features (ECG changes and cardiac assessed by a physician, paramedic, nurse,
troponin elevation) are important in the initial triage and diagnosis of or other trained emergency medical
patients with ACS, helping to risk stratify patients and guide the initial services worker who can obtain and
management strategy. However, after the acute management and sta­ interpret the ECG and deliver initial
bilization phase, most aspects of the subsequent management strategy interventions (e.g. defibrillation). FMC can
are common to all patients with ACS (regardless of the initial ECG
be either in the pre-hospital setting or
pattern or the presence/absence of cardiac troponin elevation at

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upon patient arrival at the hospital (e.g.
presentation) and can therefore be considered under a common
the emergency department)
pathway. A glossary of the terms related to invasive strategies and
STEMI diagnosis The time at which a patient with ischaemic
reperfusion therapy commonly used in this document, and their
associated definitions, is provided in Table 3. symptoms is interpreted as presenting
While they are closely related, it is important to recognize that ACS with ACS and ST-segment elevation (or
is not the same as MI.1 AMI is defined as cardiomyocyte necrosis in the ST-segment elevation equivalent)
clinical setting of acute myocardial ischaemia. This includes MI due to Primary PCIa Emergent PCI with balloon, stent, or
atherothrombotic events (Type 1 MI) and also other potential causes other approved device, performed on the
of myocardial ischaemia and myocyte necrosis (Type 2–5 MI) IRA without previous fibrinolytic
(Supplementary data online, Table S1). Myocardial injury is another treatment
distinct entity, used to describe troponin release due to mechanisms Primary PCI strategya Emergency coronary angiography and PCI
other than myocardial ischaemia and not meeting the criteria for MI of the IRA if indicated
outlined in Supplementary data online, Table S1. Myocardial injury Rescue PCIa Emergency PCI performed as soon as
can be acute or chronic depending on whether there is evidence of possible in cases of failed fibrinolytic
dynamic change in the elevated troponins on serial testing. Some
treatment
causes of myocardial injury include myocarditis, sepsis, takotsubo car­
Routine early PCI strategy Coronary angiography, with PCI of the
diomyopathy, heart valve disease, cardiac arrhythmias, and heart fail­
after fibrinolysisa IRA if indicated, performed between 2 h
ure (HF).
and 24 h after successful fibrinolysis
The focus of this guideline is largely centred on the management of
patients who will eventually receive a diagnosis of Type 1 MI. Pharmaco-invasive strategya Fibrinolysis combined with rescue PCI (in
However, at every stage of the management of patients presenting cases of failed fibrinolysis) or routine early
with ACS, physicians must carefully consider other differential diag­ PCI strategy (in cases of successful
noses in their clinical assessment because they are common, asso­ fibrinolysis)
ciated with different underlying pathological mechanisms, have Immediate invasive strategy Emergency coronary angiography (i.e. as
different prognoses, and frequently require different treatment ap­ soon as possible) and PCI/CABG of the
proaches. More information is provided in the Supplementary IRA if indicated
data online. In general, detailed information regarding the results Early invasive strategy Early coronary angiography (<24 h from
of individual trials will not be provided in the main guideline. diagnosis of ACS) and PCI/CABG of the
However, where appropriate, this information is provided in the IRA if indicated
Supplementary data online evidence tables.
© ESC 2023
Selective invasive strategy Coronary angiography ± PCI/CABG
based on clinical assessment and/or
non-invasive testing

ACS, acute coronary syndrome; CABG, coronary artery bypass grafting; ECG,
electrocardiogram; IRA, infarct-related artery; PCI, percutaneous coronary intervention;
STE-ACS, ST-segment-elevation acute coronary syndrome.
a
CABG may also be indicated instead of PCI in certain circumstances.
3732 ESC Guidelines

Clinical presentation Working diagnosisa Further investigations Final diagnosisb

hs-cTn levels
STEMI

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STEMI

ECG ± Angiography NSTEMI

If a patient has
signs/symptoms
suggestive of ACS, Unstable angina
NSTE-ACS
perform an ECG
within 10 min of FMC
± Imaging
Non-ACS diagnosis

Figure 3 Classification of patients presenting with suspected acute coronary syndrome: from a working to a final diagnosis. ACS, acute coronary syndrome;
ECG, electrocardiogram; FMC, first medical contact; hs-cTn, high-sensitivity cardiac troponin; MI, myocardial infarction; NSTE-ACS, non-ST-elevation acute
coronary syndrome; NSTEMI, non-ST-elevation myocardial infarction: STEMI, ST-elevation myocardial infarction. aThe working ACS diagnosis can be clas­
sified as STEMI or NSTE-ACS on the basis of available clinical information and ECG findings. This allows for initial triage and assessment. bThe final diagnosis is
based on symptoms, ECG and troponin for the diagnosis of MI as well as the results of other tests (i.e. imaging and/or angiography) to facilitate understanding
of the mechanism and subclassification of the type of MI. Patients initially assigned a working diagnosis of STEMI or NSTE-ACS may eventually receive a final
non-ACS diagnosis.

2.2. Epidemiology of acute coronary heart disease is the most common cause of CVD death, accounting
for 38% of all CVD deaths in females and 44% in males.3
syndromes
Cardiovascular disease (CVD) is the most common cause of mortality
and morbidity worldwide, with a substantial portion of this burden
borne by low- and middle-income countries.2,3 ACS is often the first 2.3. Number and breakdown of classes of
clinical manifestation of CVD. In 2019, there were an estimated 5.8 mil­ recommendations
lion new cases of ischaemic heart disease in the 57 ESC member coun­ The total number of recommendations in this guideline is 193. A sum­
tries.3 The median age-standardized incidence estimate per 100 000 mary of the recommendations according to Class of Recommendation
people was 293.3 (interquartile ratio 195.8–529.5). CVD remains the and Level of Evidence (LoE) is also provided. As per Class of
most common cause of death within ESC member countries, account­ Recommendation, there were 106 Class I, 70 Class II, and 17 Class III
ing for just under 2.2 million deaths in females and just over 1.9 million recommendations. As per LoE, there were 56 LoE A, 64 LoE B, and
deaths in males in the most recent year of available data. Ischaemic 73 LoE C recommendations.
ESC Guidelines 3733

2.4. What is new

Table 4 New recommendations

Recommendations Classa Levelb

Recommendations for antiplatelet and anticoagulant therapy in acute coronary syndrome

If patients presenting with ACS stop DAPT to undergo coronary artery bypass grafting, it is recommended they resume DAPT after surgery
I C
for at least 12 months.
In older ACS patients, especially if HBR, clopidogrel as the P2Y12 receptor inhibitor may be considered. IIb B
Recommendations for alternative antithrombotic therapy regimens
In patients who are event-free after 3–6 months of DAPT and who are not high ischaemic risk, single antiplatelet therapy (preferably with a

