Acute coronary syndromes

| Resident
Survival
Guide

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Acute Coronary Syndrome Chapters

Heart Attack Patient Information

Unstable Angina Patient Information

Overview

Classification

Unstable Angina
Non-ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction

Causes

Differential Diagnosis

Treatment

AHA/ACC Guidelines for Acute Coronary Syndrome

Guideline for Risk Stratification in ACS

Guideline for Pre-Hospital Evaluation and Care

Guidelines for Initial Management of ACS

Guidelines for Long-term management and secondary prevention

Guidelines for Patients with Atrial Fibrillation Complicating ACS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:  Mitra Chitsazan, M.D.[2] Yamuna Kondapally, M.B.B.S[3]; Tarek Nafee, M.D. [4]; Sabawoon Mirwais, M.B.B.S, M.D.[5]; James Nasr[6]

Synonyms and keywords: acute coronary syndrome, acute coronary syndromes, ST-elevation myocardial infarction, non-ST-segment elevation acute coronary syndrome, unstable angina, STEMI, NSTEMI, NSTE-ACS, myocardial infarction, chest pain, coronary thrombosis, high-sensitivity troponin, plaque rupture, plaque erosion, spontaneous coronary artery dissection, MINOCA

## Overview

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Acute coronary syndrome (ACS) refers to a spectrum of clinical conditions caused by a sudden reduction in blood supply to the myocardium, most commonly resulting from disruption of an unstable coronary artery atherosclerotic plaque with associated partial or complete coronary thrombosis. Plaque disruption may occur through plaque rupture, plaque erosion, or, less commonly, a calcified nodule with superimposed thrombus.[1][2]

ACS encompasses three related clinical entities that exist along a continuum of severity: unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).[2] Unstable angina is differentiated from NSTEMI by the absence of elevated cardiac troponin and therefore by the absence of detectable myocardial necrosis. The widespread use of high-sensitivity cardiac troponin assays has reduced the frequency of true unstable angina diagnoses because many patients previously classified as having unstable angina are now found to have small degrees of myocardial injury.[3]

The most common presenting symptom of ACS is chest pain or chest discomfort, classically described as pressure, heaviness, tightness, or squeezing. Pain may radiate to the left arm, both arms, neck, jaw, back, or epigastrium and may be associated with dyspnea, nausea, vomiting, diaphoresis, syncope, or fatigue.[2] ACS must be distinguished from stable angina, which is usually predictable, occurs with exertion or emotional stress, and improves with rest or nitroglycerin.

Each year, more than 7 million people worldwide are diagnosed with ACS, including more than 1 million hospitalized patients in the United States. Approximately 5% of patients hospitalized with ACS die before hospital discharge.[2] Approximately 14% of patients experiencing ACS in the United States do not survive the event.[4]

## Historical Perspective

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The clinical understanding of ACS evolved from the recognition that angina pectoris, unstable angina, and myocardial infarction represent related manifestations of acute myocardial ischemia. Earlier classifications separated unstable angina, NSTEMI, and STEMI primarily by symptoms, ECG findings, and cardiac enzyme patterns. The development of cardiac-specific biomarkers, particularly troponin, allowed more accurate detection of myocardial injury and reduced reliance on older biomarkers such as CK-MB.

The introduction of high-sensitivity cardiac troponin assays further refined the distinction between unstable angina and NSTEMI. Many patients previously diagnosed with unstable angina are now recognized to have small degrees of myocardial injury and are therefore classified as NSTEMI.[3] Contemporary ACS management has shifted toward early ECG interpretation, rapid reperfusion for STEMI, invasive risk-stratified management for NSTE-ACS, potent antiplatelet therapy, high-intensity lipid-lowering therapy, complete revascularization in selected patients, individualized beta-blocker use, and structured secondary prevention.[1]

## Classification

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ACS is classified based on clinical history, electrocardiogram (ECG) findings, and cardiac troponin levels.

ACS subtype  | ECG findings  | Troponin  | Pathophysiology

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Unstable angina | Normal ECG, nonspecific ST-T changes, transient ST depression, or T-wave inversion | No rise/fall above diagnostic threshold | Ischemia without detectable myocardial necrosis
NSTEMI | ST depression, T-wave inversion, transient ST elevation, or nonspecific changes; no persistent diagnostic ST elevation | Elevated with rise/fall pattern | Usually subtotal or partial coronary occlusion causing subendocardial infarction
STEMI | Persistent diagnostic ST-segment elevation in contiguous leads or equivalent pattern | Usually elevated with rise/fall pattern | Usually acute complete coronary occlusion causing transmural infarction

STEMI accounts for approximately 30% of ACS, whereas non-ST-segment elevation acute coronary syndrome (NSTE-ACS) accounts for approximately 70%.[2] The pathophysiology of ACS is dynamic, and patients may progress from one ACS phenotype to another during the same presentation.[1]

