Acute coronary syndrome

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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.

• Acute coronary syndrome (ACS): the suspicion or confirmed presence of acute myocardial ischemia ^[2][3]
• Acute coronary syndrome may be further classified into the following categories:
  • NSTE-ACS: acute coronary syndrome manifesting without ST elevations on ECG
    • NSTEMI: positive myocardial injury biomarkers
    • Unstable angina: absence of detectable myocardial injury biomarkers
  • STE-ACS: acute coronary syndrome manifesting with ST elevations on ECG
• See “Myocardial infarction” for more definitions.

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]

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.

• Classic presentation ^[6][7]
  • Acute retrosternal chest pain
    • Typical: dull, squeezing pressure and/or tightness
    • Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium
    • Precipitated by exertion or stress
    • Symptom relief after administration of nitrates is not a diagnostic criterion for cardiac ischemia. ^[3]
    • The peak time of occurrence is usually in the morning.
    • See also “Angina.”
  • Dyspnea (especially with exertion)
  • Pallor
  • Nausea, vomiting
  • Diaphoresis, anxiety
  • Dizziness, lightheadedness, syncope
• Other findings
  • Tachycardia, arrhythmias
  • Symptoms of CHF (e.g., orthopnea, pulmonary edema) or cardiogenic shock (e.g., hypotension, tachycardia, cold extremities)
  • New heart murmur on auscultation (e.g., new S₄)
• Atypical presentations: more likely in elderly, diabetic individuals, and women ; ^[3][8]
  • Stabbing, sharp chest pain
  • No or minimal chest pain:
  • Autonomic symptoms (e.g., nausea, diaphoresis)
  • See also “Anginal equivalents.”
• More common in inferior wall infarction
  • Epigastric pain
  • Bradycardia
  • Clinical triad in right ventricular infarction: hypotension, elevated jugular venous pressure, clear lung fields ^[2]

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

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]}

• Perform a focused clinical evaluation and ABCDE survey.
• Obtain 12-lead ECG within 10 minutes of patient arrival.
• Establish IV access and obtain blood samples for laboratory studies.
• Measure cardiac troponin as soon as possible upon clinical presentation.
• Start continuous telemetry and pulse oximetry.
• Initiate supplemental O₂ for cyanosis, respiratory distress, or SpO₂ < 90%. ^[3]
• Give aspirin if there are no contraindications.
• Consider adjunct medical therapy for ACS, e.g., sublingual nitroglycerin for chest pain relief.
• If present, manage tachyarrhythmias and treat acute heart failure, cardiogenic shock, and/or complete heart block.

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

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

• ST elevations present: : Start management of STEMI with immediate revascularization therapy, preferably PCI.
• No ST elevations present
  • ST depressions, new T-wave inversions, and/or high clinical suspicion for ACS: Begin management of NSTEMI/UA.
  • ECG nondiagnostic AND low/intermediate clinical suspicion for ACS
    • Obtain serial ECGs and repeat troponin.
    • Consider further investigations based on risk stratification for ACS.
    • See “Decision pathway for possible NSTE-ACS” for details.

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.

• Dynamic ECG changes consistent with NSTE-ACS: NSTEMI and/or unstable angina likely; begin management of NSTEMI/UA while waiting for troponin.
• No dynamic ECG changes: Check troponin or high-sensitivity troponin (hscTn).
  • Diagnosis of NSTEMI requires interpretation of both:
    • The first troponin value: e.g., detectable or undetectable, above or below the upper limit of normal (ULN) ^[4]
    • AND the change between the first and interval troponin value (Δtrop): e.g., significant or insignificant ^[4]
  • Management based on cardiac biomarkers
    • First troponin is detectable PLUS Δtrop is significant: Start management for NSTEMI
    • First troponin is above the ULN PLUS clinical suspicion is significant: Consider starting empiric management of NSTEMI before second troponin. ^[10]
    • First hscTn value is undetectable ≥ 3 hours from symptom onset PLUS clinical suspicion is low: Consider ruling out NSTEMI. ^[4][11]
• Serial ECG and troponin (or hscTn) inconclusive: Use clinical judgment based on risk stratification for ACS. ^[4]
  • Evaluate the likelihood of unstable angina.
  • Consider additional investigations (e.g., 3^rd interval troponin, cardiac stress testing, CCTA).
  • Evaluate differential diagnoses of chest pain and differential diagnoses of ↑ troponin.
  • See “Negative initial workup of ACS” for the next steps.