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IIa A
P2Y12 receptor inhibitor) should be considered.
P2Y12 inhibitor monotherapy may be considered as an alternative to aspirin monotherapy for long-term treatment. IIb A
In HBR patients, aspirin or P2Y12 receptor inhibitor monotherapy after 1 month of DAPT may be considered. IIb B
In patients requiring OAC, withdrawing antiplatelet therapy at 6 months while continuing OAC may be considered. IIb B
De-escalation of antiplatelet therapy in the first 30 days after an ACS event is not recommended. III B
Recommendations for cardiac arrest and out-of-hospital cardiac arrest
Evaluation of neurological prognosis (no earlier than 72 h after admission) is recommended in all comatose survivors after cardiac arrest. I C
Transport of patients with out-of-hospital cardiac arrest to a cardiac arrest centre according to local protocol should be considered. IIa C
Recommendations for technical aspects of invasive strategies
In patients with spontaneous coronary artery dissection, PCI is recommended only for patients with symptoms and signs of ongoing
I C
myocardial ischaemia, a large area of myocardium in jeopardy, and reduced antegrade flow.
Intravascular imaging should be considered to guide PCI. IIa A
Intravascular imaging (preferably optical coherence tomography) may be considered in patients with ambiguous culprit lesions. IIb C
Recommendations for multivessel disease in ACS patients presenting in cardiogenic shock
Staged PCI of non-IRA should be considered. IIa C
Recommendations for multivessel disease in haemodynamically stable STEMI patients undergoing primary PCI
It is recommended that PCI of the non-IRA is based on angiographic severity. I B
Invasive epicardial functional assessment of non-culprit segments of the IRA is not recommended during the index procedure. III C
Recommendations for acute coronary syndrome complications
Implantation of a permanent pacemaker is recommended when high-degree AV block does not resolve within a waiting period of at least 5
I C
days after MI.
Cardiac magnetic resonance imaging should be considered in patients with equivocal echocardiographic images or in cases of high clinical
IIa C
suspicion of LV thrombus.
Following an acute anterior MI, a contrast echocardiogram may be considered for the detection of LV thrombus if the apex is not well
IIb C
visualized on echocardiography.
In selected patients with high-degree AV block in the context of an anterior wall MI and acute heart failure, early device implantation (cardiac
IIb C
resynchronization therapy—defibrillator/pacemaker) may be considered.
In patients with recurrent life-threatening ventricular arrhythmias, sedation or general anaesthesia to reduce sympathetic drive may be
IIb C
considered.
Recommendations for acute coronary syndrome comorbid conditions
It is recommended to base the choice of long-term glucose-lowering treatment on the presence of comorbidities, including heart failure,
I A
chronic kidney disease, and obesity.
For frail older patients with comorbidities, a holistic approach is recommended to individualize interventional and pharmacological
I B
treatments after careful evaluation of the risks and benefits.
An invasive strategy is recommended in cancer patients presenting with high-risk ACS with expected survival ≥6 months. I B
A temporary interruption of cancer therapy is recommended in patients in whom the cancer therapy is suspected to be a contributing cause
I C
of ACS.
A conservative non-invasive strategy should be considered in ACS patients with poor cancer prognosis (i.e. with expected life survival <6
IIa C
months) and/or very high bleeding risk.
Aspirin is not recommended in cancer patients with a platelet count <10 000/μL. III C
Continued
3734 ESC Guidelines

Clopidogrel is not recommended in cancer patients with a platelet count <30 000/μL. III C
In ACS patients with cancer and <50 000/μL platelet count, prasugrel or ticagrelor are not recommended. III C
Recommendations for long-term management
It is recommended to intensify lipid-lowering therapy during the index ACS hospitalization for patients who were on lipid-lowering therapy
I C
before admission.
Low-dose colchicine (0.5 mg once a day) may be considered, particularly if other risk factors are insufficiently controlled or if recurrent
IIb A
cardiovascular disease events occur under optimal therapy.
Combination therapy with a high-dose statin plus ezetimibe may be considered during index hospitalization. IIb B
Recommendations for patient perspectives in acute coronary syndrome care
Patient-centred care is recommended by assessing and adhering to individual patient preferences, needs and beliefs, ensuring that patient
I B
values are used to inform all clinical decisions.

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It is recommended to include ACS patients in decision-making (as much as their condition allows) and to inform them about the risk of
I B
adverse events, radiation exposure, and alternative options. Decision aids should be used to facilitate the discussion.
It is recommended to assess symptoms using methods that help patients to describe their experience. I C
Use of the ‘teach back’ technique for decision support during the securing of informed consent should be considered. IIa B
Patient discharge information should be provided in both written and verbal formats prior to discharge. Adequate preparation and

© ESC 2023
education for patient discharge using the teach back technique and/or motivational interviewing, giving information in chunks, and checking IIa B
for understanding, should be considered.
Assessment of mental well-being using a validated tool and onward psychological referral when appropriate should be considered. IIa B

ACS, acute coronary syndrome; AV, atrioventricular; DAPT, dual antiplatelet therapy; HBR, high bleeding risk; IRA, infarct-related artery; LV, left ventricular(cle); MI, myocardial infarction;
OAC, oral anticoagulant/ation; PCI, percutaneous coronary intervention; STEMI, ST-elevation myocardial infarction.
a
Class of recommendation.
b
Level of evidence.

Table 5 Revised recommendations

Recommendations in 2017 and 2020 versions Classa LoEb Recommendations in 2023 version Classa LoEb

Recommendations for imaging for patients with suspected NSTE-ACS

In patients with no recurrence of chest pain, normal ECG In patients with suspected ACS, non-elevated (or
findings, and normal levels of cardiac troponin (preferably uncertain) hs-cTn, no ECG changes and no recurrence of
high sensitivity), but still with suspected ACS, a pain, incorporating CCTA or a non-invasive stress
I B IIa A
non-invasive stress test (preferably with imaging) for imaging test as part of the initial workup should be
inducible ischaemia or CCTA is recommended before considered.
deciding on an invasive approach.
Recommendations for timing of invasive strategy in NSTE-ACS
An early invasive strategy within 24 h is recommended in An early invasive strategy within 24 h should be
patients with any of the following high-risk criteria: considered in patients with at least one of the following
• Diagnosis of NSTEMI suggested by the diagnostic high-risk criteria:
algorithm recommended in Section 3 • Confirmed diagnosis of NSTEMI based on current
I A IIa A
• Dynamic or presumably new contiguous ST/T-segment recommended ESC hs-cTn algorithms
changes suggesting ongoing ischaemia • Dynamic ST-segment or T wave changes
• Transient ST-segment elevation • Transient ST-segment elevation
• GRACE risk score >140. • GRACE risk score >140.
Recommendations for antiplatelet and anticoagulant therapy in STEMI
A potent P2Y12 inhibitor (prasugrel or ticagrelor), or Pre-treatment with a P2Y12 receptor inhibitor may be
clopidogrel if these are not available or are contraindicated, considered in patients undergoing a primary PCI strategy.
is recommended before (or at latest at the time of) PCI, and I A IIb B
maintained over 12 months, unless there are
contraindications such as excessive risk of bleeding.
Recommendations for long-term antithrombotic therapy
After stent implantation in patients undergoing a strategy In patients who are event-free after 3–6 months of DAPT
of DAPT, stopping aspirin after 3–6 months should be and who are not high ischaemic risk, SAPT (preferably
IIa A IIa A
considered, depending on the balance between the with a P2Y12 receptor inhibitor) should be considered.
ischaemic and bleeding risks.
Continued
ESC Guidelines 3735

