Acute coronary syndrome

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Diagnostic approach

• ABCDE approach
• 12-lead ECG
• Focused clinical evaluation
• Troponin
• BMP
• CBC
• BNP or NT-pro BNP
• Coagulation panel
• HEART score for patients with NSTE-ACS
• GRACE score
• TIMI score for NSTE-ACS

Diagnostic criteria

• STEMI: ST elevations in two contiguous leads on ECG and elevated troponin
• NSTEMI: no ST elevations on ECG (may have ST depressions or nonspecific changes) and elevated troponin
• Unstable angina: no ST elevations on ECG (may have ST depressions or nonspecific changes) and normal troponin

Initial management

• Aspirin
• Anticoagulation (e.g., UFH)
• Sublingual nitroglycerin for chest pain relief
• Pulse oximetry
• Supplemental oxygen to maintain oxygen saturation ≥ 90%
• Cardiology consult
• Discuss timing of P2Y12 inhibitor loading with cardiology.
• Continuous telemetry
• STEMI management: reperfusion therapy (emergency revascularization or fibrinolysis if > 120 minutes away from a PCI-capable facility)
• NSTEMI management: Timing of invasive evaluation is based on risk of death or recurrent ischemia.

Acute coronary syndrome (ACS) is a group of conditions caused by acute myocardial ischemia, including unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). It is caused by partial or complete occlusion of a coronary artery, leading to reduced blood flow to the myocardium. The classic presentation is acute retrosternal chest pain, often described as a dull pressure or tightness, which may be accompanied by shortness of breath, sweating, and nausea. Initial diagnosis involves a 12-lead ECG and measurement of cardiac troponin (cTn) levels. Based on ECG findings, ACS is categorized as ST-elevation ACS (STE-ACS) or non-ST-elevation ACS (NSTE-ACS). NSTE-ACS is further categorized as NSTEMI if serum cTn levels are elevated, or unstable angina if cTn levels are not elevated. Initial management for all patients includes antiplatelet therapy (e.g., aspirin), anticoagulation, and analgesia. Patients with STEMI require immediate revascularization, preferably with percutaneous coronary intervention (PCI), while the timing of invasive management for NSTE-ACS is based on risk stratification. Adjunctive medical therapy includes statins, beta blockers, and RAAS inhibitors.

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

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

MI is differentiated from unstable angina by the presence of elevated troponins, while the type of MI (NSTEMI vs. STEMI) is determined by ECG findings.

• Classic presentation ; ^[5][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. ^[7]
    • 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 possible findings
  • Tachycardia, arrhythmias
  • Symptoms of heart failure (e.g., orthopnea, pulmonary edema) or cardiogenic shock (e.g., hypotension, tachycardia, cold extremities)
  • New heart murmur on auscultation (e.g., new S₄)
  • Features commonly seen in older adults, individuals with diabetes, and women, e.g.:
    • Stabbing, sharp chest pain
    • No or minimal chest pain
    • Autonomic symptoms (e.g., nausea, diaphoresis)
  • See also “Anginal equivalents.”
• Features of inferior wall infarction
  • Epigastric pain
  • Bradycardia
  • Clinical triad in right ventricular infarction: hypotension, elevated jugular venous pressure, clear lung fields

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

See “Management of chest pain” for an approach to patients with undifferentiated chest pain.

Approach ^[3][7]

• ABCDE approach
• Perform a 12-lead ECG within the first 10 minutes of care.
• IV access
• Obtain high-sensitivity cardiac troponin.
• Continuous telemetry and pulse oximetry
• Supplemental oxygen to maintain SpO2 ≥ 90%
• Aspirin if there are no contraindications
• Consider analgesics for cardiac chest pain as needed.
• Repeat testing if the initial ECG and/or cardiac troponin are nondiagnostic.
• Obtain additional laboratory studies (e.g., BMP, CBC) to guide management decisions.
• Assess risk using a risk stratification tool (e.g., GRACE score).
• Manage tachyarrhythmias and treat acute heart failure, cardiogenic shock, and/or complete heart block as needed.

Obtain an ECG immediately if ACS is a potential diagnosis.

Any patient with ST elevations on ECG requires immediate evaluation for urgent revascularization. Further diagnostic evaluation should not delay care.