Under the Fourth Universal Definition of Myocardial Infarction, myocardial infarction caused by atherosclerotic plaque rupture, erosion, fissuring, or dissection with intraluminal thrombus is classified as type 1 myocardial infarction.[5]

## Causes

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The most common cause of ACS is disruption of an atherosclerotic plaque with superimposed thrombus formation.[1][2] Important causes and mechanisms include:

* Plaque rupture with exposure of thrombogenic necrotic core material and acute coronary thrombosis.
* Plaque erosion, in which thrombus forms over an eroded endothelial surface without frank fibrous cap rupture.
* Calcified nodule, in which protruding nodular calcification disrupts the luminal surface and promotes thrombus formation.
* Coronary artery spasm, including vasospastic or Prinzmetal angina.
* Spontaneous coronary artery dissection (SCAD).
* Coronary embolism.
* Coronary arteritis.
* Myocardial infarction with nonobstructive coronary arteries (MINOCA), which is a working diagnosis requiring evaluation for ischemic and nonischemic mechanisms. MINOCA occurs in approximately 5% to 6% of patients with myocardial infarction.[4]

Other conditions may produce myocardial oxygen supply-demand mismatch and acute myocardial injury that can mimic or accompany ACS. These include hypotension, severe anemia, severe hypertension, tachycardia, bradycardia, severe aortic stenosis, hypertrophic cardiomyopathy, sepsis, severe heart failure, pulmonary embolism, myocarditis, cardiac contusion, cardiotoxic drugs, and Takotsubo cardiomyopathy.

### Risk Factors

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Traditional risk factors for atherosclerosis and ACS include dyslipidemia, hypertension, tobacco smoking, diabetes mellitus, obesity, family history of premature coronary artery disease, advanced age, male sex, chronic kidney disease, and prior coronary artery disease.

Emerging and nontraditional risk factors include hypertensive disorders of pregnancy, air pollution, psychosocial stress, disturbed sleep, chronic inflammatory disease, and alterations in the microbiome.[6]

## Pathophysiology

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The pathophysiology of ACS centers on acute coronary plaque disruption, activation of the coagulation cascade, platelet activation, and thrombosis.[1][2]

### Plaque Rupture and Thrombosis

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Progressive lipid accumulation and inflammation within an atherosclerotic plaque lead to plaque instability. Vulnerable plaques often have thin fibrous caps, large lipid cores, inflammatory cell infiltration, and increased local proteolytic activity. Rupture exposes tissue factor-rich necrotic core material to circulating blood, promoting platelet activation, thrombin generation, and thrombus formation.

### Plaque Erosion

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Plaque erosion involves endothelial denudation over an atherosclerotic plaque without frank cap rupture. It may be more frequent in younger patients and women, and it can produce ACS through thrombus formation over an eroded intimal surface.[2]

### Myocardial Ischemia and Necrosis

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The clinical phenotype depends on the degree, duration, and territory of coronary obstruction. Persistent total occlusion is more likely to produce STEMI, whereas subtotal or transient occlusion more often produces NSTEMI or unstable angina.

## Differentiating Acute Coronary Syndrome from Other Diseases

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The differential diagnosis of ACS is broad and includes life-threatening and non-life-threatening conditions. A systematic approach is required to identify alternative diagnoses while avoiding delay in treatment of true ACS.

Category  | Conditions  | Distinguishing features

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Cardiac | Pericarditis, myocarditis, Takotsubo cardiomyopathy, aortic stenosis, hypertrophic cardiomyopathy, coronary spasm | Pleuritic/positional pain, diffuse ST elevation, viral prodrome, stress trigger, murmur, dynamic spasm
Pulmonary | Pulmonary embolism, pneumothorax, pneumonia, pleuritis | Dyspnea, hypoxemia, pleuritic pain, unilateral decreased breath sounds, fever, abnormal chest imaging
Vascular | Aortic dissection, symptomatic aortic aneurysm | Abrupt tearing pain, pulse deficit, neurologic deficit, widened mediastinum, high-risk aortic imaging features
Gastrointestinal | Esophagitis, esophageal spasm, peptic ulcer disease, pancreatitis, cholecystitis | Meal-related symptoms, epigastric tenderness, dysphagia, vomiting, elevated lipase, Murphy sign
Musculoskeletal | Costochondritis, chest trauma, rib fracture, cervical radiculopathy | Reproducible tenderness, trauma history, focal chest wall pain, pain with movement
Other | Anxiety, herpes zoster, anemia, sickle cell crisis | Panic symptoms, dermatomal rash, low hemoglobin, vaso-occlusive symptoms

Acute aortic dissection is a critical diagnosis that can mimic ACS. A normal ECG and normal troponin values do not exclude aortic dissection. An elevated D-dimer may support further evaluation in the appropriate clinical setting, but imaging is required when clinical suspicion for acute aortic syndrome is significant.[7]

## Diagnosis

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Diagnosis of ACS requires integration of symptoms, electrocardiogram, cardiac troponin, risk assessment, and clinical judgment.[1][2]

### Initial Evaluation

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Patients with suspected ACS should have immediate assessment of hemodynamic stability, airway and breathing, focused cardiovascular examination, ECG, vascular access, and targeted laboratory testing. Life-threatening mimics such as aortic dissection, pulmonary embolism, tension pneumothorax, and esophageal rupture should be considered when the clinical presentation is atypical or discordant.