Recommendations for cardiac arrest and out-of-hospital cardiac arrest

Delayed as opposed to immediate angiography should be Routine immediate angiography after resuscitated cardiac
considered among haemodynamically stable patients arrest is not recommended in haemodynamically stable
IIa B III A
without ST-segment elevation successfully resuscitated patients without persistent ST-segment elevation (or
after out-of-hospital cardiac arrest. equivalents).
Targeted temperature management (also called Temperature control (i.e. continuous monitoring of core
therapeutic hypothermia), aiming for a constant temperature and active prevention of fever [i.e. >37.7°C])
temperature between 32 and 36 C for at least 24 h, is is recommended after either out-of-hospital or in-hospital
I B I B
indicated in patients who remain unconscious after cardiac arrest for adults who remain unresponsive after
resuscitation from cardiac arrest (of presumed cardiac return of spontaneous circulation.
cause).

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Recommendations for in-hospital management
When echocardiography is suboptimal/inconclusive, an When echocardiography is suboptimal/inconclusive,
alternative imaging method (CMR preferably) should be IIa C CMR imaging may be considered. IIb C
considered.
Recommendations for management of multivessel disease in haemodynamically stable STEMI patients undergoing primary PCI
Routine revascularization of non-IRA lesions should be Complete revascularization is recommended either
considered in STEMI patients with multivessel disease IIa A during the index PCI procedure or within 45 days. I A
before hospital discharge.
Recommendations for acute coronary syndrome comorbid conditions
Glucose-lowering therapy should be considered in ACS Glucose-lowering therapy should be considered in

© ESC 2023
patients with blood glucose >10 mmol/L (>180 mg/dL), patients with ACS with persistent hyperglycaemia, while
IIa B IIa C
with the target adapted to comorbidities, while episodes episodes of hypoglycaemia should be avoided.
of hypoglycaemia should be avoided.

ACS, acute coronary syndrome; CCTA, coronary computed tomography angiography; CMR, cardiac magnetic resonance; DAPT, dual antiplatelet therapy; ECG, electrocardiography/gram;
ESC European Society of Cardiology; GRACE, Global Registry of Acute Coronary Events; hs-cTn, high-sensitivity cardiac troponin; IRA, infarct-related artery; NSTE-ACS, non-ST-elevation
acute coronary syndrome; NSTEMI, non-ST-elevation myocardial infarction; PCI, percutaneous coronary intervention; SAPT, single antiplatelet therapy; STEMI, ST-elevation myocardial
infarction.
a
Class of recommendation.
b
Level of evidence.

New/revised concepts prompting consideration of the clinical diagnosis of ACS and the initi­
ation of testing aligned with specific diagnostic algorithms (Figure 4).
• ACS should be considered a spectrum, which encompasses both
Chest pain descriptors should be classified as cardiac, possibly car­
non-ST-elevation (NSTE)-ACS and ST-elevation MI (STEMI).
diac, and likely non-cardiac. Further information on the suggested use
• A section on the management of ACS in patients with cancer is
of these terms is provided in the Supplementary data online. The use
provided.
of the descriptor ‘atypical’ should be avoided. Chest pain-equivalent
• A section on patient perspectives is provided.
symptoms include dyspnoea, epigastric pain, and pain in the left or right
arm or neck/jaw.
Misdiagnosis or delayed diagnosis is sometimes due to an incomplete
3. Triage and diagnosis history or difficulty in eliciting symptoms from the patient. In order to
understand the complexity of ACS-related symptomatology, careful
3.1. Clinical presentation and physical
history taking and comprehensive interaction with the patient are
examination crucial and may help to facilitate an early and accurate diagnosis.
3.1.1. Clinical presentation Further information is provided in the Supplementary data online, in­
Acute chest discomfort—which may be described as pain, pressure, cluding Figure S1, which outlines some of the most common symptoms
tightness, heaviness, or burning—is the leading presenting symptom of ACS in women and men.
3736 ESC Guidelines

ACS
presentation

ECG Physical examination Clinical history Vital signs hs-cTna levels

Initial A.C.S.
assessment

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NSTE-ACS NSTE-ACS
STEMI
with very high-risk featuresb without very high-risk featuresb

Working
diagnosis

Immediate angiography ± Immediate angiography Consider angiography

PPCI or fibrinolysis if timely ± PCI within 24 h for NSTE-ACS
PPCI not feasible with high risk features
Early invasive
angiography
according to
patient risk PPCI ATT Fibrinolysis PCI ATT PCI ATT

Non-immediate Intravascular Non-invasive hs-cTna ECG

Echo
angiography imaging imaging levels monitoring

Further
investigations

Long-term Lifestyle Smoking

PCI CABG
medical therapy measures cessation

Further
management

Figure 4 An overview of the initial triage, management and investigation of patients who present with signs and symptoms potentially consistent with acute
coronary syndrome. ACS, acute coronary syndrome; ATT, antithrombotic therapy; CABG, coronary artery bypass grafting; ECG, electrocardiogram; hs-cTn,
high-sensitivity cardiac troponin; NSTE-ACS, non-ST-elevation acute coronary syndrome; PPCI, primary percutaneous coronary intervention; STEMI,
ST-elevation myocardial infarction. The ‘A.C.S.’ assessment is detailed in Figure 5. aResults of hs-cTn measurements are not required for the initial stratifi­
cation of ACS and the initial emergency management (i.e. for patients with a working diagnosis of STEMI or very high-risk NSTE-ACS) should not be delayed
based on this. bFor patients with NSTE-ACS with very high-risk features, immediate angiography is recommended. For patients with NSTE-ACS with high-
risk features, early invasive angiography (i.e. <24 h) should be considered and inpatient invasive angiography is recommended. See Recommendation Table 4
for details.