A normal ECG or nonspecific ECG changes do not rule out NSTE-ACS. ^[3]

Initial triage based on ECG findings ^[3][7]

Follow local rapid diagnostic protocols and tailor the workup and management to individual risk stratification for ACS.

• ST elevations: immediate revascularization in STEMI, preferably PCI
• No ST elevations: See "Decision pathway for possible NSTE-ACS."
  • ST depressions, new T-wave inversions, and/or high clinical suspicion for ACS: NSTE-ACS is likely; begin management of ACS.
  • Both nondiagnostic ECG and low or intermediate clinical suspicion for ACS
    • Serial ECGs
    • hs-cTn 1–2 hours after initial high-sensitivity test or 3–6 hours after initial conventional test ^[3]

Perform immediate cardiac catheterization (< 2 hours) in patients with NSTE-ACS and cardiogenic shock, electrical or hemodynamic instability, and/or refractory angina. ^[2][3]

Decision pathway for possible NSTE-ACS ^[3][7]

• Management based on troponin levels
  • Interpret both the initial troponin value and the change between first and interval values (Δtrop).
  • Detectable initial troponin and significant Δtrop : Start ACS management. ^[8]
  • Initial troponin above ULN and high clinical suspicion: Consider starting empiric ACS management before the second troponin.
    • Confirm diagnosis with Δtrop.
    • Consult cardiology if uncertain.
  • Undetectable hs-cTn ≥ 3 hours after symptom onset and low clinical suspicion: NSTEMI can usually be ruled out. ^[7][9]
• Inconclusive serial ECG and hs-cTn
  • Interpret results based on the patient's overall ACS risk.
  • Follow local protocols, use clinical judgment, and consult cardiology as needed. ^[7]
• MI is ruled out or remains uncertain
  • Evaluate the likelihood of unstable angina.
  • Consider additional investigations (e.g., third troponin, cardiac stress testing, CCTA).
  • Evaluate alternative causes of chest pain and differential diagnoses of elevated troponin.
  • See "Negative initial workup of ACS" for details.

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

ECG findings in ACS ^[3][8]

ECG findings change over time. Look for STEMI-equivalent ECG findings and repeat ECGs if inconclusive.

ECG changes in STEMI ^[3]

• New (or presumed new) ST-segment elevations
• ≥ 1 mm in ≥ 2 anatomically contiguous leads (other than leads V₂–V₃)
• Leads V₂–V₃
  • Men aged ≥ 40 years: ≥ 2 mm
  • Men aged < 40 years: ≥ 2.5 mm
  • Women: ≥ 1.5 mm
• Inferior myocardial infarction with right ventricular involvement may exhibit: ^[8]
  • ST elevations ≥ 1 mm in leads aVR and/or V₁
  • ST elevations ≥ 0.5 mm (or ≥ 1 mm in men aged < 30 years) in leads V₃R and V₄R

The sequence of ECG changes in ACS 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 ^[3][8]

• Posterior myocardial infarction ^[3]
  • ST depressions ≥ 0.5 mm in leads V₁–V₃
  • ST elevations ≥ 0.5 mm in leads V₇–V₉ ^[8]
• Left main coronary artery occlusion or three-vessel coronary artery disease
  • ST depressions ≥ 1 mm in ≥ 6 leads ^[10][11]
  • Combined with ST elevation in V₁ and/or aVR ST-segment elevation
• LBBB or RBBB with strong clinical suspicion for myocardial infarction ^[12]
  • New or presumed new LBBB in the absence of symptoms is not a STEMI equivalent.
  • Consider diagnostic criteria (e.g., modified Sgarbossa criteria) to evaluate the likelihood of STEMI.
• de Winter T wave: precordial J-point depression with tall, symmetrical T waves ^[13][14]
• Hyperacute T waves: can be present without ST elevations in the very early stages of ischemia.

Obtain a V₇–V₉ lead tracing if ST depressions are present in V₁–V₃, as this may be a sign of a posterior wall STEMI.

