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CLINICAL STATEMENTS AND GUIDELINES

Circulation. 2025;151:e771–e862. DOI: 10.1161/CIR.0000000000001309 April 1, 2025 e779

Abbreviation Meaning/Phrase FMC first medical contact GLP-1 glucagon-like peptide-1 HF heart failure hs-cTn high-sensitivity cardiac troponin IABP intra-aortic balloon pump ICD implantable cardioverter-defibrillator IVUS intravascular ultrasound LDL low-density lipoprotein LDL-C low-density lipoprotein cholesterol LV left ventricular LVEF left ventricular ejection fraction MACE major adverse cardiovascular event MCS mechanical circulatory support MI myocardial infarction MINOCA MI with nonobstructive coronary artery disease MVD multivessel disease NSTE-ACS non–ST-segment elevation ACS NSTEMI non–ST-segment elevation myocardial infarction OCT optical coherence tomography OR odds ratio PCI percutaneous coronary intervention PCSK9 proprotein convertase subtilisin/kexin type 9 PPCI primary percutaneous coronary intervention PPI proton pump inhibitor QOL quality of life RCT randomized controlled trial ROSC return of spontaneous circulation SGLT-2 sodium-glucose cotransporter-2 STEMI ST-segment elevation myocardial infarction UFH unfractionated heparin VA-ECMO venoarterial extracorporeal membrane oxygenation

2 OVERVIEW OF ACS

2.1 Definition and Classification of ACS

ACS are typically caused by the disruption (rupture or erosion) of an unstable coronary artery atherosclerotic plaque with associated partial or complete coronary artery thrombosis and/or microemboli, resulting in diminished blood flow to the myocardium and subsequent myocardial ischemia (Figure 1).1,2 ACS includes 3 related clinical conditions that exist along a continuum of severity: (1) unstable angina, (2) non–ST-segment elevation myocardial infarction (NSTEMI), and (3) STEMI. The initial diagnosis and classification of ACS should be based on the clinical history and symptomatology, interpretation of the ECG (Table 3), and assessment of cardiac troponin (cTn). Unstable angina is defined by transient myocardial ischemia leading to diminished flow in the absence of significant myonecrosis detected by circulating troponin. In contrast, patients with more prolonged or severe myocardial ischemia are diagnosed with MI and have elevated biomarkers of myonecrosis. Patients with NSTEMI may have a partially occluded coronary artery leading to subendocardial ischemia, while those with STEMI typically have a completely occluded vessel leading to transmural myocardial ischemia and infarction (Figure 2).3,4 The pathophysiology of ACS can be dynamic and thus patients can rapidly progress from one clinical condition (eg, unstable angina, NSTEMI, STEMI) to another during the course of their presentation and initial evaluation and treatment. Other, less common causes of myocardial ischemia, among others, include coronary artery spasm, embolism, and dissection.3

This guideline will focus on the acute management of ACS, including unstable angina, NSTEMI, and STEMI, which are presumed to result from atherosclerotic plaque rupture or plaque erosion and subsequent thrombosis.4 Under the Universal Definition of MI, these MI events would be classified as type 1 MI events (Table 4).4 The diagnostic evaluation of chest pain and the management of type 2 MI, spontaneous coronary artery dissection, and MINOCA (MI with nonobstructive coronary artery disease) are covered in separate documents.5–8 A detailed description of the approach to the evaluation of patients with chest pain can be found in the 2021 AHA/ACC/ASE/ CHEST/SAEM/SCCT/SCMR Chest Pain Guideline.5 Progressive lipid accumulation and inflammation within an atherosclerotic plaque may lead to plaque instability.1 Rupture of the atherosclerotic plaque and exposure of plaque contents to the circulation may then culminate in activation of the coagulation cascade and subsequent thrombosis. The presence of thrombus may compromise flow to the myocardium, leading to myocardial ischemia and eventual myonecrosis. Since early initiation of therapy is imperative for patients with ACS, a

Figure 1. Pathobiology of a Type 1 Myocardial Infarction Due to Atherosclerotic Plaque Disruption. Progressive lipid accumulation and inflammation within an atherosclerotic plaque may lead to plaque instability. Rupture or erosion of the atherosclerotic plaque and exposure of plaque contents to the circulation may then culminate in activation of the coagulation cascade and subsequent thrombosis. When this occurs in the epicardial vessels of the coronary circulation, the presence of thrombus may compromise flow to the myocardium, leading to myocardial ischemia and eventual myonecrosis. Illustration by Patrick Lane, ScEYEnce Studios. Copyright 2025 American College of Cardiology Foundation, and American Heart Association, Inc.

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