### Electrocardiogram

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A 12-lead ECG should be obtained and interpreted rapidly in patients with suspected ACS. Diagnostic ST-segment elevation, posterior MI, new or presumed new left bundle branch block with ischemic features, diffuse ischemic ST depression with ST elevation in aVR, or other STEMI-equivalent patterns should prompt urgent reperfusion planning.[1]

### Cardiac Troponin

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High-sensitivity cardiac troponin assays improve early diagnosis and risk stratification. A rise and/or fall in troponin above the assay-specific 99th percentile upper reference limit supports acute myocardial injury; ischemic symptoms, ECG changes, imaging findings, or angiographic evidence are needed to classify the injury as myocardial infarction.[5]

### Initial ACS Diagnostic Algorithm

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| Suspected ACS: chest pain, dyspnea, diaphoresis, syncope, nausea, or ischemic equivalent|

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| Immediate ECG, vital signs, focused exam, aspirin if no contraindication, troponin testing, and assessment for life-threatening mimics|

| Diagnostic STEMI or STEMI-equivalent pattern?|

| Yes|

| No|

| Activate reperfusion pathway: primary PCI if available in recommended timeframe; fibrinolysis if indicated and PCI delay is excessive|

| Serial ECGs, serial high-sensitivity troponin, risk stratification, anti-ischemic therapy, antithrombotic therapy, and invasive strategy according to risk|

## Treatment

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* To view the detailed treatment of Unstable angina/NSTEMI click here.
* To view the detailed treatment of STEMI click here.

## 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for Acute Coronary Syndromes. Contemporary Updates (Please do not edit)

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The 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for acute coronary syndrome updates several areas of ACS care, including beta-blocker use after myocardial infarction, multivessel revascularization, intracoronary imaging, antithrombotic strategies, lipid-lowering therapy, cardiogenic shock management, colchicine, SGLT2 inhibitor use, and evaluation of myocardial infarction with nonobstructive coronary arteries (MINOCA).[1][8]

### Beta-Blockers After Myocardial Infarction

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Early oral beta-blocker therapy remains appropriate in selected patients with ACS in the absence of contraindications, especially in patients with hypertension, tachycardia, ongoing ischemia, reduced left ventricular systolic function, or ventricular arrhythmias.[1] However, long-term routine beta-blocker therapy after myocardial infarction is now more individualized according to left ventricular ejection fraction (LVEF), heart failure status, arrhythmia burden, recurrent angina, blood pressure, and tolerability.[1]

Clinical scenario  | Contemporary interpretation

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MI with LVEF ≤40% or clinical heart failure | Long-term beta-blocker therapy remains indicated unless contraindicated.
MI with mildly reduced LVEF, approximately 40%-49% | Individual-patient meta-analysis data suggest benefit; long-term therapy is generally favored when tolerated.[9]
MI with preserved LVEF ≥50%, no heart failure, and no other beta-blocker indication | Recent randomized data do not show clear reduction in death, recurrent MI, or heart failure hospitalization with routine long-term beta-blocker therapy.[10][11]
Stable post-MI patient without heart failure or LV systolic dysfunction who has already received beta-blocker therapy for ≥1 year | Discontinuation may be reasonable in selected stable patients when there is no other indication, based on noninferiority data.[12]

In REDUCE-AMI, 5,020 patients with acute myocardial infarction who underwent coronary angiography and had LVEF ≥50% were randomized to long-term beta-blocker therapy or no beta-blocker. At a median follow-up of 3.5 years, the primary endpoint of death from any cause or new myocardial infarction occurred in 7.9% versus 8.3%, respectively (hazard ratio 0.96; 95% CI, 0.79-1.16; P=0.64).[10] In REBOOT, beta-blocker therapy after MI without reduced EF did not reduce the composite of death, reinfarction, or heart failure hospitalization.[11] A 2026 individual-patient-data meta-analysis of randomized trials in patients with MI and LVEF ≥50% similarly found no significant reduction in death, myocardial infarction, or heart failure with beta-blocker therapy.[13]

### Multivessel Revascularization in ACS

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Complete revascularization has an expanded role in selected patients with ACS and multivessel coronary artery disease (MVD), but the timing and extent of revascularization depend on hemodynamic stability, STEMI versus NSTE-ACS presentation, lesion complexity, and cardiogenic shock status.[1]