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

ECG changes in NSTE-ACS ^[3][8]

• No persistent ST elevations
• Nonspecific signs of ischemia may be present, including:
  • New (or presumed new) ST-segment depressions
    • ≥ 0.5 mm in ≥ 2 anatomically contiguous leads
    • Typically horizontal or down-sloping
  • T-wave inversions of > 1 mm in V₁–V₆ with any of the following:
    • Prominent R wave
    • R/S ratio > 1
    • Transient ST-segment elevation
• Wellens syndrome after resolution of ischemia ^[15]
  • Biphasic or markedly inverted T waves in leads V₂–V₃ (sometimes extending to lead V₆)
  • Absence of Q waves

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

Laboratory studies ^[3]

Cardiac troponin ^[3]

Acute myocardial infarction is characterized by the rise and/or fall of cardiac troponin on repeat testing with at least one elevated value.

• > 99^thpercentile ULN: myocardial injury (i.e., NSTEMI or STEMI) ^[8]
• No detectable elevation (with ECG features of ACS): unstable angina
• Testing intervals
  • 1–2 hours after initial high-sensitivity test
  • 3–6 hours after initial conventional test
  • At symptom recurrence (if suspicion for ACS remains high) and/or appearance of new ECG changes ^[16]
  • Consider at 72 hours as a marker of infarct size. ^[17]
• Other cardiac biomarkers (e.g., CK-MB, myoglobin): not recommended unless cardiac troponin is unavailable ^[8]

In patients with a normal ECG, a single high-sensitivity troponin result below the limit of detection ≥ 3 hours after symptom onset is considered sufficient to rule out myocardial infarction. ^[7]

Additional studies

Obtain the following studies for risk stratification and to help guide management decisions.

• BMP: e.g., to check renal function for GRACE score and anticoagulation dosing ^[2]
• CBC: to assess for anemia requiring blood transfusion
• BNP or NT-proBNP: to assess for heart failure
• Coagulation panel: for anticoagulation management and assessment of bleeding risk
• Lipid panel

Imaging ^[3]

• Indication: suspected or confirmed ACS
• Timing: prior to hospital discharge
• Preferred modality: transthoracic echocardiography (TTE)
• Alternatives
  • Cardiac MRI (if TTE is nondiagnostic)
  • Myocardial perfusion imaging
• Possible findings
  • Wall motion abnormalities
  • Decreased LV function
  • Signs of different conditions that cause chest pain (see “Differential diagnoses of chest pain”)
  • Mechanical complications of ACS (e.g., papillary muscle rupture)
  • LV thrombus

Urgent TTE is indicated for patients presenting with hemodynamic instability, cardiogenic shock, or suspected mechanical complications of ACS.

Do not delay treatment of ACS for imaging.

Risk stratification tools ^[3]

• In patients with NSTE-ACS, multiple scoring systems are used to:
  • Help identify high-risk vs. low-risk patients
  • Guide timing of PCI and disposition
  • Guide further diagnostic studies
• In patients with STEMI , these tools may be used to calculate mortality risk but are not used to determine management.

Risk stratification tools are not a substitute for clinical judgment.

GRACE score for risk of mortality in ACS ^[3][18][19]

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

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

• 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.
• Criteria
  • Age ≥ 65 years
  • Coronary artery disease (CAD) risk factors (e.g., family history of CAD, diabetes mellitus, smoking, hypertension, hypercholesterolemia)
  • Known CAD (stenosis > 50%)
  • Episodes of severe angina in the last 24 hours
  • Aspirin use in the past 7 days
  • ST deviation
  • Elevated cardiac biomarkers

HEART score ^[21][22]

• The HEART score is an acronym of its components:
  • History
  • ECG
  • Age
  • Risk factors
  • 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

Approach ^[2][3]

• Consult cardiology; decisions regarding revascularization for ACS are ideally made by a multidisciplinary heart team.
• Continue or initiate continuous telemetry, serial ECGs, and serial troponins (frequency and duration are determined by cardiac risk).
• Supplement oxygen as needed to maintain saturation ≥ 90%. ^[3]
• Provide pharmacological treatment for ACS.
  • Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor
  • Parenteral anticoagulation (with, e.g., UFH)
  • Analgesia as needed to relieve cardiac chest pain
  • Statin therapy, beta blocker therapy, and RAAS inhibitor therapy
• Consider a liberal transfusion strategy for patients with anemia (i.e., target hemoglobin ≥ 10 g/dL). ^[3]
• Consider checking cardiac troponin 3–6 hours after PCI to assess for cardiac procedural myocardial injury. ^[8]
• See “Management of cardiogenic shock,” e.g., for patients with inferior myocardial infarction causing severe RV dysfunction.