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]

12-lead ECG ^[2][3]

• Indicated for every patient with suspected ACS (best initial test) within 10 minutes of presentation ^[3]
• Findings: should always be interpreted in the context of clinical findings and patient history
  • ECG changes in STEMI (see also “STEMI-equivalent ECG findings”)
  • ECG changes in NSTEMI/unstable angina
• If nondiagnostic, consider obtaining V₇–V₉ and/or V₃R–V₆R lead tracings (see “Localization of myocardial infarct on ECG”).
• Repeat every 15–30 minutes in the first hour (especially if the first ECG is inconclusive or symptoms recur or change in quality).
• Compare with previous ECGs (if available).

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]

• Routine studies: CBC, BMP, coagulation panel
• Troponin: all patients at arrival (see also “Cardiac biomarkers”) ^[2][3][13]
  • Repeat interval
    • Conventional assay: 3–6 hours
    • High-sensitivity troponin (hscTn): 1–3 hours
    • At symptom recurrence and/or appearance of new ECG changes
    • Consider at 72 hours as a marker of infarct size.
  • Interpretation alongside clinical findings
    • STEMI/NSTEMI: elevation > 99^thpercentile PLUS change ≥ 20% on repeat testing
    • Unstable angina: no detectable elevation
    • Detectable elevation without serial increase or decrease: Consider differential diagnoses of ↑ troponin.
    • hscTn undetectable in patients with ≥ 3 hours of symptoms: MI can be ruled out; unstable angina may still be possible depending on clinical suspicion. ^[4]

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.

• Indications include:
  • Cardiogenic shock
  • Infarct-like symptoms but inconclusive ECG findings
  • Evaluation for complications of myocardial infarction
• Findings
  • Wall motion abnormalities
  • Decreased LV function ^[2]
  • Signs of different conditions that cause chest pain (see “Differential diagnoses of chest pain”)

Do not delay treatment of ACS for imaging.

• 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:
  • Patient age
  • Vital signs
  • Cardiac and renal function
  • Cardiac arrest on presentation
  • ECG findings
  • Troponin levels

HEART score ^[16]

• The HEART score is an acronym of its components: history, ECG, age, risk factors, and troponin values.
• Risk assessment for major adverse cardiovascular events (MACE) in patients with chest pain presenting to the emergency department
  • Can be integrated into decision pathways for early discharge
  • Potentially reduces hospital admissions of low-risk patients
  • Should not be used in patients with STEMI or those who are hemodynamically unstable

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

• Estimates the risk of mortality, new or recurrent myocardial infarction, or the need for urgent revascularization in patients with NSTE-ACS
• Can help determine the therapeutic regimen and timing for revascularization.

Overview

• Identify patients with STEMI as soon as possible for immediate revascularization.
• Treatment of choice: PCI within 90 minutes of first medical contact (FMC).
• Consider intravenous fibrinolytics if:
  • PCI cannot be performed within 120 minutes
  • AND there are no contraindications to fibrinolytics for STEMI

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

ECG changes in STEMI ^{[2][8][13][23]}

• Definition: significant ST elevation in two contiguous leads
• Specific criteria: elevation measured at the J point in reference to the onset of the Q wave
  • In all leads except V₂ and V₃: ≥ 1 mm (≥ 0.1 mV)
  • In V₂ and V₃: depends on patient's sex and age
    • Men < 40 years: ≥ 2.5 mm (≥ 0.25 mV)
    • Men ≥ 40 years: ≥ 2.0 mm (≥ 0.2 mV)
    • Women of any age: ≥ 1.5 mm (≥ 0.15 mV)
  • The criteria are valid only in the absence of left ventricular hypertrophy and LBBB.
• Additional considerations
  • ECG findings may change over time (see “Timeline of ECG changes in STEMI”)
  • Hyperacute T waves can be present without ST elevations in the very early stages of ischemia.
  • If inferior myocardial infarction is suspected, investigate for signs of right ventricular involvement (see “Localization of myocardial infarct on ECG”)