Scenario  | 2025 ACS guideline direction

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Hemodynamically stable STEMI with MVD after successful culprit-artery PCI | PCI of significantly stenosed non-infarct-related arteries is recommended to reduce death or MI and improve angina-related quality of life.[1]
STEMI with low-complexity MVD | Same-setting multivessel PCI may be preferred over staged PCI in selected stable patients.[1]
STEMI with complex MVD involving LAD or left main territory | Elective CABG after successful culprit-artery PCI may be reasonable depending on coronary anatomy and Heart Team assessment.[1]
NSTE-ACS with MVD, no left main stenosis, and not intended for CABG | PCI of significant nonculprit lesions at the index procedure or as a staged procedure is recommended to reduce MACE.[1]
STEMI or NSTE-ACS complicated by cardiogenic shock | Routine PCI of nonculprit arteries during the index procedure should not be performed because of increased risk of death or renal failure.[1]

Important supporting trials include COMPLETE, BIOVASC, and MULTISTARS AMI. COMPLETE demonstrated that staged complete revascularization in STEMI with MVD reduced cardiovascular death or myocardial infarction at 3 years. BIOVASC supported immediate complete revascularization as noninferior to staged complete revascularization in selected patients. MULTISTARS AMI showed improved composite outcomes with immediate multivessel PCI compared with staged PCI in selected patients with STEMI and MVD.[1]

### Intravascular Imaging Guidance During PCI

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File:Coronary angiography.jpgCoronary angiography during invasive evaluation of coronary artery disease. Image available through Wikimedia Commons under a free license; verify local WikiDoc file availability before publication.

In patients with ACS undergoing coronary stent implantation in the left main artery or in complex lesions, intracoronary imaging with intravascular ultrasound (IVUS) or optical coherence tomography (OCT) is recommended for procedural guidance to reduce ischemic events.[1]

Imaging modality  | Practical role in ACS PCI  | Limitations

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IVUS | Useful for left main disease, vessel sizing, plaque burden, stent expansion, and assessment of deep vessel wall structures. | Lower image resolution than OCT.
OCT | High-resolution assessment of calcium thickness, lipid plaque, thrombus, plaque rupture, plaque erosion, stent expansion, and stent apposition. | Requires blood clearance with contrast; less useful in renal dysfunction or some ostial left main lesions.

RENOVATE-Complex PCI demonstrated lower target-vessel failure with intravascular imaging guidance compared with angiography guidance in complex coronary lesions.[14] ILUMIEN IV did not significantly reduce target-vessel failure in the overall population, but OCT guidance improved minimal stent area and reduced definite or probable stent thrombosis in high-risk patients and lesions.[15]

### Colchicine After ACS

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Low-dose colchicine may be considered for selected patients after ACS to reduce recurrent ischemic events, but evidence is mixed and the 2025 ACS guideline recommendation is cautious.[1]

Trial  | Population / timing  | Main result

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COLCOT | Post-MI patients, colchicine started within 30 days | Reduced composite cardiovascular events: 5.5% vs. 7.1%; HR 0.77; 95% CI, 0.61-0.96.[16]
CLEAR SYNERGY | Acute MI patients, colchicine started early after MI | Neutral: 9.1% vs. 9.3%; HR 0.99; 95% CI, 0.85-1.16.[17]

The clinical role of colchicine after ACS remains individualized. Benefit may be more likely when initiated after the early unstable phase in selected patients with residual inflammatory risk, whereas routine immediate initiation during acute MI is not clearly supported.[1][17][18]

### Mechanical Circulatory Support in Infarct-Related Cardiogenic Shock

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In selected patients with STEMI-related cardiogenic shock who meet DanGer Shock-like criteria, use of a microaxial flow pump may be reasonable at experienced centers, balancing survival benefit against device-related complications.[1]

In DanGer Shock, 360 patients with STEMI-related cardiogenic shock were randomized to microaxial flow pump plus standard care versus standard care alone. All-cause mortality at 180 days was 45.8% versus 58.5%, respectively (hazard ratio 0.74; 95% CI, 0.55-0.99; P=0.04), corresponding to an absolute risk reduction of 12.7%.[19]

However, microaxial pump therapy increased complications. In DanGer Shock, the composite safety endpoint of severe bleeding, limb ischemia, hemolysis, device failure, or worsening aortic regurgitation occurred in 24.0% versus 6.2% of patients.[19] Therefore, patient selection is critical. The evidence is most applicable to patients with STEMI-related cardiogenic shock without coma after cardiac arrest, without overt right ventricular failure, and treated in centers with experience using temporary mechanical circulatory support.[1][19]

| STEMI-related cardiogenic shock|

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| Immediate culprit-vessel revascularization and shock-team evaluation|

| DanGer Shock-like profile? No coma after cardiac arrest, no overt RV failure, experienced MCS center|