It is important that awareness of the symptoms associated with the public to seek urgent medical help. Continuous education, pro­
ACS is high among the general population, in particular red flag motion, and advocacy efforts are important to make sure that this
symptoms such as prolonged chest pain (>15 min) and/or recurrent information is as widely available as possible to the general
pain within 1 h, which should prompt patients or other members of population.
ESC Guidelines 3737

3.1.2. History taking and physical examination 3.2. Diagnostic tools | Electrocardiogram
Patients with suspected ACS present in a broad range of clinical scen­ The resting 12-lead ECG is the first-line diagnostic tool in the assess­
arios, including in the community, at the emergency department (ED), ment of patients with suspected ACS. It is recommended that an
or in the inpatient setting. It is crucial to take a focused medical history ECG is obtained immediately upon FMC and interpreted by a qualified
and accurately characterize the presenting symptoms in order to emergency medical technician or physician within 10 min.4,5 It should
manage the patient via the appropriate care pathway as soon as be repeated as necessary, especially if symptoms have waned at FMC.
possible. Based on the initial ECG, patients with suspected ACS can be differen­
Prompt assessment of vital signs is recommended at first medical tiated into two working diagnoses:
contact (FMC), at the same time as acquisition of an initial ECG
(Figure 5). In patients presenting with suspected ACS, physical examin­ • Patients with acute chest pain (or chest pain-equivalent
ation is recommended and is useful both to eliminate differential diag­ signs/symptoms) and persistent ST-segment elevation
noses and to identify very high-risk and high-risk ACS features. This may (or ST-segment elevation equivalents) on ECG (working

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be particularly relevant for patients presenting with cardiac arrest, signs diagnosis: ST-segment elevation MI: STEMI). The vast major­
of CS, and/or haemodynamic or electrical instability.4 Focused physical ity of these patients will sustain myocardial necrosis and troponin ele­
examination should include checking for the presence of all major vation, fulfilling the criteria for an MI, but MI will not be the final
pulses, measurement of blood pressure in both arms, auscultation of diagnosis in all patients with a working diagnosis of STEMI.
the heart and lungs, and assessing for signs of HF or circulatory • Patients with acute chest pain (or chest pain-equivalent
compromise. signs/symptoms) but without persistent ST-segment

A C S
Abnormal Clinical Stable
ECG? context? patient?

Perform an ECG to assess Consider the clinical Perform an exam to assess

for evidence of ischaemia context and available if the patient is clinically
or other abnormalities investigations and vitally stable

Figure 5 The A.C.S. assessment for the initial evaluation of patients with suspected acute coronary syndrome. ECG, electrocardiogram. This figure sum­
marizes the initial ‘A.C.S. assessment’ that can be performed for a patient presenting with suspected ACS. ‘A’ stands for ‘Abnormal ECG?’: an ECG should be
performed within 10 min of FMC and assessed for evidence of abnormalities or ischaemia. ‘C’ stands for ‘Clinical Context?’: it is important to consider the
clinical context of the patient’s presentation and the results of any investigations that are available. This should also include a targeted history with the aim of
determining the patient’s symptoms and elucidating any other relevant background information. ‘S’ stands for ‘Stable Patient?’: the patient should be quickly
assessed to determine if they are clinically stable—this should include assessment of the clinical vital signs, including heart rate, blood pressure, and oxygen
saturations, if possible, as well as checking for potential signs of CS.
3738 ESC Guidelines

elevation (or ST-segment elevation equivalents) on ECG in aVR and/or V1, suggests multivessel ischaemia or left main coronary
(working diagnosis: non-ST-elevation [NSTE]-ACS). artery obstruction, particularly if the patient presents with haemo­
These patients may exhibit other ECG alterations, including transient dynamic compromise.9–11
ST-segment elevation, persistent or transient ST-segment depres­ Bundle branch block (BBB). In patients with a high clinical sus­
sion, and T wave abnormalities, including hyperacute T waves, T picion of ongoing myocardial ischaemia, the presence of LBBB, right
wave inversion, biphasic T waves, flat T waves, and pseudo- bundle branch block (RBBB), or a paced rhythm precludes an accurate
normalization of T waves. Alternatively, the ECG may be normal. assessment of the presence or absence of ST-segment elevation.
The majority of patients in this category who subsequently display Therefore, patients presenting with these ECG patterns in combination
a typical rise and fall in cardiac troponin levels (i.e. fulfilling MI criteria with signs/symptoms that are highly suspicious for ongoing myocardial
as per the fourth universal definition of MI) will receive a final diagno­ ischaemia should be managed similarly to those with clear ST-segment
sis of non-ST-elevation MI (NSTEMI). In other patients, the troponin elevation, regardless of whether the BBB is previously known (see
level will remain below the 99th centile and they will receive a final Supplementary data online).4
diagnosis of UA, although with high-sensitivity troponin assays this

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diagnosis has become less common. It is also important to recognize 3.2.2. Acute coronary syndrome without persistent
that NSTEMI or UA will not be the final diagnosis in all patients with ST-segment elevation (non-ST elevation acute
an initial working diagnosis of NSTE-ACS. coronary syndrome)
While the ECG in the setting of NSTE-ACS may be normal in more
than one-third of patients, characteristic ECG abnormalities are fre­
3.2.1. Acute coronary syndrome with persistent quently present and increase the diagnostic probability of ACS.12–16
ST-segment elevation (suspected ST-elevation These ECG abnormalities include ST depression and T wave changes
myocardial infarction) (especially biphasic T waves or prominent negative T waves
The priority for these patients is the implementation of reperfusion ther­ [Wellens’ sign, related to severe proximal left anterior descending ar­
apy as soon as possible (see Section 5). In the appropriate clinical context, tery stenosis]), (see Supplementary data online, Figure S3).
ST-segment elevation (measured at the J-point) is considered suggestive
of ongoing coronary artery acute occlusion in the following cases:
New ST elevation at the J-point in at least two contiguous leads: Recommendation Table 1 — Recommendations for
clinical and diagnostic tools for patients with suspected
• ≥2.5 mm in men <40 years, ≥2 mm in men ≥40 years, or ≥1.5 mm acute coronary syndrome
in women regardless of age in leads V2–V3
• and/or ≥1 mm in the other leads (in the absence of left ventricular Recommendations Classa Levelb
[LV] hypertrophy or left bundle branch block [LBBB]). It is recommended to base the diagnosis and initial
short-term risk stratification of ACS on a
In patients with suspected inferior STEMI, it is recommended to re­ I B
combination of clinical history, symptoms, vital signs,
cord right precordial leads (V3R and V4R) in order to assess for
other physical findings, ECG, and hs-cTn.1,17,18
ST-segment elevation.6 Posterior leads (V7–V9) can also be recorded
to investigate for posterior STEMI, particularly in patients with ongoing ECG
symptoms and an inconclusive standard 12-lead ECG. Twelve-lead ECG recording and interpretation is
The diagnosis of ongoing acute coronary artery occlusion on ECG recommended as soon as possible at the point of I B
can sometimes be challenging, and some cases may warrant prompt FMC, with a target of <10 min.5,19
management and triage for immediate reperfusion therapy despite Continuous ECG monitoring and the availability of
the absence of ST-segment elevation. It is also important to recognize defibrillator capacity is recommended as soon as
that while the most sensitive sign for ongoing acute coronary possible in all patients with suspected STEMI, in I B
artery occlusion is ST-segment elevation, there are other ECG find­ suspected ACS with other ECG changes or ongoing
ings that can be suggestive of ongoing coronary artery occlusion (or
chest pain, and once the diagnosis of MI is made.20,21
severe ischaemia). If these findings are present, prompt triage for
The use of additional ECG leads (V3R, V4R, and V7–
immediate reperfusion therapy is indicated (see Supplementary data
V9) is recommended in cases of inferior STEMI or if
online, Figure S2). I B
total vessel occlusion is suspected and standard leads
ST-segment depression in leads V1–V3 (especially when the terminal
are inconclusive.22–24
T wave is positive) and/or ST-segment elevation in V7–V9 are highly
suggestive of posterior coronary artery occlusion (often the left cir­ An additional 12-lead ECG is recommended in cases
I C
cumflex artery).1,7 ST-segment elevation in V3R and V4R is highly sug­ with recurrent symptoms or diagnostic uncertainty.
gestive of ongoing RV ischaemia.8 ST depression ≥1 mm in ≥6 surface Continued
leads (inferolateral ST depression), coupled with ST-segment elevation
ESC Guidelines 3739

