Acute coronary syndrome

Last updated: November 2, 2023

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Summarytoggle arrow icon

Acute coronary syndrome (ACS) is the clinical manifestation of myocardial infarct and commonly the default working diagnosis in patients with new-onset chest pain suspected to be of cardiac ischemic origin. Clinical findings (e.g., onset and characteristics of pain, patient history) in combination with ECG and troponin are the mainstays of diagnosis. Based on ECG findings, patients are categorized into those with ST-elevation (STE-ACS) or non-ST-elevation ACS (NSTE-ACS). Depending on serum levels of cardiac troponin (cTn), NSTE-ACS can be categorized as NSTEMI or unstable angina (UA). STE-ACS patients require immediate revascularization therapy with percutaneous coronary intervention (PCI) or fibrinolytic therapy. The timing and necessity of revascularization therapy in NSTE-ACS is determined based on multiple risk factors. All ACS patients receive dual antiplatelet therapy and initially anticoagulation. Adjunctive therapy (e.g., beta blockers, oxygen) helps reduce symptoms and can have a positive impact on mortality.

This article concerns the initial management of ACS patients. See “Myocardial infarction” for more details regarding, e.g., histopathology and long-term management.

Definitiontoggle arrow icon

Overviewtoggle arrow icon

Recommendations in this article are consistent with the 2021 American Heart Association (AHA) guidelines on chest pain, and 2013 AHA guidelines on STEMI and NSTE-ACS. [2][3][4]

Overview of acute coronary syndrome (ACS) [2][3]
Unstable angina (UA) Non-ST-segment elevation myocardial infarction (NSTEMI) ST-segment elevation myocardial infarction (STEMI)
Clinical presentation
  • Partial occlusion of coronary vessel decreased blood supply → ischemic symptoms without infarction
Cardiac troponin
  • Not elevated
  • Elevated (within 1–6 hours)
ECG findings

Subtypes of ACS cannot be differentiated based on clinical presentation alone.

Unstable angina is differentiated from MI by the presence of positive troponins, while the type of MI (NSTEMI vs. STEMI) is determined based on ECG findings.

Clinical featurestoggle arrow icon

Classically, it has been taught that STEMI manifests with more severe symptoms than NSTEMI, but this is not always the case.

Management approachtoggle arrow icon

The following applies to patients with acute chest pain and suspected ACS. See “Management of chest pain” for an approach to patients with undifferentiated chest pain.

Immediate management [2][3][4][8][9]

Obtain an ECG immediately if ACS is considered a potential diagnosis.

Initial triage based on ECG findings [2][3][4][8][9]

Evaluate patients with suspected STEMI immediately for revascularization therapy.

Decision pathway for possible NSTE-ACS [3][4][9]

For patients without ST elevations on ECG, determine the likelihood of NSTE-ACS using serial ECGs and troponin levels. Follow local rapid diagnostic protocols if available and tailor workup and management to individual risk stratification for ACS.

Unstable angina is a clinical diagnosis associated with normal troponin levels. Suggestive ECG changes can support the diagnosis but are not required to establish it.

Perform urgent PCI (< 2 hours) in patients with NSTE-ACS who have unstable hemodynamics, intractable angina, suspected posterior infarction, and/or left main-vessel occlusion (see “Risk-dependent timing of revascularization in NSTE-ACS”). [2][3][8]

Diagnosticstoggle arrow icon

12-lead ECG [2][3]

Consider serial ECGs if the initial ECG is negative or inconclusive, as ECG findings are dynamic and signs of ischemia can appear or disappear within minutes.

Obtain a V7–V9 lead tracing if ST depressions are present in V1–V4, as this may be a sign of a posterior wall STEMI.

Laboratory studies [3][4][12]

In patients with a normal ECG, a single result below the limit of detection using a high-sensitivity troponin assay ≥ 3 hours after symptom onset is considered sufficient to rule out myocardial infarction. [4]

Transthoracic echocardiography (TTE) [2][3][12][13]

TTE is generally not necessary and should not delay reperfusion therapy. However, it may be a helpful study in patients with atypical symptoms or if the diagnosis is unclear.