Yes|

| No / uncertain|

Consider microaxial flow pump plus standard care, balancing bleeding, limb ischemia, hemolysis, sepsis, and renal replacement risk|

| Standard shock care, culprit PCI, vasopressors/inotropes, selective MCS only if individualized benefit exceeds risk

### SGLT2 Inhibitors and GLP-1 Receptor Agonists After ACS

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The cardiovascular benefits of SGLT2 inhibitors and glucagon-like peptide-1 receptor agonists are well established in selected patients with stable atherosclerotic cardiovascular disease, type 2 diabetes, chronic kidney disease, heart failure, or obesity, but the early post-ACS evidence base is more limited.[1]

DAPA-MI and EMPACT-MI evaluated SGLT2 inhibitors after acute myocardial infarction in patients at risk for heart failure. Neither trial significantly reduced the primary composite of cardiovascular death or heart failure hospitalization, although EMPACT-MI showed reduction in heart failure hospitalization alone. No major new safety signals were observed.[1]

Patients with an existing indication for SGLT2 inhibitor therapy do not necessarily need to defer initiation or continuation at hospital discharge after ACS if clinically stable. SGLT2 inhibitors should be stopped before scheduled surgery, including CABG, because of risk of diabetic or euglycemic ketoacidosis: at least 3 days before surgery for canagliflozin, dapagliflozin, or empagliflozin, and at least 4 days before surgery for ertugliflozin.[1]

Semaglutide reduced major adverse cardiovascular events in patients with established stable atherosclerotic cardiovascular disease and overweight or obesity without diabetes in SELECT, but semaglutide has not been specifically tested as an early post-ACS therapy.[1][20]

### Antiplatelet Therapy, Short DAPT, and De-Escalation

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The default strategy after ACS remains dual antiplatelet therapy with aspirin and a P2Y12 receptor inhibitor for at least 12 months in patients who are not at high bleeding risk.[1] The 2025 ACS guideline also supports more individualized approaches to reduce bleeding risk in selected patients.[8]

Strategy  | Contemporary role

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Ticagrelor monotherapy after initial DAPT | In patients with ACS who tolerate DAPT with ticagrelor after PCI, transition to ticagrelor monotherapy after at least 1 month may reduce bleeding risk.[1][8]
Short DAPT followed by P2Y12 inhibitor monotherapy | Reasonable in selected PCI patients to reduce bleeding events, typically after 1-3 months depending on ischemic and bleeding risk.[1]
De-escalation from ticagrelor or prasugrel to clopidogrel | May be reasonable after the early high-risk period, often after 1 month, to reduce bleeding risk in selected patients.[1]
ACS requiring oral anticoagulation | Aspirin is generally discontinued after 1-4 weeks of triple therapy, with continuation of oral anticoagulation plus a P2Y12 inhibitor, preferably clopidogrel.[1]

### Lipid-Lowering Therapy After ACS

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High-intensity statin therapy should be initiated or continued as early as possible after ACS unless contraindicated.[1] The 2025 ACS guideline strengthens recommendations for adding nonstatin lipid-lowering therapy in selected patients.[1][8]

LDL-C / treatment scenario  | 2025 ACS update

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ACS patient already on maximally tolerated statin with LDL-C ≥70 mg/dL | Add a nonstatin lipid-lowering agent to further reduce MACE.[1]
ACS patient with LDL-C 55-69 mg/dL despite maximally tolerated statin | Adding a nonstatin lipid-lowering agent is reasonable in selected patients.[1]
Statin intolerance after ACS | Nonstatin lipid-lowering therapy is recommended.[1]
Initial ACS hospitalization | Concurrent initiation of ezetimibe with maximally tolerated statin may be considered rather than waiting for outpatient LDL-C reassessment.[1]

Nonstatin options include ezetimibe, PCSK9 inhibitor therapy such as evolocumab or alirocumab, inclisiran, and bempedoic acid, selected according to LDL-C level, expected LDL-C reduction, patient risk, cost, access, and tolerability.[1][21]

### MINOCA Evaluation and Treatment

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Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a working diagnosis rather than a final diagnosis. It occurs in approximately 5% to 6% of patients with myocardial infarction and requires evaluation for ischemic and nonischemic mechanisms.[4]

MINOCA component  | Recommended approach

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Early cardiac MRI | Cardiac MRI within approximately 7-10 days can identify myocarditis, Takotsubo cardiomyopathy, infarction, or normal myocardium and may reclassify the diagnosis.[22]
Intracoronary imaging | OCT or IVUS may identify plaque rupture, plaque erosion, calcified nodule, thrombus, or spontaneous coronary artery dissection when angiography is nondiagnostic.[22]
Vasospasm testing | Provocative testing may be considered when vasospasm is suspected and expertise is available.[22]
Treatment | Therapy should be etiology-specific: aspirin and statin for atherosclerotic MINOCA, calcium channel blockers for vasospasm, and conservative management for many cases of SCAD when stable.[22]

