What are the types of acute coronary syndrome (ACS)?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 18, 2026 • View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Types of Acute Coronary Syndrome

Acute coronary syndrome comprises three distinct clinical entities: ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina, all sharing a common pathophysiology of atherosclerotic plaque disruption with coronary thrombosis but differing in the degree of vessel occlusion and myocardial necrosis. 1, 2

Primary Classification Framework

The classification of ACS is based on two key diagnostic elements that determine both prognosis and treatment urgency:

1. ST-Segment Elevation Myocardial Infarction (STEMI)

  • Definition: Myocardial ischemia with necrosis (elevated troponin above the 99th percentile) accompanied by persistent ST-segment elevation lasting more than 20 minutes on the 12-lead ECG 2
  • Pathophysiology: Results from complete coronary artery occlusion causing transmural myocardial ischemia and infarction 2
  • Clinical urgency: Requires immediate reperfusion therapy (primary PCI within 120 minutes or fibrinolytic therapy if PCI unavailable) as mortality reduction depends on rapid treatment 1

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

  • Definition: Myocardial ischemia with necrosis evidenced by cardiac troponin levels above the 99th percentile, but without persistent ST-segment elevation on ECG 1, 2
  • Pathophysiology: Typically arises from a partially occluded coronary artery producing subendocardial ischemia 2
  • ECG findings: May show transient ST-segment elevation, persistent or transient ST-segment depression, T-wave inversion, flat T waves, pseudo-normalization of T waves, or the ECG may be completely normal 1
  • Clinical spectrum: Ranges from asymptomatic patients at presentation to individuals with ongoing ischemia, electrical or hemodynamic instability, or cardiac arrest 1

3. Unstable Angina

  • Definition: Myocardial ischemia at rest or minimal exertion in the absence of cardiomyocyte necrosis (normal troponin levels) 1
  • Pathophysiology: Transient myocardial ischemia with reduced coronary flow but without myocardial cell death 2
  • Declining prevalence: With high-sensitivity cardiac troponin assays, unstable angina diagnoses have decreased by 4% absolute (20% relative), with a reciprocal increase in NSTEMI detection 1
  • Prognostic significance: Patients with unstable angina have substantially lower risk of death compared to NSTEMI patients and derive less benefit from intensified antiplatelet therapy and early invasive strategy 1

Diagnostic Algorithm

The initial 12-lead ECG obtained within 10 minutes of presentation determines the immediate management pathway 1:

  • Persistent ST-elevation present → STEMI pathway with immediate reperfusion therapy 1
  • No persistent ST-elevation → Non-ST-elevation ACS (NSTE-ACS) pathway requiring high-sensitivity cardiac troponin testing 1, 2
    • Troponin above 99th percentile with rise/fall pattern → NSTEMI 1, 2
    • Troponin normal → Unstable angina 1, 2

Universal Definition Context: Type 1 Myocardial Infarction

All three ACS entities correspond to Type 1 MI under the Universal Definition of Myocardial Infarction, characterized by atherosclerotic plaque rupture, ulceration, fissure, erosion, or dissection with resulting intraluminal thrombus leading to decreased myocardial blood flow and subsequent myocardial necrosis 1

This distinguishes ACS from:

  • Type 2 MI: Myocardial necrosis from supply-demand mismatch (coronary spasm, endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anemia, respiratory failure, hypotension, severe hypertension) rather than plaque instability 1
  • Other coronary etiologies: Coronary artery spasm, embolism, or dissection that can mimic ACS clinically but require distinct management 1

Critical Clinical Pitfalls

  • Dynamic progression: ACS is not static—patients can rapidly evolve from unstable angina to NSTEMI to STEMI during initial evaluation as a partially occlusive thrombus extends to complete occlusion 1, 2
  • Normal ECG does not exclude ACS: Up to 41% of NSTE-ACS patients present with neither ST-segment depression nor T-wave inversion on initial ECG, and 1-6% of patients with completely normal ECGs will have myocardial infarction 1, 3
  • Atypical presentations: Women, elderly patients, and individuals with diabetes frequently present with atypical symptoms (dyspnea, nausea, generalized weakness, syncope, epigastric pain) and non-diagnostic ECGs, requiring heightened clinical vigilance 1
  • Serial assessment mandatory: Continuous ECG monitoring and serial troponin measurements at 1-3 hours (high-sensitivity assays) or 6-12 hours (standard assays) are essential because initial values may be normal in evolving MI 1, 2

References

1
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

2
Guideline

Acute Coronary Syndrome: Core Definitions and Diagnostic Framework

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Related Questions

What is the appropriate initial evaluation and management for an adult presenting with chest discomfort suggestive of acute coronary syndrome or angina?
What are the diagnostic criteria for acute coronary syndrome (ACS)?
Which components are included in unified protocols among emergency care units (UPAs), hospitals, and the regulatory network for suspected acute coronary syndrome?
What is the initial management for a patient presenting with Acute Coronary Syndrome (ACS)?
What is the recommended inpatient workup and management for a patient presenting with Acute Coronary Syndrome (ACS)?
When should treatment be started in a reproductive‑age woman with polycystic ovary syndrome (PCOS) and what are the indications?
Why is thrombolytic therapy contraindicated in subarachnoid hemorrhage?
What oral dose of sodium polystyrene sulfonate (Kayexalate) is recommended for an adult with a serum potassium of 5.7 mmol/L and no contraindications?
Why would a patient with chronic nasal obstruction refractory to optimal medical therapy (saline irrigations, intranasal corticosteroid sprays, antihistamines, decongestants, allergy immunotherapy) require nasal turbinate surgery?
What is ameloblastoma?
What are the steps of cardiopulmonary resuscitation for an unresponsive person not breathing normally, regardless of age?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.

Ask Question