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EMERGENCY

Acute Coronary Syndrome (ACS)

High EvidenceUpdated: 2025-12-22

On This Page

Red Flags

  • ST elevation on ECG (STEMI)
  • Ongoing ischaemic chest pain
  • Haemodynamic instability (hypotension, shock)
  • Cardiogenic shock
  • Ventricular arrhythmias (VT, VF)
  • New heart failure
  • Cardiac arrest
Overview

Acute Coronary Syndrome (ACS)

1. Topic Overview

Summary

Acute coronary syndrome (ACS) encompasses a spectrum of conditions caused by acute myocardial ischaemia, most commonly due to atherosclerotic plaque rupture and coronary thrombus formation. The spectrum includes ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina. STEMI represents complete coronary occlusion and requires emergent reperfusion therapy (primary PCI or fibrinolysis). NSTEMI/unstable angina are managed with antithrombotic therapy and a risk-stratified approach to invasive management. Early recognition, timely reperfusion, and optimal medical therapy significantly reduce mortality.

Key Facts

  • Definition: Acute myocardial ischaemia due to coronary thrombus
  • Spectrum: Unstable Angina → NSTEMI → STEMI
  • STEMI: Complete occlusion, ST elevation, urgent reperfusion required
  • NSTEMI: Partial occlusion, troponin positive, no persistent ST elevation
  • Unstable Angina: Troponin negative, high-risk angina
  • Door-to-Balloon Target: <90 minutes for primary PCI
  • Door-to-Needle Target: <30 minutes for fibrinolysis if PCI not available

Clinical Pearls

"Time is Myocardium": Every minute of delay in STEMI increases mortality. Primary PCI within 90 minutes is the goal.

"STEMI Equivalents": New LBBB, posterior MI, de Winter T-waves, and hyperacute T-waves may represent acute occlusion despite no classic ST elevation — treat as STEMI.

"DAPT for All": Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) is the cornerstone of management in all ACS patients.

Why This Matters Clinically

ACS is a leading cause of death worldwide. Rapid diagnosis and treatment save lives. Every minute counts in STEMI — delayed reperfusion leads to larger infarcts, heart failure, and higher mortality.


2. Epidemiology

Incidence

MeasureValue
UK Incidence~100,000 ACS admissions/year
Mortality (STEMI)In-hospital 5-8%; 1-year 10%
Mortality (NSTEMI)In-hospital 3-5%; 1-year 12-15%

Demographics

FactorDetails
AgeRisk increases with age; peak >65
SexMen more common; women present later, atypically
TrendDeclining due to prevention and reperfusion

Risk Factors (Coronary Artery Disease)

ModifiableNon-Modifiable
SmokingAge
HypertensionMale sex
DiabetesFamily history
DyslipidaemiaGenetic factors
Obesity
Physical inactivity
Stress

3. Pathophysiology

Mechanism of ACS

Step 1: Atherosclerotic Plaque

  • Lipid-rich necrotic core
  • Thin fibrous cap (vulnerable plaque)

Step 2: Plaque Rupture or Erosion

  • Exposes thrombogenic core to blood
  • Platelet aggregation
  • Thrombus formation

Step 3: Coronary Occlusion

  • Complete occlusion → STEMI
  • Subtotal occlusion → NSTEMI/UA

Step 4: Myocardial Ischaemia and Necrosis

  • Subendocardial → transmural
  • Troponin release
  • Myocardial stunning, hibernation

Consequences

DurationEffect
<20 minReversible ischaemia
20-60 minSubendocardial necrosis
>60 minTransmural necrosis
HoursInfarct expansion, complications

4. Clinical Presentation

Classic Symptoms

Atypical Presentations

PopulationFeatures
ElderlyDyspnoea, confusion, fatigue
DiabeticSilent MI, atypical pain
WomenAtypical location, fatigue, nausea
Post-operativeMay be masked

Red Flags

[!CAUTION] Immediate Red Flags:

  • ST elevation on ECG
  • Ongoing ischaemic pain
  • Haemodynamic instability
  • Cardiogenic shock
  • Ventricular arrhythmias
  • Cardiac arrest

Central crushing/heavy chest pain (>20 min)
Common presentation.
Radiation to left arm, jaw, neck, back
Common presentation.
Dyspnoea
Common presentation.
Sweating (diaphoresis)
Common presentation.
Nausea, vomiting
Common presentation.
Pallor, anxiety
Common presentation.
5. Clinical Examination

Physical Examination

General:

  • Pallor, sweating, distress
  • Cool peripheries

Cardiovascular:

  • May be normal
  • Tachycardia, hypotension (cardiogenic shock)
  • S3 (LV dysfunction)
  • Murmur (MR if papillary muscle dysfunction)
  • Elevated JVP (RV infarct or failure)

Pulmonary:

  • Crackles (pulmonary oedema)

Killip Classification (Acute MI)

ClassFeaturesMortality
INo heart failure6%
IIS3, crackles17%
IIIPulmonary oedema38%
IVCardiogenic shock81%

6. Investigations

Immediate

TestPurpose
12-lead ECGSTEMI diagnosis, localisation
Troponin (hs-cTn)NSTEMI diagnosis; check 0h and 3h (or 1h algorithm)
Serial ECGsDynamic changes