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.

Coronary revascularization ^[2][3]

See "Revascularization in STEMI" and "Revascularization in NSTE-ACS" for details.

• Coronary angiography with PCI; , i.e., balloon dilation with stent implantation, is the preferred revascularization strategy in ACS. ^[2][3]
  • Primary PCI: PCI that is not preceded by fibrinolysis
  • PCI after thrombolysis: PCI performed after fibrinolysis for STEMI
• Coronary artery bypass grafting (CABG) may be indicated in selected cases, e.g.: ^[2][3]
  • Large area of myocardium at risk, cardiogenic shock, or hemodynamic instability alongside either of the following:
    • Coronary anatomy poorly suited to PCI
    • Unsuccessful PCI
  • Mechanical complications (e.g., papillary muscle rupture, ventricular septal rupture) requiring surgery
• Fibrinolytic therapy is used for patients with STEMI if timely access to PCI is not available.

See "Prevention of recurrent myocardial infarction" for long-term management.

Antiplatelet therapy ^[2][3]

• DAPT with aspirin and a P2Y12 inhibitor reduces the risk of major adverse cardiac events after acute myocardial infarction.
• Timing of aspirin: at presentation
• Timing of P2Y12 inhibitor therapy ^[23]
  • Recommended after assessment of coronary anatomy (i.e., during cardiac catheterization) for most patients with NSTE-ACS
  • If delayed (> 24 hours from presentation) cardiac cathetherization is planned, consider pretreatment with P2Y12 inhibitor in consultation with cardiology.
  • There is insufficient evidence on pretreatment in patients with STEMI; follow local protocols.
• See "Prevention of recurrent myocardial infarction" for more information on the duration of DAPT after acute management.
• See "Perioperative management of antiplatelet therapy in patients undergoing CABG" for more information on this patient group.

Do not administer prasugrel to patients who have had a TIA or stroke. ^[3]

Pretreatment with P2Y12 inhibitor therapy prior to cardiac catheterization is not recommended for most patients with NSTE-ACS due to the increased risk of bleeding, but it can be considered if cardiac catheterization is planned > 24 hours after presentation. ^[3]

IV cangrelor may be used for patients undergoing PCI who have not received a loading dose of a P2Y12 inhibitor. ^[2][3]

Anticoagulation ^[3]

• The choice and duration are determined by the diagnosis and treatment strategy.
• Duration of therapy
  • Patients undergoing PCI: Continue until revascularization (and post-PCI for bivalirudin).
  • Patients receiving fibrinolytic therapy without planned invasive strategy: Continue for the duration of the hospital stay (maximum 8 days). ^[3]
  • Patients with NSTE-ACS without planned invasive strategy: Continue for the duration of the hospital stay.

Glycoprotein IIb/IIIa inhibitors are not routinely recommended but may be administered to selected patients undergoing PCI.

Fondaparinux is contraindicated in patients undergoing PCI because of the risk of catheter thrombosis. ^[3]

Analgesics for cardiac chest pain ^[3]

• Nitrates
  • Sublingual nitroglycerin for hemodynamically stable patients with SBP ≥ 90 mm Hg ^[3]
  • IV nitroglycerin ^[3]
    • Use for pain refractory to sublingual nitroglycerin and/or ACS with hypertension or pulmonary edema.
    • Avoid in patients with suspected RV infarction; , SBP < 90 mm Hg, or ↓ SBP > 30 mm Hg below baseline. ^[3]
  • Avoid nitrates in patients who have recently taken a PDE5 inhibitor (e.g., within 24 hours for sildenafil; , or 48 hours for tadalafil). ^[3]
• Opioids: for pain resistant to maximally tolerated nitroglycerin
  • Morphine ^[3]
  • Fentanyl ^[3]

Patients with cardiac chest pain that is not relieved with nitrates should receive rapid coronary revascularization. Opioids may improve chest pain symptoms but do not preclude the need for revascularization. ^[3]

NSAIDs should not be used in patients with suspected or confirmed ACS because they are associated with an increased risk of MACE. ^[3]

Lipid-lowering therapy ^[3]

These recommendations apply to patients diagnosed with ACS within the last 12 months.

