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

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Treatment

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

• Arrhythmias: a common cause of death in MI patients in the first 24 hours
  • Sinus bradycardia is the most common arrhythmia, especially in inferior wall myocardial infarction
    • Due to occlusion of the right coronary artery (RCA). The RCA usually supplies blood to the sinoatrial node, the atrioventricular node, and most of the bundle of His
    • Managed with intravenous atropine
  • Ventricular tachyarrhythmias
  • Atrioventricular block (e.g., complete heart block)
  • Conduction blocks

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