Other

TestPurpose
FBCAnaemia
U&ERenal function (contrast, ACE-I)
GlucoseDiabetes
Lipid profileBaseline for statin
CoagulationBefore anticoagulation
CXRPulmonary oedema, cardiomegaly
EchocardiographyLV function, RWMA, complications
Coronary AngiographyDefinitive anatomy

7. Management

Immediate (All ACS)

  • Aspirin 300mg
  • P2Y12 inhibitor (Ticagrelor 180mg or Clopidogrel 300-600mg)
  • Anticoagulation (Fondaparinux, Enoxaparin, or UFH)
  • GTN, Morphine (caution)
  • Oxygen if hypoxic

STEMI

  • Primary PCI (<90 min) — gold standard
  • Fibrinolysis if PCI not available <120 min

NSTEMI/UA

  • Risk stratification (GRACE score)
  • Invasive strategy based on risk
  • Optimal medical therapy

Secondary Prevention

TherapyDuration
AspirinLifelong
P2Y12 inhibitor12 months
High-intensity statinLifelong
ACE-ILifelong (especially if EF <40%)
Beta-blockerLifelong (especially if EF <40%)
EplerenoneIf EF ≤40% + HF/diabetes

8. Complications

Early (In-Hospital)

ComplicationNotes
ArrhythmiasVT/VF (most common cause of sudden death)
Cardiogenic ShockKillip IV; mortality 50%+
Heart FailureAcute LV dysfunction
MechanicalVSD, papillary muscle rupture, free wall rupture
PericarditisEarly (24-48h) or late (Dressler's)
StrokeLV thrombus embolism
BleedingAnticoagulation, vascular access

Late

ComplicationNotes
Heart FailureRemodelling, chronic LV dysfunction
Recurrent ACSIn-stent restenosis or thrombosis
ArrhythmiasVentricular tachycardia (scar)
LV AneurysmUsually anterior MI

9. Prognosis & Outcomes

Mortality

TypeIn-Hospital1-Year
STEMI5-8%10%
NSTEMI3-5%12-15%

Prognostic Factors

  • Age, Killip class, heart rate, BP
  • Anterior MI worse than inferior
  • Delayed reperfusion worsens outcome
  • EF most important long-term predictor

10. Evidence & Guidelines

Key Guidelines

  1. ESC Guidelines for STEMI (2017) — Ibanez B, et al.

  2. ESC Guidelines for NSTE-ACS (2020) — Collet JP, et al.

Landmark Trials

PLATO (2009) — Ticagrelor vs Clopidogrel

  • Key finding: Ticagrelor reduced CV death, MI, stroke
  • Clinical Impact: Ticagrelor preferred over clopidogrel in ACS

HORIZONS-AMI (2008) — Bivalirudin in STEMI

  • Key finding: Bivalirudin reduced bleeding vs heparin+GPIIb/IIIa

Evidence Strength

InterventionLevelKey Evidence
Primary PCI for STEMI1aMultiple RCTs
DAPT for 12 months1aCURE, PLATO, TRITON-TIMI 38
High-intensity statin1aPROVE IT-TIMI 22, MIRACL

11. Patient/Layperson Explanation

What is ACS?

Acute coronary syndrome is a group of conditions caused by reduced blood flow to your heart. It includes heart attacks (STEMI and NSTEMI) and unstable angina.

What happens?

A fatty deposit (plaque) in your heart's arteries can rupture, forming a blood clot that blocks blood flow. This damages heart muscle.

What are the symptoms?

  • Crushing chest pain lasting more than 15-20 minutes
  • Pain spreading to your arm, jaw, or back
  • Shortness of breath
  • Sweating, nausea, feeling unwell

How is it treated?

  1. Emergency treatment: Aspirin, blood thinners, and opening the blocked artery (angioplasty with stent or clot-busting drugs)
  2. Long-term medicines: Blood thinners, cholesterol tablets, blood pressure tablets
  3. Lifestyle changes: Stop smoking, healthy diet, exercise, cardiac rehabilitation

What to expect

  • Most people recover well with prompt treatment
  • You'll need medications for life to prevent future heart attacks
  • Cardiac rehabilitation helps recovery

When to call 999

Call 999 immediately if:

  • You have crushing chest pain lasting more than 15 minutes
  • Pain spreads to your arm or jaw
  • You feel short of breath, sweaty, or unwell

12. References

Primary Guidelines

  1. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177. PMID: 28886621

  2. Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021;42(14):1289-1367. PMID: 32860058

Key Trials

  1. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes (PLATO). N Engl J Med. 2009;361(11):1045-1057. PMID: 19717846

Further Resources

  • British Heart Foundation: bhf.org.uk
  • Heart UK: heartuk.org.uk


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. If you suspect a heart attack, call 999 immediately.

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22
Emergency Protocol

Red Flags

  • ST elevation on ECG (STEMI)
  • Ongoing ischaemic chest pain
  • Haemodynamic instability (hypotension, shock)
  • Cardiogenic shock
  • Ventricular arrhythmias (VT, VF)
  • New heart failure

Clinical Pearls

  • **"Time is Myocardium"**: Every minute of delay in STEMI increases mortality. Primary PCI within 90 minutes is the goal.
  • **"STEMI Equivalents"**: New LBBB, posterior MI, de Winter T-waves, and hyperacute T-waves may represent acute occlusion despite no classic ST elevation — treat as STEMI.
  • **"DAPT for All"**: Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) is the cornerstone of management in all ACS patients.
  • **Immediate Red Flags:**
  • - ST elevation on ECG

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines