Acute coronary syndrome

graph TD
    CAD["Coronary Artery Disease (CAD)"]
    StableAngina["Chronic Stable Angina"]
    ACS["Acute Coronary Syndrome (ACS)"]
    UnstableAngina["Unstable Angina"]
    NSTEMI["NSTEMI"]
    STEMI["STEMI"]
	Variant["Variant (Prinzmetal) Angina"]

    CAD --> StableAngina
    CAD --> ACS
	CAD --> Variant
    ACS --> UnstableAngina
    ACS --> NSTEMI
    ACS --> STEMI

Etiology

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Pathophysiology

Possibilities

1. Left anterior descending artery (45%): infarction of the anterior wall and anterior septum of the LV
2. Right coronary artery: infarction of the posterior wall, posterior septum, and papillary muscles** of the LV
3. Left circumflex artery: infarction of the lateral wall of the LV

LV vs RV

Feature	Left Ventricle	Right Ventricle
Muscle mass	High	Low
Resting oxygen extraction	High	Low
Coronary perfusion	During diastole only	Throughout cardiac cycle
Collateral circulation	Less developed	More developed
Ischemic preconditioning	Low	High

The relatively low systolic pressure of the RV (eg, ≤25 mm Hg) allows for coronary perfusion throughout the cardiac cycle

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Clinical features

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Diagnostics

Pathology

Time After Myocardial Infarction	Predominant Light Microscopic Changes
0-4 hours	No visible change
4-12 hours	Wavy fibers with narrow, elongated myocytes
12-24 hours	Myocyte hypereosinophilia with pyknotic (shrunken) nuclei
1-3 days	Coagulation necrosis (loss of nuclei & striations) Prominent neutrophilic infiltrate
3-7 days	Disintegration of dead neutrophils & myofibers Macrophage infiltration at border areas
7-10 days	Robust phagocytosis of dead cells by macrophages Beginning formation of granulation tissue at margins
10-14 days	Well-developed granulation tissue with neovascularization
2-8 weeks	Progressive collagen deposition & scar formation

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Treatment

Acute Coronary Syndrome (ACS: UA, NSTEMI, STEMI)

• Immediate Tx (All ACS):
  • DAPT: Aspirin + P2Y₁₂ inhibitor (e.g., Clopidogrel, Ticagrelor).
  • Anticoagulation: Heparin (UFH or LMWH).
  • High-Intensity Statin.
  • Symptom Control: NTG, Morphine, Beta-blockers (if stable).
• STEMI-Specific Tx:
  • IMMEDIATE REPERFUSION.
  • PCI: Gold standard. Goal: door-to-balloon < 90 min.
  • Thrombolysis: If PCI is not available (>120 min away).
• NSTEMI / UA-Specific Tx:
  • Risk Stratify (TIMI score).
  • High-risk: Early invasive strategy (angiography ± PCI).
  • Low-risk: Conservative medical management initially.

Link to original

Arrythmia

Class IB antiarrhythmics treat ventricular arrhythmias, especially in ischemic tissue (e.g. post-MI)

Note

Ischemia leads to slow cellular depolarization that inactivates sodium channels, and therefore enhanced binding of IB drugs.

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Complications

Complication	Time course	Clinical findings
Papillary muscle rupture/dysfunction*	Acute or within 3-5 days	Severe pulmonary edema, respiratory distress New early systolic murmur (acute MR) Hypotension/cardiogenic shock
Interventricular septum rupture	Acute or within 3-5 days	Chest pain New holosystolic murmur Hypotension/cardiogenic shock Step up in O2 level from RA to RV
Free wall rupture**	Within 5 days or up to 2 weeks	Chest pain Distant heart sounds Shock, rapid progression to cardiac arrest
Left ventricular aneurysm**	Up to several months	Heart failure Angina, ventricular arrhythmias

*Usually due to right coronary artery occlusion.

**Usually due to left anterior descending artery occlusion

0–24 hours post-infarction

• Sudden cardiac death (SCD)
  • Definition: A sudden death presumably caused by cardiac arrhythmia or hemodynamic catastrophe, which occurs either within an hour of symptom onset in patients with cardiovascular symptoms, or within 24 hours of being asymptomatic in patients with no cardiovascular symptoms.
  • Pathophysiology: Fatal ventricular arrhythmia is considered to be the underlying mechanism of SCD.
  • Underlying conditions
    • Coronary artery disease: present in ∼ 70% of cases in adults over 35 years
    • Dilated cardiomyopathy/hypertrophic cardiomyopathy
    • Myocarditis
    • Hereditary ion channelopathies (e.g., long QT syndrome, Brugada syndrome)
  • Prevention: installation of the implantable cardioverter-defibrillator device
• Arrhythmias: a common cause of death in MI patients in the first 24 hours
  • Immediate Phase (0–48 hours)
    • Ventricular Fibrillation/Tachycardia (VF/VT):
      • The most common cause of death in the immediate post-MI period.
      • Due to acute electrical instability.
    • Bradycardia & AV Block:
      • Most common with Inferior MI (RCA occlusion affecting SA/AV nodes).
      • Usually transient and resolves with reperfusion.
      • AV block with Anterior MI (LAD occlusion) is less common but indicates extensive necrosis and carries a poor prognosis.
    • Accelerated Idioventricular Rhythm (AIVR):
      • Regular, wide-complex rhythm (60-110 bpm).
      • Generally benign and often considered a sign of successful reperfusion.
  • Subacute/Chronic Phase (>2 days)
    • Atrial Fibrillation (AFib):
      • The most common sustained arrhythmia post-MI.
      • Caused by atrial ischemia, inflammation, or high LA pressure from LV dysfunction.
      • Worsens prognosis (↑ risk of stroke, heart failure).
    • Sustained Monomorphic VT:
      • Caused by a stable re-entry circuit that forms around the healed infarct scar.
      • A major cause of late sudden cardiac death.

1–3 days post-infarction

• Early infarct-associated pericarditis
  • This pericarditis is a reaction to necrosis of the myocardium near the epicardial surface; usually localized to the areas overlying the necrotic myocardial segment.
  • Clinical features of acute pericarditis, including:
    • Friction rub
    • Pleuritic chest pain
    • Dry cough
      • Due to inflammation of the mediastinal pleura adjoining the pericardium.
    • Diffuse ST elevations on ECG
    • Pericardial effusion
  • Prognosis: usually self-limiting

Tip

• Early: peri-infarction pericarditis
• Late: Dressler syndrome

2 weeks to months post-infarction

Postmyocardial infarction syndrome (Dressler syndrome)

Pericarditis occurring 2–10 weeks post-MI without an infective cause

• Pathophysiology: thought to be due to circulating antibodies against cardiac muscle cells (autoimmune etiology) → immune complex deposition → inflammation
• Clinical features
  • Signs of Pericarditis: pleuritic chest pain , dry cough , friction rub
  • Fever
  • Laboratory findings: leukocytosis, ↑ serum troponin levels
  • ECG: diffuse ST elevations
• Treatment: NSAIDs (e.g., aspirin), colchicine
• Complications (rare): hemopericardium