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

• Acute stage: myocardial damage ongoing
  • Hyperacute T waves (peaked T wave)
  • ST elevations in two contiguous leads with reciprocal ST depressions
• Intermediate stage: myocardial necrosis present
  • Absence of R wave
  • T-wave inversions
  • Pathological Q waves
    • Duration ≥ 0.04 seconds
    • Amplitude ≥ ¼ of the R wave or ≥ 0.1 mV
    • Any Q wave in leads V1–3
• Chronic stage: permanent scarring
  • Persistent, broad, and deep Q waves
  • Often incomplete recovery of R waves
  • Permanent T-wave inversion is possible.

The sequence of ECG changes over several hours to days: hyperacute T wave → ST elevation → pathological Q wave → T-wave inversion → ST normalization → T-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).

• Posterior myocardial infarction
  • ST depression ≥ 0.5 mm in leads V₁–V₄
  • ST elevations ≥ 0.5 mm in leads V₇–V₉
• Left main-vessel occlusion or three-vessel disease
  • ST depression ≥ 1 mm in ≥ 6 leads ^[8][23]
  • Combined with ST elevation in leads aVR and/or V₁
• LBBB or RBBB with strong clinical suspicion for MI ^[8][24][25]

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:
  • Concordant ST elevation of ≥ 1 mm in any lead
  • Concordant ST depression of ≥ 1 mm in any of leads V₁–V₃
  • Discordant ST elevation ≥ 1 mm and ≥ 25% of preceding S wave

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

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]

• Patients < 120 minutes away from a PCI-capable facility
  • Immediate cardiology consult and evaluation for emergency revascularization (code STEMI)
  • Start antiplatelet therapy and anticoagulation for STEMI.
• Patients > 120 minutes away from a PCI-capable facility and symptom onset < 12 hours
  • Immediate cardiology consult (code STEMI), even if no PCI is available
  • Check for contraindications to fibrinolysis in STEMI and STEMI-equivalents.
  • If no absolute contraindications present: Administer fibrinolytic therapy for STEMI.
  • Start antiplatelet therapy and anticoagulation for STEMI.
• All patients with STEMI
  • Adjunctive medical therapy for ACS
  • Continuous telemetry, serial ECG, and serum troponins every 4–6 hours
  • ICU level of care

Immediate revascularization ^[2]

PCI for STEMI ^[2]

• Indication: : preferred method of revascularization in patients suspected of having STEMI
  • STEMI and STEMI equivalents
  • LBBB with positive modified Sgarbossa criteria
  • LBBB or RBBB with strong clinical suspicion of myocardial ischemia
• Procedure: coronary angiography with PCI; , i.e., balloon dilatation with stent implantation
  • Primary PCI: PCI that is not preceded by fibrinolysis for STEMI
  • PCI after thrombolysis: PCI performed after successful or unsuccessful fibrinolysis for STEMI
• First medical contact (FMC) to PCI time
  • Ideally ≤ 90 minutes.
  • Should not exceed 120 minutes

Fibrinolytic therapy in STEMI ^[2]

• Indications (in STEMI and STEMI equivalents, if all of the following apply):
  • PCI cannot be performed ≤ 120 minutes after FMC.
  • Symptom onset
    • ≤ 12 hours
    • OR 12–24 hours with clinical signs of ongoing ischemia (PCI is even more preferable in this context) ^[2]
  • No contraindications to fibrinolysis present
• Timing: within < 30 minutes of patient arrival at the hospital ^[2]
• Contraindications
  • If > 24 hours after symptom onset
  • See “Contraindications to fibrinolysis for STEMI.”
• Regimens (one of the following)
  • Tenecteplase
  • Alteplase
  • Reteplase
  • Streptokinase
• Postfibrinolysis: Evaluate for evidence of reperfusion (i.e., resolution of chest pain and ST-elevations) and transfer to a PCI-capable facility.