Blood sampling Some of the clinical implications of hs-cTn assays are detailed in
Supplementary data online, Table S2.
It is recommended to measure cardiac troponins
It is also important to consider that there are other clinical conditions
with high-sensitivity assays immediately after
I B apart from Type 1 MI in which elevations in cTn can be observed (see
presentation and to obtain the results within 60 min
Supplementary data online, Section 3.3.1 and Table S3).
of blood sampling.15,25–27
It is recommended to use an ESC algorithmic
3.3.2. Central laboratory vs. point of care
approach with serial hs-cTn measurements (0 h/1 h I B
The vast majority of cTn assays that run on automated platforms in the
or 0 h/2 h) to rule in and rule out NSTEMI.28–44
central laboratory are sensitive (i.e. allow for the detection of cTn in
Additional testing after 3 h is recommended if the ∼20–50% of healthy individuals) or high-sensitivity (i.e. allow for the de­
first two hs-cTn measurements of the 0 h/1 h tection of cTn in ∼50–95% of healthy individuals) assays.
algorithm are inconclusive and no alternative I B High-sensitivity assays are recommended over lower-sensitivity assays,

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diagnoses explaining the condition have been as they provide higher diagnostic accuracy at an identical low
made.45,46 cost.1,12,15,25–27,57,63
The use of established risk scores (e.g. GRACE risk The majority of currently used point-of-care (POC) tests cannot be
score) for prognosis estimation should be IIa B considered high-sensitivity assays.64 The advantage of POC tests is a
considered.47–49 shorter turnaround time. However, this is counterbalanced by lower
Triage for emergency reperfusion strategy sensitivity, lower diagnostic accuracy, and lower negative predictive va­
lue (NPV). A randomized trial in low-risk chest pain patients with sus­

© ESC 2023
It is recommended that patients with suspected
pected NSTE-ACS and onset of symptoms ≥2 h before ambulance
STEMI are immediately triaged for an emergency I A
50–52
presentation reported that the use of a pre-hospital rule-out strategy
reperfusion strategy. (with a single POC conventional troponin T test) resulted in a signifi­
ACS, acute coronary syndrome; ECG, electrocardiogram; ESC, European Society of cant reduction of 30-day healthcare costs and a comparable major ad­
Cardiology; FMC, first medical contact; GRACE, Global Registry of Acute Coronary verse cardiovascular event (MACE) rate in comparison to an ED
Events; hs-cTn, high-sensitivity cardiac troponin; MI, myocardial infarction; NSTEMI, rule-out strategy (with evaluation as per standard local practice).65
non-ST-elevation myocardial infarction; STEMI, ST-elevation myocardial infarction.
a
Class of recommendation. Overall, automated assays have been more thoroughly evaluated
b
Level of evidence. than POC tests and are currently preferred.1,12–15,26,34,35,53,55–58
However, this is a rapidly developing field and it will be important to
re-evaluate this preference when more extensively validated high-
sensitivity POC tests are clinically available.66–68

3.3. Diagnostic tools | Biomarkers 3.3.3. Confounders of cardiac troponin concentration

3.3.1. High-sensitivity cardiac troponins In patients presenting with suspected NSTE-ACS, four clinical variables
After excluding clinical and ECG signs suggestive of STEMI or very high- affect hs-cTn concentrations beyond the presence or absence of MI.
risk NSTE-ACS, biomarkers play a complementary role in the diagnosis, These variables are: age (concentrations in healthy very young vs.
risk stratification, and management of patients with suspected ACS. ‘healthy’ very old individuals differ by up to 300%); renal dysfunction
Measurement of a biomarker of cardiomyocyte injury, preferably high- (differences between otherwise healthy patients with very high vs.
sensitivity cardiac troponin (hs-cTn), is recommended in all patients very low estimated glomerular filtration rate [eGFR] of up to 300%);
with suspected ACS.15,17,25–27,53,54 If the clinical presentation is com­ time from chest pain onset (>300%); and, to a lesser extent, sex
patible with myocardial ischaemia, then a rise and/or fall in cTn above (≈40%).28,34,35,69–76 Despite the potential baseline differences in
the 99th percentile of healthy individuals points to a diagnosis of MI hs-cTn values based on these four variables, absolute changes in
as per the criteria in the fourth universal definition of MI.1 In patients hs-cTn levels are still of diagnostic and prognostic value. Current data
with MI, levels of cTn rise rapidly (i.e. usually within 1 h if using high- on the use of sex-specific hs-cTn values in the diagnosis of MI have
sensitivity assays) after symptom onset and remain elevated for a vari­ been controversial and failed to demonstrate a clear clinical bene­
able period of time (usually several days).1,15,26,53,55–58 fit.74,75,77–80 Therefore, until automated tools (i.e. risk assessment cal­
Advances in technology have led to a refinement in cTn assays and culators) incorporating the effect of all four clinical variables (age,
have improved their accuracy in detecting and quantifying cardiomyo­ eGFR, time from chest pain onset, and sex) are available, the use of uni­
cyte injury.1,12–15,18,26,34,35,53,55–60 Data from large multicentre studies form cut-off concentrations should remain the standard of care for the
have consistently shown that hs-cTn assays increase diagnostic accuracy early diagnosis of MI.28,30,31,34,35,73,81,82
for MI at the time of presentation in comparison to conventional assays,
especially in patients presenting early after chest pain onset, enabling 3.3.4. Rapid ‘rule-in’ and ‘rule-out’ algorithms
more rapid ‘rule-in’ and ‘rule-out’ of MI.1,12–15,26,34,35,53,55–58 Overall, Due to their higher sensitivity and diagnostic accuracy for the detection
hs-cTn T and hs-cTn I subunit assays appear to provide comparable of MI at presentation, the time interval to the second cTn assessment
diagnostic accuracy in the early diagnosis of MI.28,32,61,62 The use of can be shortened with the use of hs-cTn assays. This substantially re­
the terms ‘normal’ and ‘abnormal’ to describe hs-cTn levels should duces the delay to diagnosis, translating into shorter stays in the ED,
be avoided; instead, the terms ‘non-elevated’ and ‘elevated’ should be lower costs, and less diagnostic uncertainty for patients.15,83–88 It is re­
used to refer to hs-cTn levels below and above the 99th percentile. commended to use the 0 h/1 h algorithm (best option) or the 0 h/2 h
3740 ESC Guidelines

algorithm (second-best option) (Figure 6). These algorithms have been ‘rule-in’ pathway patients with diagnoses other than MI still have condi­
derived and validated in large multicentre diagnostic studies using cen­ tions that require specialist cardiology input and either coronary angi­
tral adjudication of the final diagnosis for all currently available hs-cTn ography or non-invasive imaging in order to establish an accurate
assays.27–39,62,70,73,82,89–93 Optimal thresholds for rule-out were se­ final diagnosis.28,30,31,34,35,73,82 Therefore, the vast majority of patients
lected to allow a sensitivity and NPV of at least 99%. Optimal thresholds triaged towards the ‘rule-in’ pathway by these algorithms will require
for rule-in were selected to allow a positive predictive value (PPV) of at hospital admission and invasive coronary angiography (ICA).
least 70%. These algorithms were developed from large derivation co­
horts and then validated in large independent validation cohorts. The
previous ESC 0 h/3 h algorithm was considered as an alternative,40,56 3.3.4.1.3. Observe. Patients who do not qualify for the ‘rule-out’ or
but three recent large diagnostic studies suggested that the ESC 0 h/ ‘rule-in’ pathways are assigned to the ‘observe’ pathway. These patients re­
3 h algorithm appears to balance efficacy and safety less well than present a heterogeneous group and have been shown to have a mortality
more rapid protocols using lower rule-out concentrations, including rate that is comparable to rule-in patients.98 Therefore, an individual as­
the ESC 0 h/1 h algorithm.41–43 The very high safety and high efficacy sessment based on the particular risk profile of the patient (i.e. risk scores)

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of applying the ESC 0 h/1 h algorithm was recently confirmed in three is of paramount importance for patients in this group. Additionally, a third
real-life implementation studies, including one randomized controlled measurement of cTn at 3 h (± echocardiography) is recommended as the
trial (RCT).44,94,95 Therefore, the ESC 0 h/3 h algorithm is an alternative next step in order to guide further management.45,46
for cases where the ESC 0 h/1 h or 0 h/2 h algorithms are not available. Most patients in the observe zone with a high degree of clinical
Of note, patients assigned to the ‘rule-out’ pathway using the ESC 0 h/ suspicion of ACS (e.g. relevant increase in cTn from presentation
1 h or 0 h/2 h algorithms have a very low rate of clinical events through to 3 h) are candidates for ICA. Conversely, most patients with a
to 30 days.95,96 low to intermediate likelihood for ACS according to clinical judg­
ment are candidates for non-invasive imaging after transfer from
the ED to the ward. Computed tomography (CT) angiography can
3.3.4.1. European Society of Cardiology 0 h/1 h and 0 h/2 h
be used to aid diagnosis and, in particular, to identify patients with
algorithms
non-obstructed coronary arteries who can be discharged if other
The ESC 0 h/1 h and 0 h/2 h algorithms are based on two underlying relevant diseases have been excluded. CT angiography can also iden­
concepts: firstly, hs-cTn is a continuous variable and the probability tify patients with obstructive coronary disease in whom revascular­
of MI increases with increasing hs-cTn values.28,30,31,34,35,73,82 ization may be considered. In the appropriate clinical context, if
Secondly, early absolute changes in the levels within 1 h or 2 h can be alternative conditions have been identified that explain the cTn va­
used as surrogates for absolute changes over 3 h or 6 h and provide in­ lues (i.e. rapid ventricular rate response to atrial fibrillation [AF],
cremental diagnostic value to the single cTn assessment at presenta­ marked anaemia, or a hypertensive emergency), further diagnostic
tion.27,28,30,31,34,35,73,82,97 The cut-off concentrations within the 0 h/ testing (i.e. ICA) may not be required.
1 h and 0 h/2 h algorithms are assay specific (Supplementary data The same concepts apply to the 0 h/2 h algorithm. Cut-off levels for
online, Table S4).27,28,30,31,34,35,73,82 both the 0 h/1 h and 0 h/2 h algorithms are also assay specific, and these
cut-off levels are shown in Supplementary data online, Table S4.99
3.3.4.1.1. Rule-out. The NPV for MI in patients assigned to the The ESC 0 h/1 h and 0 h/2 h algorithms should always be integrated
‘rule-out’ pathway has exceeded 99% in several large validation with a detailed clinical assessment and a 12-lead ECG. Repeat blood
cohorts.28–30,34,35,73 Assignment to the rule-out pathway does not al­ sampling is mandatory in cases where there is ongoing or recurrent
ways equal outpatient management. However, when used in conjunc­ chest pain. Recently, artificial intelligence models that include serial
tion with clinical and ECG findings, the 0 h/1 h and 0 h/2 h algorithms hs-cTn measurements in conjunction with individual risk profiles have
will enable the identification of appropriate candidates for early dis­ been proposed to be useful to facilitate a personalized diagnostic evalu­
charge and outpatient management. Even after the ruling out of MI, ation of patients with suspected MI. Similarly, risk-assessment models
elective non-invasive or invasive imaging may be appropriate according combining hs-cTn values at presentation and after early or late resam­
to clinical and risk assessment, and an alternative diagnosis to MI should pling have been developed to predict MI events during the first 30 days.
be identified. These models may facilitate alternative hs-cTn cut-offs based on the
balance between NPV and PPV best suited to individual clinical sites.27
3.3.4.1.2. Rule-in. The PPV for MI in patients meeting the ‘rule-in’ A diagnostic approach to the use of the ESC 0 h/1 h and 0 h/2 h algo­
pathway criteria in several studies has been ∼70–75%. Most of the rithms is shown in Figure 6.
ESC Guidelines 3741

Patient presents with a suspected NSTEMI and

without an indication for immediate invasive angiography

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Take hs-cTn at 0 h and 1 h/2 h

Very low initial hs-cTna Patients who do not meet High initial hs-cTn
the criteria for either of OR
OR
the other two pathways
Low initial hs-cTn and no Increase in 1 h/2 h hs-cTn
increase in 1 h/2 h hs-cTn