No completed randomized trial has established a universal MINOCA-specific medication strategy. Therefore, treatment should be directed by the identified mechanism whenever possible.[22]

| MI criteria met, but coronary angiography shows no obstructive CAD|

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| Treat as working diagnosis of MINOCA; exclude nonischemic myocardial injury and missed obstructive disease|

| Cardiac MRI within 7-10 days when feasible; consider OCT/IVUS and vasospasm testing if clinically appropriate|

| Identify mechanism: plaque disruption, spasm, SCAD, embolism, myocarditis, Takotsubo, or other cause|

| Use mechanism-specific therapy rather than universal empiric MINOCA regimen|

## 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization. Recommendations to prefer PCI or CABG (Please do not edit)

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### Patients With Complex Disease

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Recommendation  | Class  | Level of Evidence

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In patients who require revascularization for significant left main CAD with high-complexity CAD, CABG is recommended over PCI to improve survival.  | Class I | A
In patients who require revascularization for multivessel CAD with complex or diffuse CAD, such as SYNTAX score >33, CABG is reasonable over PCI to confer a survival advantage.  | Class IIa | B-R

### Patients with Diabetes

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Recommendation  | Class  | Level of Evidence

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In patients with diabetes and multivessel CAD with involvement of the LAD who are appropriate candidates for CABG, CABG with a LIMA to the LAD is recommended in preference to PCI to reduce mortality and repeat revascularizations.  | Class I | A
In patients with diabetes who have multivessel CAD amenable to PCI and an indication for revascularization but are poor candidates for surgery, PCI can be useful to reduce long-term ischemic outcomes.  | Class IIa | B-NR
In patients with diabetes who have left main stenosis and low- or intermediate-complexity CAD in the rest of the coronary anatomy, PCI may be considered an alternative to CABG to reduce major adverse cardiovascular outcomes.  | Class IIb | B-R

### Patients With Previous CABG

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Recommendation  | Class  | Level of Evidence

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In patients with previous CABG with a patent LIMA to the LAD who need repeat revascularization, if PCI is feasible, it is reasonable to choose PCI over CABG.  | Class IIa | B-NR
In patients with previous CABG and refractory angina on GDMT that is attributable to LAD disease, it is reasonable to choose CABG over PCI when an internal mammary artery can be used as a conduit to the LAD.  | Class IIa | C-LD
In patients with previous CABG and complex CAD, it may be reasonable to choose CABG over PCI when an internal mammary artery can be used as a conduit to the LAD.  | Class IIb | B-NR

## 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization. Pharmacological Strategies in Patients Undergoing Revascularization (Please do not edit)

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### Antiplatelet Therapy in Patients After PCI

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Recommendation  | Class  | Level of Evidence

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In patients undergoing PCI, a loading dose of aspirin, followed by daily aspirin, is recommended to reduce ischemic events.  | Class I | B-R
In patients with ACS undergoing PCI, a P2Y12 inhibitor should be given in addition to aspirin and continued for at least 12 months to reduce ischemic events.  | Class I | A

### Oral Anticoagulant and Antiplatelet Therapy in Patients With Atrial Fibrillation Undergoing PCI

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Recommendation  | Class  | Level of Evidence

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In patients with atrial fibrillation undergoing PCI and taking oral anticoagulant therapy, it is recommended to discontinue aspirin treatment after 1 to 4 weeks while maintaining P2Y12 inhibitor therapy in addition to oral anticoagulant therapy to reduce the risk of bleeding.  | Class I | B-R

## 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization. Revascularization Outcomes (Please do not edit)

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### Assessment of Outcomes in Patients After Revascularization

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Recommendation  | Class  | Level of Evidence

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With the goal of improving patient outcomes, it is recommended that cardiac surgery and PCI programs participate in state, regional, or national clinical data registries and receive periodic reports of their risk-adjusted outcomes as a quality assessment and improvement strategy.  | Class I | B-NR
With the goal of improving patient outcomes, it is reasonable for cardiac surgery and PCI programs to have a quality improvement program that routinely reviews institutional quality programs and outcomes, reviews individual operator outcomes, provides peer review of difficult or complicated cases, and performs random case reviews.  | Class IIa | C-LD

## Prevention

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Secondary prevention after ACS includes smoking cessation, lipid-lowering therapy, antiplatelet therapy, blood pressure control, diabetes management, cardiac rehabilitation, weight management, physical activity, vaccination where appropriate, and management of psychosocial risk factors.[1]

### Smoking Cessation

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In patients who use tobacco and have ACS or have undergone coronary revascularization, a combination of behavioral interventions plus pharmacotherapy is recommended to maximize cessation and reduce adverse cardiac events.[1]