PCI is indicated even after successful thrombolysis.

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

Other

• 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]

• Timing: Initiate therapy without delaying revascularization.

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

• Immediate cardiology consult and evaluation for emergency revascularization (code STEMI)
• Transfer to cath lab for angiography.
• Start antiplatelets and anticoagulation (see “Antiplatelet therapy and anticoagulation in STEMI”).
  • Aspirin
  • ADP receptor inhibitor (can also be given at time of PCI)
  • Start anticoagulation with UFH, bivalirudin, or fondaparinux.
  • Consider glycoprotein (GP) IIb/IIIa receptor antagonist.

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

• Immediate cardiology consult (code STEMI), even if no PCI is available
• Check for contraindications to fibrinolysis (see “Contraindications for fibrinolysis in STEMI and STEMI-equivalents”).
• If no absolute contraindications present: Administer fibrinolytic (see “Fibrinolytic therapy in STEMI”).
• Start antiplatelets and anticoagulation (see “Antiplatelet therapy and anticoagulation in STEMI”).
  • Aspirin (as soon as possible)
  • ADP receptor inhibitor: clopidogrel
  • Start anticoagulation with UFH, enoxaparin, or fondaparinux.
• Postfibrinolysis: Evaluate for evidence of reperfusion (i.e., resolution of chest pain and ST-segment elevations).
• Transfer to a PCI-capable facility.

For all patients with STEMI

• Adjunctive medical therapy for ACS
  • Supplemental oxygen as needed: target SpO₂ > 90%
  • Nitroglycerin for patients with ongoing chest pain or hypertension
  • Analgesia with morphine only for patients with very strong pain.
  • High-intensity statin
  • Consider a beta blocker if there are no contraindications.
  • Consider an ACE inhibitor if there are no contraindications.
• Order continuous telemetry, serial ECG, and serum troponins every 4–6 hours.
• Consider ICU level of care

Overview

• Patients with NSTE-ACS are classified based on the presence (NSTEMI) or absence (UA) of significantly elevated cardiac troponin (cTn) levels.
• A key element of management is to assess the necessity for and timing of PCI (fibrinolytics are not indicated in NSTE-ACS).
• Hemodynamically unstable patients and those with intractable angina require immediate PCI (i.e., they are managed like STEMI patients).
• Multiple risk scores (e.g., HEART, TIMI, GRACE) can help to determine an adequate strategy but are no substitute for individual clinical judgment.
• Dual antiplatelet therapy and anticoagulation is indicated initially and the preferred regimens vary based on patient risk factors and timing of revascularization.
• Some low-risk NSTE-ACS patients can be managed conservatively.

• Findings ^[3]
  • No ST elevations present
  • Nonspecific signs of ischemia may be present, including:
    • ST depression, especially if horizontal or downsloping
    • Transient ST deviations ≥ 0.5 mm (≥ 0.05 mV) in symptomatic patients at rest
    • T-wave inversions of ≥ 2 mm (≥ 0.2 mV) in V₁–V₆
• Additional considerations
  • Normal ECG may be seen in up to 15% of patients with NSTEMI. ^[3][30]
  • Be wary of STEMI-equivalent ECG findings (e.g., signs of posterior myocardial infarction) and repeat ECGs if inconclusive.

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

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]

• Management of NSTE-ACS depends on a patient's mortality risk (e.g., TIMI score), clinical findings, and the availability of resources.
• Invasive strategy for NSTE-ACS (very high- to intermediate-risk patients): coronary angiography within 2–72 hours
• Ischemia-guided strategy for NSTE-ACS (in stable, low-risk patients): noninvasive cardiac stress testing (e.g., exercise ECG, stress echocardiography) to evaluate the need for coronary angiography

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]

• 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.

