Harvey's Garden

Acute coronary syndrome

5 min read

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

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

FeatureLeft VentricleRight Ventricle
Muscle massHighLow
Resting oxygen extractionHighLow
Coronary perfusionDuring diastole onlyThroughout cardiac cycle
Collateral circulationLess developedMore developed
Ischemic preconditioningLowHigh

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

Clinical features

Diagnostics

  • Best Initial Test: ECG (Do within 10 mins).
    • Serial ECGs should be performed (at baseline, then every 15–30 minutes initially) to identify progression to MI. c
  • Most Specific Test: Cardiac Troponin I or T.
    • Rises in 3-4 hours; peaks at 24 hours.
    • Step 2 Tip: If initial troponin is negative but suspicion is high, repeat in 2-3 hours.
  • CXR: To rule out aortic dissection (widened mediastinum) if presentation is tearing pain.

Pathology

Time After Myocardial InfarctionPredominant Light Microscopic Changes
0-4 hoursNo visible change t
4-12 hoursWavy fibers with narrow, elongated myocytes
12-24 hoursMyocyte hypereosinophilia with pyknotic (shrunken) nuclei
1-3 daysCoagulation necrosis (loss of nuclei & striations)
Prominent neutrophilic infiltrate
3-7 daysDisintegration of dead neutrophils & myofibers
Macrophage infiltration at border areas
7-10 daysRobust phagocytosis of dead cells by macrophages
Beginning formation of granulation tissue at margins
10-14 daysWell-developed granulation tissue with neovascularization
2-8 weeksProgressive collagen deposition & scar formation

Loss of cardiomyocyte contractility occurs within 60 seconds after the onset of total ischemia. When ischemia lasts less than 30 minutes, restoration of blood flow leads to reversible contractile dysfunction (myocardial stunning), with contractility gradually returning to normal over the next several hours to days. However, after about 30 minutes of total ischemia, ischemic injury becomes irreversible. t

Treatment

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

  • Immediate Stabilization (All ACS):
    • ABC, IV access, Cardiac Monitor.
    • Aspirin: 325mg chewable (loading dose) - Mortality benefit.
    • P2Y12 Inhibitor: Clopidogrel/Ticagrelor (DAPT).
    • Anticoagulation: Unfractionated Heparin (esp if PCI planned) or LMWH. c
    • Nitroglycerin: SL or IV for pain/HTN (Avoid in Right Ventricular MI - II, III, aVF; preload dependent). c
    • Beta-Blocker: Metoprolol (within 24h if stable, no HF/bradycardia).
    • Statin: High-intensity (Atorvastatin 80mg).
  • Reperfusion Strategy (STEMI):
    • PCI (Gold Std): Door-to-balloon <90 min (or <120 min if transferrequired).
    • Fibrinolysis (tPA): If PCI unavailable within 120 min. Door-to-needle <30 min.
  • NSTEMI/UA Strategy:
    • TIMI/GRACE Score: Risk stratify.
    • Early Invasive (Angio): Refractory angina, hemodynamic instability, new HF, high risk score.
    • Ischemia-Guided: Medical mgmt, stress test prior to discharge.

Right Ventricular Infarct (Inferior Wall MI)

  • Clue: ST elevation in II, III, aVF. Hypotension, Clear lungs, JVD.
  • Next Step: Get Right-sided ECG (look for ST elevation in V4R).
  • Management: IV Fluids (maximize preload). Avoid Nitrates/Diuretics (they drop preload).
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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.

Complications

ComplicationTime courseClinical findings
Papillary muscle rupture/dysfunction*Acute or within 3-5 daysSevere pulmonary edema, respiratory distress
New early systolic murmur (acute MR)
Hypotension/cardiogenic shock
Interventricular septum ruptureAcute or within 3-5 daysChest 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 weeksChest pain
Distant heart sounds
Shock, rapid progression to cardiac arrest
Left ventricular aneurysm**Up to several monthsHeart 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
    • Prevention: installation of the implantable cardioverter-defibrillator device
  • Papillary Muscle Dysfunction (not papillary muscle rupture)
    • Mechanism: Acute ischemia (transient) or infarction of the papillary muscle (without rupture).
    • Risk: Posteromedial muscle (fed by RCA) is most susceptible due to single blood supply.
    • Clinical: New onset Mitral Regurgitation (usually mild-to-moderate), worsening pulmonary edema. t
  • 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

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