### Cardiac Rehabilitation

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Referral to comprehensive cardiac rehabilitation is recommended after ACS, particularly after MI, PCI, CABG, or hospitalization for acute ischemia. Cardiac rehabilitation improves functional capacity, medication adherence, risk-factor control, and cardiovascular outcomes.[1]

### Psychological Interventions

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Depression, anxiety, and stress are common after ACS and are associated with worse quality of life and outcomes. Screening and referral or treatment may be reasonable when symptoms are present, and cognitive behavioral therapy, counseling, or pharmacologic therapy may improve recovery in selected patients.[1]

## Special Populations

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### Older Adults

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Older adults with ACS often have atypical symptoms, frailty, chronic kidney disease, polypharmacy, cognitive impairment, and higher bleeding risk. Management should balance ischemic benefit, bleeding risk, patient goals, frailty, and expected quality of life.[1]

### Women

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Women with ACS may have atypical symptoms, delayed presentation, higher prevalence of MINOCA, spontaneous coronary artery dissection, and coronary microvascular dysfunction. Diagnostic and therapeutic decisions should not be delayed or minimized because symptoms are atypical.[2][1]

### Chronic Kidney Disease

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Patients with chronic kidney disease have higher ischemic and bleeding risk. Contrast minimization, renal-adjusted medication dosing, and careful selection of invasive strategy are important. OCT may require additional contrast and should be used cautiously in patients at high risk of contrast-associated kidney injury.[1]

### Diabetes Mellitus

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Patients with diabetes have higher risk of recurrent ischemic events and multivessel coronary disease. High-intensity statin therapy, strict risk-factor control, and selection of revascularization strategy according to coronary anatomy are essential.[1]

## Prognosis

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Prognosis after ACS depends on age, ACS subtype, infarct size, LVEF, renal function, diabetes, cardiogenic shock, success and timing of reperfusion, completeness of revascularization, bleeding complications, adherence to secondary prevention, and participation in cardiac rehabilitation.[1][2]

STEMI with cardiogenic shock carries particularly high mortality. In selected patients matching DanGer Shock criteria, microaxial flow pump support reduced 180-day mortality but increased serious complications, emphasizing the need for experienced centers and careful patient selection.[19]

## Indications for Referral

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Referral to emergency medical services or emergency department evaluation is indicated for suspected ACS, ongoing chest pain, ischemic equivalent symptoms, syncope, hemodynamic instability, new heart failure, or concerning ECG changes.

Urgent cardiology or interventional cardiology involvement is indicated for STEMI, high-risk NSTE-ACS, refractory ischemia, hemodynamic instability, cardiogenic shock, malignant arrhythmias, mechanical complications, suspected left main disease, complex multivessel disease, or suspected MINOCA requiring advanced diagnostic evaluation.

Referral to cardiac rehabilitation is recommended after ACS hospitalization, PCI, CABG, or MI when clinically feasible.[1]

## See Also

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* Unstable angina
* Non-ST-segment elevation myocardial infarction
* ST-segment elevation myocardial infarction
* Myocardial infarction
* Coronary artery disease
* Cardiogenic shock
* Percutaneous coronary intervention
* Coronary artery bypass grafting
* Myocardial infarction with nonobstructive coronary arteries
* Cardiac rehabilitation

## References

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1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 1.43 1.44 1.45 1.46 1.47 Rao SV, O'Donoghue ML, Ruel M, et al. (2025). "2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes". J Am Coll Cardiol. 85 (22): 2135–2237. doi:10.1016/j.jacc.2024.11.009. PMID 40013746 Check `|pmid=` value (help).
2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Bhatt DL, Lopes RD, Harrington RA (2022). "Diagnosis and Treatment of Acute Coronary Syndromes: A Review". JAMA. 327 (7): 662–675. doi:10.1001/jama.2022.0358. PMID 35166796 Check `|pmid=` value (help).
3. ↑ 3.0 3.1 Braunwald E, Morrow DA (2013). "Unstable angina: is it time for a requiem?". Circulation. 127 (24): 2452–2457. doi:10.1161/CIRCULATIONAHA.113.001258. PMID 23775194.
4. ↑ 4.0 4.1 4.2 Kamran H, Jneid H, Kayani WT, et al. (2021). "Oral Antiplatelet Therapy After Acute Coronary Syndrome: A Review". JAMA. 325 (15): 1545–1555. doi:10.1001/jama.2021.0716. PMID 33683880 Check `|pmid=` value (help).
5. ↑ 5.0 5.1 Thygesen K, Alpert JS, Jaffe AS, et al. (2018). "Fourth Universal Definition of Myocardial Infarction (2018)". J Am Coll Cardiol. 72 (18): 2231–2264. doi:10.1016/j.jacc.2018.08.1038. PMID 30153967.
6. ↑ Zaman S, Wasfy JH, Kapil V, et al. (2025). "The Lancet Commission on Rethinking Coronary Artery Disease: Moving From Ischaemia to Atheroma". Lancet. 405 (10486): 1264–1312. doi:10.1016/S0140-6736(25)00055-8. PMID 40179933 Check `|pmid=` value (help).
7. ↑ Vilacosta I, San Román JA, di Bartolomeo R, et al. (2021). "Acute Aortic Syndrome Revisited: JACC State-of-the-Art Review". J Am Coll Cardiol. 78 (21): 2106–2125. doi:10.1016/j.jacc.2021.09.022. PMID 34794692 Check `|pmid=` value (help).
8. ↑ 8.0 8.1 8.2 8.3 Kumbhani DJ, Cibotti-Sun M, Moore MM (2025). "2025 Acute Coronary Syndromes Guideline-at-a-Glance". J Am Coll Cardiol. 85 (22): 2128–2134. doi:10.1016/j.jacc.2025.01.018. PMID 40108936 Check `|pmid=` value (help).
9. ↑ Rossello X, Prescott E, Kristensen A, et al. (2025). "Beta blockers after myocardial infarction with mildly reduced ejection fraction: an individual patient data meta-analysis of randomised controlled trials". Lancet. 406 (10508): 1128–1137. doi:10.1016/S0140-6736(25)01592-2. Vancouver style error: initials (help)
10. ↑ 10.0 10.1 Yndigegn T, Lindahl B, Mars K, et al. (2024). "Beta-blockers after myocardial infarction and preserved ejection fraction". N Engl J Med. 390 (15): 1372–1381. doi:10.1056/NEJMoa2401479. PMID 38587241 Check `|pmid=` value (help).
11. ↑ 11.0 11.1 Ibanez B, Latini R, Rossello X, et al. (2025). "Beta-blockers after myocardial infarction without reduced ejection fraction". N Engl J Med. 393 (19): 1889–1900. doi:10.1056/NEJMoa2504735.
12. ↑ Choi KH, Kang D, Kim W, et al. (2026). "Discontinuation of beta-blocker therapy after myocardial infarction". N Engl J Med. 394 (13): 1302–1312. doi:10.1056/NEJMoa2601005.
13. ↑ Kristensen A, Rossello X, Atar D, et al. (2026). "Beta-blockers after myocardial infarction with normal ejection fraction". N Engl J Med. 394 (6): 540–550. doi:10.1056/NEJMoa2512686. Vancouver style error: initials (help)
14. ↑ Lee JM, Choi KH, Song YB, et al. (2023). "Intravascular imaging-guided or angiography-guided complex PCI". N Engl J Med. 388 (18): 1668–1679. doi:10.1056/NEJMoa2216607. PMID 37158966 Check `|pmid=` value (help).
15. ↑ Ali ZA, Landmesser U, Maehara A, et al. (2024). "OCT-guided vs angiography-guided coronary stent implantation in complex lesions: an ILUMIEN IV substudy". J Am Coll Cardiol. 84 (4): 368–378. doi:10.1016/j.jacc.2024.04.037.
16. ↑ Tardif JC, Kouz S, Waters DD, et al. (2019). "Efficacy and safety of low-dose colchicine after myocardial infarction". N Engl J Med. 381 (26): 2497–2505. doi:10.1056/NEJMoa1912388. PMID 31733140.
17. ↑ 17.0 17.1 Jolly SS, d'Entremont MA, Lee SF, et al. (2025). "Colchicine in acute myocardial infarction". N Engl J Med. 392 (7): 633–642. doi:10.1056/NEJMoa2405922. PMID 39555823 Check `|pmid=` value (help).
18. ↑ Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK (2025). "Inflammation and cardiovascular disease: 2025 ACC Scientific Statement". J Am Coll Cardiol. doi:10.1016/j.jacc.2025.08.047.
19. ↑ 19.0 19.1 19.2 19.3 Møller JE, Engstrøm T, Jensen LO, et al. (2024). "Microaxial flow pump or standard care in infarct-related cardiogenic shock". N Engl J Med. 390 (15): 1382–1393. doi:10.1056/NEJMoa2312572. PMID 38587242 Check `|pmid=` value (help).
20. ↑ Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. (2023). "Semaglutide and cardiovascular outcomes in obesity without diabetes". N Engl J Med. 389 (24): 2221–2232. doi:10.1056/NEJMoa2307563. PMID 37952131 Check `|pmid=` value (help).
21. ↑ Blumenthal RS, Morris PB, Gaudino M, et al. (2026). "2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia". J Am Coll Cardiol. doi:10.1016/j.jacc.2025.11.016. PMID 40128129 Check `|pmid=` value (help).
22. ↑ 22.0 22.1 22.2 22.3 22.4 Tamis-Holland JE, Gulati M, Reynolds HR, et al. (2025). "Nonobstructive coronary artery disease and myocardial infarction with nonobstructive coronary arteries: a scientific statement from the American Heart Association". Circulation.

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