• Evaluate for very-high risk factors requiring urgent coronary angiography : If present, follow STEMI checklist. ^[3]
• Start antiplatelet therapy and anticoagulation.
  • Aspirin
  • ADP receptor inhibitor: ticagrelor or clopidogrel
  • Anticoagulation with UFH, enoxaparin, bivalirudin, or fondaparinux
• Calculate TIMI score and GRACE score.
• Cardiology consult for discussion of strategy (see “Risk-dependent timing of revascularization in NSTE-ACS”)
• Adjunctive medical therapy for ACS
  • Supplemental oxygen as needed: target SpO₂ > 90%
  • Nitroglycerin for patients with ongoing chest pain or hypertension
  • Analgesia with morphine only for patients with very strong pain
  • High-intensity statin
  • Consider beta blocker if no contraindications.
  • Consider ACE inhibitor if no contraindications.
• Order continuous telemetry, serial ECG, and serum troponins every 3–6 hours.
• Transfer to cardiac telemetry floor or (cardiac) ICU.

Monitoring

• 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]

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

• Oxygen therapy for patients with:
  • Cyanosis
  • Severe dyspnea
  • SpO₂ < 90%
• Fluid management: see “Management of acute heart failure.”
  • Intravenous fluids (e.g., normal saline)
    • Consider for inferior myocardial infarction causing RV dysfunction
    • Increasing the preload optimizes left and right ventricular filling and reduces hemodynamic instability.
  • Loop diuretic (e.g., furosemide ): consider for patients with pulmonary edema, acute heart failure

Subsequent measures

• See “Prevention of myocardial infarction.”
• See “Coronary artery bypass surgery.”

STEMI ^[2]

Provide ICU-level care to all patients.

• At PCI-capable site: Consult cardiology immediately and transfer to cath lab as soon as possible for primary PCI.
• < 120 minutes from nearest PCI-capable site: Arrange immediate interfacility transfer for primary PCI at referral center.
• > 120 minutes from nearest PCI-capable site
  • If symptom onset < 12 hours AND no contraindications to fibrinolysis for STEMI: Administer fibrinolytic prior to transfer to PCI-capable site.
  • All other patients: Transfer to PCI-capable site.

NSTEMI and unstable angina ^[3]

• Cardiology consult
• Hospital admission
  • Continuing angina, hemodynamic instability, uncontrolled arrhythmias, or large-territory MI: Admit to cardiac ICU.
  • All other patients: Admit to step down unit.
• Assess risk-dependent timing of revascularization in NSTEMI and consider the need for transfer to the nearest PCI-capable site.

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:

• Rule out other potential causes of chest pain.
• Use risk stratification for ACS (e.g., the HEART score) to determine the short-term risk of a MACE.
• Consider the need for observation or admission for further diagnostics based on the risk.

Risk-based management ^[4]

• High-risk (e.g., HEART score ≥ 7)
  • Inpatient admission
  • Obtain invasive coronary angiography during admission.
• Intermediate-risk (e.g., HEART score 4–6)
  • Noninvasive testing (i.e., cardiac stress test or coronary CT angiography) is usually required prior to discharge.
  • In patients with a recent negative workup for CAD , no further testing is indicated prior to discharge.
• Low-risk (e.g., HEART score ≤ 3)
  • No further testing is indicated prior to discharge from the ED.
  • Ensure outpatient follow-up.
  • Outpatient coronary artery calcium scoring may be considered for ASCVD risk evaluation.

See “Differential diagnoses of chest pain.”

Differential diagnoses of increased troponin ^[12]

• Cardiovascular causes
  • Myocarditis
  • Decompensated congestive heart failure
  • Pulmonary embolism
  • Cardiac arrhythmia, tachycardia
  • Aortic dissection
  • Hypertensive emergencies
  • Structural heart disease
  • Myocardial drug toxicity (e.g., doxorubicin)
  • Cardiac trauma (including iatrogenic/periprocedural)
  • Takotsubo cardiomyopathy
  • Stroke
• Noncardiovascular causes
  • Renal failure
  • Critical illness (e.g., sepsis)
  • Hypothyroidism or hyperthyroidism

Differential diagnoses of ST elevations on ECG ^[2]

• Early repolarization
• LBBB
• Brugada syndrome
• Myocarditis
• Pericarditis
• Pulmonary embolism
• Hyperkalemia
• Tricyclic antidepressant use
• Poor ECG lead placement

The differential diagnoses listed here are not exhaustive.

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