A 58-year-old man with a history of anterior wall myocardial infarction 3 months ago presents with recurrent episodes of sustained monomorphic ventricular tachycardia (VT). Electrophysiology study confirms a re-entrant circuit in the scar tissue. He is haemodynamically stable during VT. What is the drug of choice for acute termination and long-term suppression of this arrhythmia?

Explanation

## Drug of Choice for Sustained Monomorphic VT **Key Point:** Amiodarone is the most effective antiarrhythmic agent for sustained monomorphic ventricular tachycardia, particularly in the setting of structural heart disease (post-MI scar-related re-entry). ## Why Amiodarone? **High-Yield:** Amiodarone possesses properties of all four Vaughan-Williams classes: - Class I (sodium channel blockade) → slows conduction - Class II (beta-blockade) → reduces automaticity - Class III (potassium channel blockade) → prolongs refractoriness - Class IV (calcium channel effects) → AV nodal slowing This multi-modal action makes it superior for complex re-entrant arrhythmias in post-infarction scar tissue. ## Efficacy in Post-MI VT | Feature | Amiodarone | Procainamide | Sotalol | Verapamil | |---------|-----------|--------------|--------|----------| | **Efficacy in structural VT** | Excellent (70–80%) | Moderate (40–50%) | Moderate (50–60%) | Poor | | **Class of action** | I, II, III, IV | I (IA) | II, III | IV | | **Haemodynamic stability** | Good (even in VT) | Can worsen LV function | Moderate | Contraindicated in VT | | **Acute termination** | Yes (IV form) | Yes (IV form) | No (oral only) | No | **Clinical Pearl:** In haemodynamically stable sustained monomorphic VT post-MI, IV amiodarone is the agent of choice for acute termination, followed by oral amiodarone for long-term suppression. The drug's broad spectrum of action addresses both the re-entrant substrate and any residual automaticity. **Warning:** Amiodarone has significant side effects (thyroid, lung, liver, QT prolongation) but remains the standard of care for life-threatening VT in structural heart disease because efficacy outweighs toxicity risk in this high-risk population. ## Mechanism in This Case The post-MI scar creates a re-entrant circuit. Amiodarone's Class I effect slows conduction through the circuit, while Class III effect prolongs refractoriness, breaking the re-entry loop. Its beta-blocking properties also reduce automaticity from any residual ischaemic tissue.