What does acute coronary syndrome (ACS) include?

Acute Coronary Syndrome Components

Acute coronary syndrome (ACS) includes three distinct clinical entities: unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). 1

The Three Components of ACS

1. Unstable Angina (UA)

• Transient myocardial ischemia with diminished coronary flow but WITHOUT myocardial necrosis 1
• Cardiac troponin remains below the 99th percentile upper reference limit 1, 2
• Represents the mildest form on the ACS spectrum, though still life-threatening 3

2. Non-ST-Segment Elevation Myocardial Infarction (NSTEMI)

• Myocardial ischemia WITH myonecrosis (elevated cardiac troponin above 99th percentile) but WITHOUT persistent ST-segment elevation on ECG 1
• Typically results from partially occluded coronary artery causing subendocardial ischemia 1
• ECG may show ST-segment depression ≥0.5 mm, T-wave inversion >1 mm, transient ST elevation, or may be completely normal 1, 2
• Accounts for approximately 70% of all ACS cases 4

3. ST-Segment Elevation Myocardial Infarction (STEMI)

• Myocardial ischemia WITH myonecrosis (elevated troponin) AND persistent ST-segment elevation >20 minutes on ECG 1
• Results from completely occluded coronary vessel causing transmural myocardial ischemia and infarction 1
• Represents approximately 30% of ACS cases 4
• Requires immediate reperfusion therapy (primary PCI within 120 minutes or fibrinolytic therapy) 4

Underlying Pathophysiology

All three ACS entities share the same fundamental mechanism: atherosclerotic plaque disruption (rupture or erosion) with subsequent partial or complete coronary artery thrombosis, resulting in diminished myocardial blood flow. 1, 2

• Progressive lipid accumulation and inflammation destabilize the plaque, leading to rupture or erosion 2
• Exposure of plaque contents activates the coagulation cascade and platelet aggregation, forming intracoronary thrombus 2
• The degree of vessel occlusion determines the clinical presentation along the ACS spectrum 1

Critical Diagnostic Distinctions

Initial Classification Based on ECG

• Obtain 12-lead ECG within 10 minutes of presentation to distinguish STEMI from non-ST-elevation ACS (NSTE-ACS, which includes both UA and NSTEMI) 1, 4
• Persistent ST elevation → STEMI pathway 1
• No persistent ST elevation → NSTE-ACS pathway (requires troponin to differentiate UA from NSTEMI) 1

Troponin Distinguishes UA from NSTEMI

• High-sensitivity cardiac troponin (hs-cTn) T or I with at least one value above the 99th percentile upper reference limit separates NSTEMI from unstable angina 1, 2
• Serial troponin measurements are essential, as initial values may be normal in early presentation 2

Dynamic Nature of ACS

The pathophysiology of ACS is dynamic—patients can rapidly progress from unstable angina to NSTEMI to STEMI during their presentation and initial evaluation. 1, 2

• Continuous monitoring and serial assessments are mandatory 2
• A partially occlusive thrombus can propagate to complete occlusion 1
• Treatment must be adjusted as the clinical condition evolves 2

Important Caveats

• A normal ECG does NOT exclude ACS—many NSTE-ACS patients have nonspecific changes or completely normal ECGs at presentation 2
• Approximately 40% of men and 48% of women present with atypical symptoms (dyspnea, diaphoresis, nausea) without classic chest pain 5, 4
• All three ACS entities represent Type 1 myocardial infarction in the Universal Definition of MI classification 1
• Less common causes of myocardial ischemia (coronary spasm, embolism, dissection) can mimic ACS but are managed differently 1