• All patients: high-intensity statin therapy
• Add a nonstatin lipid-lowering agent (e.g., ezetimibe, PCSK9 inhibitor, bempedoic acid) for patients with :
  • LDL-C ≥ 70 mg/dL and already on a high-intensity statin
  • Statin intolerance
• Consider adding a nonstatin lipid-lowering agent for patients already on a high-intensity statin with LDL-C ≥ 55 mg/dL.
• See “Lipid-lowering therapy for ASCVD” for agents and dosages.

Beta-blocker therapy ^[3]

• Initiate low-dose oral beta-blocker therapy; within 24 hours of presentation, unless there are contraindications to beta blockers.
• Titrate as tolerated by heart rate and blood pressure.
• Avoid or discontinue in patients with heart failure symptoms or cardiogenic shock.

RAAS inhibitor therapy ^[3]

• Initiate ACEi or ARB for patients with high-risk features, i.e. :
  • LVEF ≤ 40%
  • Hypertension
  • Diabetes
  • Anterior STEMI
• Initiate mineralocorticoid receptor antagonist therapy (i.e., eplerenone) for patients with LVEF ≤ 40% who also have diabetes mellitus and/or symptoms of heart failure.

Other adjunctive therapy ^[3]

• Low-dose colchicine: Consider to reduce the risk of MACE.
• SGLT-2 inhibitors and GLP-1 receptor agonists: Initiate or continue in patients with indications (e.g., diabetes, heart failure); ACS alone is not an indication.

Approach ^[2][3][24]

• Identify patients with STEMI as soon as possible for immediate revascularization. ^[3]
• Immediate cardiology consult (code STEMI)
• Continuous telemetry
• Treatment of choice: primary PCI within 90 minutes of first medical contact ^[3]
• Consider intravenous fibrinolytic therapy in STEMI in patients with both of the following:
  • PCI cannot be performed within 120 minutes (i.e., in patients who require hospital transfer for PCI) ^[3]
  • No contraindications to fibrinolytics for STEMI
• Start pharmacological treatment for ACS.
  • Planned PCI
    • DAPT with aspirin and P2Y12 inhibitor (e.g., prasugrel or ticagrelor); follow local protocols regarding timing of P2Y12 inhibitor administration.
    • Anticoagulation with UFH
  • Planned fibrinolytic therapy
    • DAPT with aspirin and clopidogrel
    • Anticoagulation with LMWH (e.g., enoxaparin)
• Serial troponin levels and ECGs to monitor for cardiac procedural myocardial injury

"Time is muscle": Revascularization should be performed immediately in patients with STEMI. All other interventions can wait.

Percutaneous coronary intervention ^[2][3]

• Indications
  • Onset of ischemic symptoms < 12 hours prior to first medical contact
  • Cardiogenic shock or hemodynamic instability (regardless of symptom duration)
  • Patients who have received fibrinolytic therapy
  • May be considered in stable patients 12–24 hours after symptom onset
• Contraindication: stable patients (e.g., no ongoing ischemia, acute severe heart failure, or life-threatening arrhythmia) with occluded artery > 24 hours after onset of symptoms

Fibrinolytic therapy in STEMI ^[3]

• Indications (all of the following must apply)
  • PCI cannot be performed within 120 minutes of first medical contact.
  • Symptom onset: < 12 hours or ≥ 12 hours with hemodynamic instability or large infarct size
  • No contraindications to fibrinolysis in STEMI
• Timing: within 30 minutes of first medical contact ^[3]
• Contraindications: See “Contraindications for fibrinolysis in STEMI and STEMI equivalents.”
• Regimens (one of the following)
  • Tenecteplase ^[3]
  • Alteplase ^[3]
  • Reteplase
  • Streptokinase
• Postfibrinolysis: Evaluate for evidence of reperfusion (i.e., resolution of chest pain and ST-elevations) and transfer to a PCI-capable facility.

