Acute Coronary Syndrome (ACS)

Last updated: April 6, 2026, 6:54 PM Pacific Time (PDT)

Disease Pathway

Risk factors -> diagnostics -> diagnostic criteria -> management

Clinical Risk Factors

Who should trigger ACS reasoning?

Pressure-like, exertional, radiating, or persistent chest discomfort
Dyspnea, diaphoresis, nausea, syncope, or unexplained weakness
Known CAD, prior MI/PCI/CABG, diabetes, CKD, PAD, smoking, hypertension, dyslipidemia
Older age or atypical symptoms in higher-risk groups
Hemodynamic instability, pulmonary edema, malignant arrhythmia, or refractory symptoms

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Diagnostics

Look for ischemia and myocardial injury

Evaluation setting

Inpatient / ED Outpatient

Core labs

Serial high-sensitivity troponin
BMP
CBC
Coagulation studies

Additional labs

Lipid panel
Hemoglobin A1c

Imaging / diagnostics

12-lead ECG
Chest x-ray
Transthoracic echo

Procedures

Coronary angiography
PCI
Intravascular imaging / physiology

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Differential Diagnosis

Keep high-stakes mimics in parallel

Inpatient / ED

Aortic dissection / acute aortic syndrome
Pulmonary embolism
Pericarditis / myocarditis
Pneumothorax / pneumonia / pleurisy
Esophageal spasm / GERD / biliary pain

Outpatient

Stable angina vs noncardiac chest pain
GERD / esophageal spasm / biliary disease
Costochondritis / chest wall pain
Anxiety / panic symptoms after red flags excluded
Pulmonary embolism / pneumonia / pericarditis if symptoms suggest them

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Confirm Diagnosis

Classify the ACS phenotype

STEMI: ischemic symptoms plus ST-elevation or STEMI-equivalent ECG pattern requiring emergent reperfusion.
NSTEMI: ischemic syndrome with rise/fall in cardiac troponin above the assay threshold, without STEMI ECG pattern.
Unstable angina: ischemic symptoms without biomarker evidence of myocardial necrosis.
Type 2 MI / myocardial injury: troponin elevation from supply-demand mismatch or non-ischemic injury rather than plaque rupture.
Safety check: keep dissection, PE, myocarditis, pericarditis, and noncardiac mimics in parallel when the story does not fit.

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Management

Tailor treatment to suspected diagnosis

Suspected diagnosis

STEMI NSTEMI Unstable angina Type 2 MI / myocardial injury

Stable Angina vs ACS Spectrum

Toggle diagnosis, treatment, or prognosis rows

Feature

Stable Angina

Unstable Angina

NSTEMI

STEMI

Pathophysiology

Fixed stenosis
Demand ischemia with exertion

Active plaque
Partial occlusion or vasospasm

Active plaque with partial occlusion
Myocardial necrosis

Complete coronary occlusion
Transmural myocardial necrosis

Clinical presentation

Predictable exertional pain
Relieved by rest or nitro within 5 min

New, crescendo, or rest angina
Often >20 min

Prolonged rest pain >20 min
May have pulmonary edema or new MR murmur

Prolonged rest pain >20 min
May have pulmonary edema or new MR murmur

Troponin

Normal

Normal / negative

Elevated

Elevated
Do not wait to reperfuse if ECG diagnostic

ECG

May be normal
Ischemic changes during stress testing

ST depression >=0.5 mm
T-wave inversion, transient ST elevation, or normal ECG

ST depression >=0.5 mm or T-wave inversion >1 mm
No persistent ST elevation

ST elevation >=1 mm in >=2 contiguous leads
Higher V2-V3 thresholds, e.g. >=2 mm in men >=40 years

Coronary anatomy

CAC may be 0 or elevated
CCTA: nonobstructive or obstructive plaque
ICA if high-risk ischemia or refractory symptoms

Cath may show nonocclusive culprit plaque
May also show vasospasm or nonobstructive CAD

Cath often shows culprit stenosis or thrombus
Partial occlusion or severe plaque rupture pattern

Cath often shows acute culprit occlusion
Goal is rapid culprit-artery reperfusion

Aspirin

75-100 mg daily for secondary prevention

Load 162-325 mg chewed
Then 75-100 mg daily

Load 162-325 mg chewed
Then 75-100 mg daily

Load 162-325 mg chewed
Then 75-100 mg daily

P2Y12 inhibitor

Not routine unless prior MI or PCI

Ticagrelor preferred
Clopidogrel if unavailable
Prasugrel if PCI planned

Ticagrelor or prasugrel preferred for PCI
Ticagrelor if no invasive strategy
Clopidogrel if others unavailable

Ticagrelor or prasugrel for PPCI
Clopidogrel with fibrinolytics

DAPT duration

Not applicable unless separate PCI/MI indication

At least 12 months after ACS unless bleeding risk changes plan

At least 12 months after ACS unless bleeding risk changes plan

At least 12 months after ACS unless bleeding risk changes plan

Anticoagulation

Not acutely indicated

Parenteral anticoagulant during hospitalization
UFH, LMWH, bivalirudin, or fondaparinux

Parenteral anticoagulant during hospitalization
UFH, LMWH, bivalirudin, or fondaparinux

Parenteral anticoagulant during hospitalization
Agent depends on reperfusion strategy

Beta-blocker

First-line for symptom control

Early oral initiation within 24 hr if no contraindications

Early oral initiation within 24 hr if no contraindications

Early oral initiation within 24 hr if no contraindications

Statin

High-intensity statin for secondary prevention

High-intensity statin at presentation

High-intensity statin at presentation

High-intensity statin at presentation

Reperfusion strategy

Not applicable

Early invasive strategy if high risk
Otherwise ischemia-guided

Early invasive strategy if high risk
Otherwise ischemia-guided

Immediate reperfusion
PPCI within 120 min, or fibrinolysis if PCI unavailable

Revascularization goal

Improve symptoms and quality of life
Usually after trial of medical therapy

Reduce MACE
Prevent MI

Reduce MACE
Prevent recurrent MI

Restore perfusion
Salvage myocardium
Reduce mortality

Prognosis

~3-4% annual MI/death risk

Higher short-term risk than stable angina
Risk stratification guides management

Higher risk than unstable angina
Early invasive strategy reduces events in high-risk patients

Highest acute mortality risk
Time to reperfusion is critical

Resident Pearls

Bedside Use

Do not wait for troponin to activate reperfusion for a convincing STEMI pattern.
When NSTE-ACS is suspected, the key decision is not just diagnosis but timing of invasive evaluation.
Antithrombotic intensity should be checked against bleeding risk, renal function, planned procedures, and possible mimics.
Secondary prevention is part of the ACS treatment pathway, not an afterthought.

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