Do not delay treatment of ACS for imaging.

Risk stratificationtoggle arrow icon

  • Multiple scoring systems are used in patients with NSTE-ACS to:
    • Help identify high-risk vs. low-risk patients
    • Guide further diagnostic studies
    • Guide timing of PCI and disposition
  • They are not appropriate for patients with STEMI who require immediate revascularization.

Risk stratification tools are not a substitute for clinical judgment.

GRACE score for risk of mortality in ACS [3][14][15]

  • Based on the Global Registry of Acute Coronary Events (GRACE)
  • May be used to inform management and disposition (e.g., ICU admission, timing of intervention in NSTE-ACS).
  • Incorporates different criteria to estimate risk of mortality in patients with ACS, including:

HEART score [16]

HEART score for the risk of MACE [16]
Component Characteristic Points
History Slightly suspicious 0
Moderately suspicious 1
Highly suspicious 2
ECG Normal 0
Nonspecific repolarization changes 1
Significant ST depression 2
Age < 45 years 0
45–65 years 1
≥ 65 years 2
Risk factors None 0
1–2 1
≥ 3 or history of atherosclerotic disease 2
Troponin (initial) [17][18] normal 0
1–2 x upper limit 1
> 2 x upper limit 2


  • Score ≤ 3 (low risk): consider early discharge
  • Score 4–6 (intermediate risk): hospital admission
  • Score ≥ 7 (high risk): consider early invasive strategy
  • Any positive troponin level: usually considered non-low risk and requires further evaluation [19]

TIMI score for NSTE-ACS [3][20][21]

TIMI score for NSTE-ACS [21]
Characteristics Points
Age ≥ 65 years 1

≥ 3 CAD risk factors (e.g., family history of CAD, DM, smoking, HTN, hypercholesterolemia)

Known CAD (stenosis > 50%) 1
≥ 2 episodes of severe angina in the last 24 hours 1
ASA use in the past 7 days 1
ST deviation (≥ 0.5 mm) 1
Elevated cardiac biomarkers 1

Interpretation [22]

  • Score of 0–1 (low-risk): favors an ischemia-guided strategy [20]
  • Score ≥ 2 (non-low-risk): favors an invasive strategy [22]

STEMItoggle arrow icon


Avoid excluding a diagnosis of STEMI based on a single ECG as findings can change over time and with symptom fluctuation.

ECG changes in STEMItoggle arrow icon

ECG changes in STEMI [2][8][13][23]

Any patient with ST elevations on ECG requires immediate evaluation for urgent revascularization. The administration of other therapies should not delay care.

Classical timeline of ECG changes in STEMI

The sequence of ECG changes over several hours to days: hyperacute T waveST elevation → pathological Q waveT-wave inversionST normalizationT-wave normalization

STEMI-equivalent ECG findings [2][8][23]

Presence of any of the following findings requires immediate evaluation for revascularization therapy (i.e., management is the same as that for STEMI).

Modified Sgarbossa criteria [8][26][27]

  • A set of ECG criteria that can help identify STEMI in patients with LBBB and high clinical suspicion of ACS.
  • The criteria can also be used in right-ventricular pacing with LBBB configuration but are less specific in this scenario.
  • Acute STEMI is likely if any of the following are present:

Positive modified Sgarbossa criteria can help identify STEMI in symptomatic patients with LBBB for whom ST-segment assessment is difficult.

Managementtoggle arrow icon

The following recommendations are generally consistent with the 2013 AHA/ACC guidelines for the management of STE-ACS. [2]

"Time is muscle": Revascularization should occur as soon as possible in patients with STEMI! All other interventions can wait!

Approach [2]

Immediate revascularization [2]

PCI for STEMI [2]

Fibrinolytic therapy in STEMI [2]

PCI is indicated even after successful thrombolysis.

Common contraindications for fibrinolysis in STEMI and STEMI-equivalents [2][8][28]
Absolute contraindications
Relative contraindications

Streptokinase is nonfibrin-specific and highly antigenic. It is contraindicated within 6 months of previous exposure to streptokinase.


  • Coronary artery bypass grafting: Not routinely recommended for acute STEMI [2]
    • Consider in the following cases:
      • Coronary anatomy poorly suited to PCI
      • After unsuccessful PCI
      • STEMI occurring at the time of surgical repair of a mechanical defect

Antiplatelet therapy and anticoagulation in STEMI [2]

Dual antiplatelet therapy (DAPT) and anticoagulation in STEMI [2]
Class Regimen if undergoing PCI Regimen if undergoing fibrinolysis
Dual antiplatelet therapy (DAPT) [2]
Anticoagulation [2]

Glycoprotein IIb/IIIa inhibitor (GPI) [2]

  • Not routinely recommended

Acute management checklist for STEMItoggle arrow icon

For patients < 120 min away from a PCI-capable facility

For patients > 120 min away from a PCI-capable facility and symptom onset < 12 hours

For all patients with STEMI

NSTEMI/UAtoggle arrow icon


ECG changes in NSTEMI/UAtoggle arrow icon

To identify STEMI or STEMI-equivalent ECG findings, repeat ECGs if the initial one is inconclusive or any changes in symptoms occur.

Managementtoggle arrow icon

The following recommendations are generally consistent with the 2014 AHA/ACC guidelines for the management of NSTE-ACS. [3]

Risk-dependent timing of revascularization [3][12]

Risk-dependent timing of revascularization in NSTE-ACS [3][12]
Revascularization strategy Risk group Criteria
Urgent revascularization (< 2 hours)
  • Very high
Early invasive strategy (< 24 hours)
  • High
Delayed invasive (24–72 hours)
  • Intermediate
  • Low
  • None of the criteria above
  • GRACE score < 109
  • TIMI score 0 or 1
  • Individual decision based on patient and physician preferences

Selection of an ischemia-guided strategy via shared decision-making may be appropriate in intermediate-risk patients without serious comorbidities or contraindications. [3]

Fibrinolytic therapy is not indicated in patients with unstable angina or NSTEMI.

Antiplatelet therapy and anticoagulation in NSTE-ACS [3]

Dual antiplatelet therapy (DAPT) and anticoagulation in NSTEMI [3]
Class Regimen
Dual antiplatelet therapy (DAPT) [3]

Anticoagulation [3]

Glycoprotein IIb/IIIa inhibitor (GPI) [3]

  • Timing [3]
    • Start DAPT as soon as possible; duration depends on whether PCI is performed or not.
    • Start anticoagulation as soon as possible; continue for the duration of hospitalization or until PCI is performed.
    • GPI should only be started in high-risk patients undergoing PCI and in consultation with a cardiologist.

Acute management checklist for NSTE-ACStoggle arrow icon

Monitoring and adjunctive medical therapytoggle arrow icon


  • Continuous cardiac monitoring
  • Serial 12-lead ECG every 15–30 minutes for the first hour
  • Serial serum troponin measurement (every 1–6 hours)

Adjunct medical therapy in ACS [2][3]

Adjunct medical therapy in ACS [2][3][8][12]
Class Options Indications Contraindications and additional considerations


Beta blockers

  • Initiate within 24 hours.


ACE inhibitors/ARBs

Aldosterone antagonists [2][3][8]

High-intensity statin

Options for initial MI treatment include “MONA-BASH”: Morphine, Oxygen, Nitroglycerin, Antiplatelet drugs (aspirin + ADP receptor inhibitor), Beta blockers, ACE inhibitors, Statins, and Heparin. The scope of interventions depends on the patient's risk profile (see “Indications”).

Supportive measures

Subsequent measures

Dispositiontoggle arrow icon


Provide ICU-level care to all patients.

NSTEMI and unstable angina [3]

Negative initial workup for ACS [4]

If the initial evaluation for ACS is negative or inconclusive based on serial ECGs and cardiac troponin but clinical suspicion remains:

Risk-based management [4]

Differential diagnosestoggle arrow icon

See “Differential diagnoses of chest pain.”

Differential diagnoses of increased troponin [12]

Differential diagnoses of ST elevations on ECG [2]

The differential diagnoses listed here are not exhaustive.

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Referencestoggle arrow icon

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