Transfer to a PCI-capable facility after fibronolytic therapy. ^[3][24]

Approach ^[2][3]

• Management of NSTE-ACS is determined by the patient's risk of mortality and recurrent ischemic events.
• Hemodynamically or electrically unstable patients and those with intractable angina require an immediate invasive approach (i.e., cardiac catheterization).
• Calculate the GRACE score and/or TIMI score for NSTE-ACS for all patients, to help guide the timing of cardiac catheterization. ^[2]
• Start pharmacological treatment for ACS, including:
  • DAPT with ASA and P2Y12 inhibitor (e.g., ticagrelor); P2Y12 inhibitor is not generally recommended prior to cardiac catheterization.
  • Anticoagulation
    • UFH if cardiac catheterization is planned
    • LMWH if initial noninvasive approach is planned
• Perform noninvasive cardiac stress testing or coronary CTA for clinically stable patients at low risk of MACE.
• Duration of telemetry and length of stay are determined by ongoing cardiac risk.

Fibrinolytic therapy is not indicated in patients with NSTE-ACS.

Invasive strategy for NSTE-ACS

In the management of NSTE-ACS, an invasive approach involves cardiac catheterization with the intention of proceeding with revascularization (e.g., PCI or CABG) if significant blockages are found. Patient risk stratification guides the timing of cardiac catheterization (i.e., immediate, early, or delayed).

See “Differential diagnoses of chest pain.”

Differential diagnoses of increased troponin ^[8][27]

• 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
  • Ischemia with nonobstructive coronary arteries
  • Stroke
  • Wellens syndrome ^[15]
• Noncardiovascular causes
  • Renal failure
  • Critical illness (e.g., sepsis)
  • Hypothyroidism or hyperthyroidism

Differential diagnoses of ST elevations on ECG ^[28]

• Early repolarization
• LBBB
• Brugada syndrome
• Myocarditis
• Pericarditis
• Left ventricular aneurysm ^[29]
• Ischemia with nonobstructive coronary arteries (e.g., coronary artery spasm, coronary microvascular dysfunction)
• Pulmonary embolism
• Hyperkalemia
• Tricyclic antidepressant use
• Poor ECG lead placement

The differential diagnoses listed here are not exhaustive.

See also “Complications of myocardial infarction.”

Mechanical complications ^[3]

• Ventricular septal rupture (i.e., acute ventricular septal defect)
• Contained ventricular rupture (pseudoaneurysm)
• Papillary muscle rupture or infarction
• Ventricular free wall rupture

Patients with mechanical complications after acute MI should be managed in a dedicated cardiac surgery center. ^[3]

Electrical complications ^[3]

• Ventricular arrhythmias
  • Ventricular tachycardia
  • Ventricular fibrillation
• Bradyarrhythmias
  • Mobitz type II AV block
  • High-grade AV block
  • Alternating bundle branch block
  • Third-degree AV block

Other ^[3]

• Heart failure (see "Management of acute heart failure" for more details, including guidance on fluid management)
• Early infarct-associated pericarditis
• Postmyocardial infarction syndrome (Dressler syndrome)
• LV thrombus

We list the most important complications. The selection is not exhaustive.

Cardiac intensive care unit or ICU ^[3]

• Ongoing angina
• Hemodynamic instability
• Uncontrolled arrhythmias
• Suboptimal reperfusion
• Cardiogenic shock

Telemetry unit ^[3]

• Patients at low risk for cardiac arrhythmias: Monitor for up to 24 hours (or until coronary revascularization).
• Patients at intermediate or high risk of cardiac arrhythmias: Consider monitoring for > 24 hours.

Negative initial workup for ACS ^[7]

Approach

• Rule out other potential causes of chest pain, including myocardial infarction in the absence of obstructive coronary artery disease (MINOCA). ^[30]
• Use risk stratification for ACS (e.g., the HEART score) to determine the short-term risk of MACE.
• Consider the need for observation or admission for further diagnostics based on the risk of MACE.

Risk-based management ^[7]

• 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.

• Prompt primary care and cardiology follow-up
• Confirm referral to cardiac rehabilitation. ^[3]
• Screen for and treat depression and anxiety. ^[2]
• Lipid profile 4–8 weeks after discharge; adjust therapy as needed (see “Lipid management in the first 12 months post-ACS”). ^[3]
• Repeat TTE 6–12 weeks after discharge if LV function was decreased during hospitalization. ^[3]
• Ensure annual influenza vaccination. ^[3]
• Perform a medication reconciliation and reinforce adherence. ^[3]

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