Appropriate management can be determined

based on the hs-cTn levels and clinical situation

Rule-out pathway Observe pathway Rule-in pathway

Figure 6 The 0 h/1 h or 0 h/2 h rule-out and rule-in algorithms using high-sensitivity cardiac troponin assays in patients presenting to the emergency de­
partment with suspected NSTEMI and without an indication for immediate invasive angiography. hs-cTn, high-sensitivity cardiac troponin; NSTEMI,
non-ST-elevation myocardial infarction. Patients are classified into one of three pathways as per the results of their hs-cTn values at 0 h (time of initial blood
test) and 1 h or 2 h later. Patients with a very low initial hs-cTn value or patients with a low initial value and no 1 h/2 h change in hs-cTn are assigned to the
‘rule-out’ pathway. Patients with a high initial hs-cTn value or a 1 h/2 h change in hs-cTn are assigned to the ‘rule-in’ pathway. Patients who do not meet the
criteria for the rule-out or rule-in strategies are assigned to the ‘observe’ pathway, and these patients should have hs-cTn levels checked at 3 h ± echocar­
diography in order to decide on further management. Cut-offs are assay specific (see Supplementary material online, Table S4) and derived to meet
pre-defined criteria for sensitivity and specificity for NSTEMI. Potential management and testing options for each of the three strategies are provided in
the relevant sections of the main text.12–15,26,27,53,55–58,100,101 aOnly applicable if the chest pain onset was >3 h prior to the 0 h hs-cTn measurement.
3742 ESC Guidelines

3.3.4.2. Practical guidance on how to implement the European recommended. However, CCTA may provide added value in certain clin­
Society of Cardiology 0 h/1 h algorithm ical settings (i.e. for patients in the observe zone in whom cTn and ECG
In order to maximize the safety and feasibility of implementing the 0 h/ results remain inconclusive). A normal CCTA (ruling out both obstructive
1 h algorithm, blood samples for hs-cTn at 0 h and 1 h should be ob­ and non-obstructive plaque) has a high NPV to exclude ACS and is asso­
tained irrespective of other clinical details and pending results (see ca­ ciated with excellent clinical outcomes.
veats of using rapid algorithms in Supplementary data online, Section 3.3. The systematic use of CCTA in rule-out patients after hospital dis­
2.2). This may result in unnecessary cTn measurements in the ∼10– charge may identify the presence of obstructive or non-obstructive pla­
15% of patients with very low 0 h concentrations and chest pain onset que and guide preventative medical therapies.118 CCTA can also be
>3 h, but substantially facilitates the process and thereby further in­ used to risk stratify selected low-risk NSTEMI patients. Such patients,
creases patient safety. Similarly, the 0 h blood sample should be ob­ who are found to have normal coronary arteries, non-obstructive cor­
tained immediately after admission to the ED. onary disease, or distal obstructive disease, may then not require
ICA.119–121 Of note, the utility of CCTA may be limited in patients
with tachycardia, established coronary artery disease (CAD), previous

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3.3.5. Other biomarkers
stents, or extensive coronary calcification.
The use of biomarkers other than cTn for the diagnosis of ACS is not
recommended (unless cTn is not available). Among the multitude of
additional biomarkers evaluated for the diagnosis of NSTEMI, only cre­ 3.4.3. Cardiac magnetic resonance imaging with or
atine kinase myocardial band isoenzyme, myosin-binding protein C, and without stress testing
copeptin may have clinical relevance when used in combination with Cardiac magnetic resonance (CMR) imaging delineates cardiac struc­
(standard) cTn T/I, although in most clinical situations their incremental ture and function, and also has the ability to provide assessments of
value above and beyond cTn is limited.45,46,83,102–114 myocardial perfusion and the pattern of myocardial injury. CMR is
the imaging test of choice when poor echocardiographic windows pre­
3.4. Diagnostic tools | Non-invasive imaging clude diagnostic echocardiographic evaluation. CMR allows direct visu­
3.4.1. Echocardiography alization of infarcted regions, providing information on scarring and
In emergency rooms and chest pain units, transthoracic echocardiog­ viability that can be differentiated from other forms of myocardial injury
raphy (TTE) performed or interpreted by trained healthcare profes­ (e.g. myocarditis). CMR is therefore of particular clinical value in estab­
sionals should be routinely available. In cases of suspected ACS with lishing a diagnosis of AMI where there is diagnostic uncertainty. CMR
diagnostic uncertainty, TTE can be useful to identify signs suggestive of can also be useful in identifying the culprit vascular territory and in con­
ongoing ischaemia or prior MI. However, this should not result in rele­ firming a diagnosis of myocarditis or takotsubo cardiomyopathy,
vant delays in transfer to the cardiac catheterization laboratory if there amongst other differentials. CMR is of particular value in establishing
is suspicion of an acute coronary artery occlusion. TTE can also be useful a diagnosis in patients presenting with a working diagnosis of myocardial
to suggest alternative aetiologies associated with chest pain (i.e. acute infarction with non-obstructive coronary arteries (MINOCA) following
aortic disease, RV signs in pulmonary embolism [PE]). All patients pre­ invasive angiography and is the gold standard for the assessment of LV
senting with CS or haemodynamic instability should undergo emergency thrombus.
TTE to try to identify the underlying cause—in particular, to assess LV
and RV function and look for evidence of mechanical complications.
Recommendation Table 2 — Recommendations for
non-invasive imaging in the initial assessment of patients
3.4.2. Computed tomography with suspected acute coronary syndrome
Upon clinical presentation, CT is often the diagnostic tool of choice for
ruling out alternative potentially life-threatening differential diagnoses Recommendations Classa Levelb
of ACS, like PE or aortic dissection (this should be an ECG-gated con­
Emergency TTE is recommended in patients with
trast CT angiogram with full coverage of the thoracic aorta and the
suspected ACS presenting with cardiogenic shock or I C
proximal head and neck vessels). Generally, CT does not have a role
suspected mechanical complications.
in patients presenting with suspicion of ongoing acute coronary occlu­
sion, for whom emergency ICA is the priority. In patients with suspected ACS, non-elevated (or
Coronary CT angiography (CCTA) has been investigated in many trials uncertain) hs-cTn levels, no ECG changes and no
for the assessment of patients presenting to the ED with suspected recurrence of pain, incorporating CCTA or a IIa A
NSTE-ACS. However, trials investigating CCTA in the era of hs-cTn as­ non-invasive stress imaging test as part of the initial
says may be of greater relevance for contemporary practice. The workup should be considered.116,122–127
BEACON (Better Evaluation of Acute Chest Pain with Coronary Emergency TTE should be considered at triage in
Computed Tomography Angiography) study showed no reduction of in- cases of diagnostic uncertainty but this should not
hospital duration of stay or hospital admission in the CCTA arm com­ result in delays in transfer to the cardiac IIa C
pared with patients investigated with hs-cTn, with similar results to those catheterization laboratory if there is suspicion of an
observed in the ROMICAT II (Rule Out Myocardial Ischemia/Infarction by
© ESC 2023

acute coronary artery occlusion.

Computer Assisted Tomography) and RAPID-CTCA (Rapid Assessment Routine, early CCTA in patients with suspected ACS
of Potential Ischaemic Heart Disease with CTCA) trials.115–117 In the lat­ is not recommended.117
III B
ter study, a default approach using early non-invasive CCTA in patients
with suspected NSTE-ACS did not improve clinical outcomes at 1 year ACS, acute coronary syndrome; CCTA, coronary computed tomography angiography;
ECG, electrocardiogram; hs-cTn, high-sensitivity cardiac troponin; TTE, transthoracic
and was associated with a modest increase in the duration and cost of
echocardiography.
the hospital stay. A default approach using CCTA as the first-line imaging a
Class of recommendation.
investigation in patients with suspected NSTE-ACS is therefore not b
Level of evidence.
ESC Guidelines 3743

Cardiac magnetic resonance can also assess myocardial perfusion 4.1.1. Time to treatment
with pharmacological stress. This can be used as an alternative to Time to treatment is vital for the care of patients triaged to the STEMI
CCTA in the assessment of patients in the observe zone following pathway. Components of the total ischaemic time, contributors to delays
ECG and hs-cTn assessments, particularly in those with advanced, es­ in initial management, and the selection of reperfusion strategy for STEMI
tablished CAD, in whom assessments of myocardial perfusion and via­ patients are shown in Figure 7. Treatment times reflect the efficiency and
bility may provide more useful information than CCTA. Some quality of care of a system taking care of patients with suspected STEMI.
additional information on CMR, single-photon emission computerized The multidisciplinary STEMI treatment pathway should be subject to
tomography (SPECT) perfusion imaging and stress echocardiography continuous clinical audit in order to assess the treatment times for indi­
is provided in the Supplementary data online. vidual patients and identify opportunities for healthcare improvement
Depending on local expertise and availability, other forms of stress through quality indicators (QIs). If projected QIs are not met, interven­
imaging (e.g. SPECT, nuclear, stress echo) can be used to assess patients tions are needed to improve the performance of the system.
in the observe zone. Recognition of ischaemic symptoms by individuals in the community

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has pivotal importance in activation of the out-of-hospital pathway, and
3.5. Differential diagnosis for acute chest this is especially relevant to first responders without healthcare training.
The recommended action should be to contact the EMS rather than to
pain
self-present to an ED or primary care clinician.
Several cardiac and non-cardiac conditions that may mimic ACS should
The time from symptom onset to ‘first call for help’ is associated with
be considered in the differential diagnosis of acute chest pain as part of
socioeconomic factors and sex.128 In order to avoid delays through fail­
the clinical assessment. More information about the differential diagno­
ure to recognize and act on symptoms of a ‘heart attack’, community
sis of acute chest pain is provided in the sections on MINOCA and Type
education initiatives should target less well-served groups (i.e. those
2 MI and in the Supplementary data online, Table S5.
from deprived communities, ethnic minority groups) and use targeted
public health messaging (i.e. avoiding stereotyped messaging that under­
pins a negative bias based on sex, ethnicity, or social background, and
4. Initial measures for patients using language and images that will resonate with those groups).
presenting with suspected acute System delays are representative of the quality of care and it is recom­
coronary syndrome | Initial mended to measure these as QIs.

treatment 4.1.2. Healthcare systems and system delays

4.1. Pre-hospital logistics of care For patients with suspected STEMI, the system delay (the time from
when the patient contacts the healthcare system to reperfusion) is
Individuals experiencing acute chest pain in the community represent
amenable to improvement by organizational measures, whereas patient
an undifferentiated population, often presenting ad hoc to first med­
delay is multifactorial. System delay is a predictor of mortality in STEMI
ical responders in the pre-hospital setting. These patients should
patients treated with primary PCI (PPCI).129–131 When a working diag­
undergo immediate risk assessment and triage following local proto­
nosis of STEMI is made in the pre-hospital setting (EMS), immediate ac­
cols established within the emergency medical service (EMS)
tivation of the catheterization laboratory team reduces treatment
(Figures 7 and 8).
delays and mortality.132–136
If the first responding medical professional suspects ACS, a 12-lead
When a STEMI working diagnosis is made by the EMS in the pre-
ECG should be acquired and analysed as soon as possible. It is recom­
hospital setting and the patient is triaged for emergency invasive manage­
mended that all medical and paramedical personnel caring for ACS pa­
ment, they should bypass the ED and go straight to the catheterization
tients within the EMS setting have access to defibrillation equipment
laboratory. Bypassing the ED is associated with a significant saving in the
and are trained in basic cardiac life support. Patients with suspected
time from FMC to wire crossing and may be associated with improved
ACS are initially categorized on the basis of the 12-lead ECG and
survival.137–139 For patients presenting to a non-PCI centre with a sus­
triaged into two initial treatment pathways: (i) one for patients with
pected STEMI, the ‘door-in to door-out time’—defined as the duration
an ECG consistent with STEMI (persistent ST-segment elevation or
between arrival of the patient at the hospital to discharge of the patient
equivalent ECG patterns) (Figure 7); and (ii) one for patients without
in an ambulance ‘en route’ to the PCI centre—is also an important clinical
ST-segment elevation or equivalent ECG patterns (suspected
performance measure, and a door-in to door-out time of ≤30 min is re­
NSTE-ACS) (Figure 8). The initial ECG-guided risk stratification should
commended to expedite reperfusion therapy.140
also trigger treatment decisions in the pre-hospital setting, including the
choice of target hospital, and serve to determine the sequence of initial
investigations and interventions (including pharmacological), in particu­ 4.1.3. Emergency medical services
lar, the timing of ICA. At a national level, an EMS with an easily recalled and well-publicised un­
An initial diagnosis of suspected STEMI portends a higher risk of im­ ique medical dispatching number (112 for most European Union coun­
mediate, life-threatening complications (e.g. ventricular fibrillation tries) is important to speed-up system activation. Parallel circuits
[VF]). Accordingly, there is an indication for initiating an emergency re­ for the referral and transport of patients with suspected STEMI that by­
perfusion strategy and direct transfer to a centre with 24/7 PCI capabil­ pass the EMS should be avoided. The ambulance system plays a critical
ities. Patients who present with an ECG without ST-segment elevation role in the early management of patients with suspected STEMI, including
(or equivalent ECG patterns) but have ongoing ischaemic symptoms immediately establishing the initial diagnosis, triage, and treatment.129,141
should undergo pre-hospital triage in accordance with protocols for pa­ Ambulances in the EMS must be equipped with ECG recorders, de­
tients in the STEMI pathway, since they also face immediate risks, in­ fibrillators, telemetry devices, and at least one person trained in ad­
cluding ventricular arrhythmias. vanced life support. The quality of the care provided depends on the