A 65-year-old woman with dilated cardiomyopathy (ejection fraction 25%) presents with recurrent episodes of polymorphic ventricular tachycardia. She is intolerant to beta-blockers (severe hypotension). Which drug is the preferred first-line choice for long-term suppression of polymorphic VT in this setting?

Explanation

## Drug of Choice for Polymorphic VT in Cardiomyopathy **Key Point:** Amiodarone is the preferred first-line agent for polymorphic ventricular tachycardia in patients with structural heart disease (dilated cardiomyopathy) and reduced ejection fraction, especially when beta-blockers are contraindicated. ## Why Amiodarone in Polymorphic VT? **High-Yield:** Polymorphic VT in cardiomyopathy often involves: 1. Abnormal automaticity from failing myocardium 2. Triggered activity (early and delayed afterdepolarisations) 3. Micro-re-entry in areas of fibrosis Amiodarone's multi-class action addresses all three mechanisms simultaneously. ## Comparison of Agents in Polymorphic VT with Cardiomyopathy | Agent | Mechanism | Efficacy | LV Function Impact | Safety in Cardiomyopathy | |-------|-----------|----------|-------------------|------------------------| | **Amiodarone** | Class I, II, III, IV | Excellent (70–80%) | Neutral/improves | Excellent (gold standard) | | **Flecainide** | Class IC (pure Na blockade) | Moderate (40–50%) | Negative inotrope | **Contraindicated** (CAST trial) | | **Mexiletine** | Class IB (Na blockade) | Poor (20–30%) | Minimal | Weak; not recommended | | **Disopyramide** | Class IA (Na blockade + anticholinergic) | Moderate (50–60%) | Strong negative inotrope | **Contraindicated** in cardiomyopathy | **Clinical Pearl:** The CAST (Cardiac Arrhythmia Suppression Trial) demonstrated that Class IC agents (flecainide, encainide) increase mortality in post-MI patients with reduced ejection fraction. This principle extends to all cardiomyopathy patients: pure sodium-channel blockers are harmful. **Warning:** Disopyramide and flecainide are absolutely contraindicated in dilated cardiomyopathy because their negative inotropic effects can precipitate acute decompensation or sudden death. Mexiletine has insufficient efficacy. ## Why Amiodarone Works Here 1. **Class III effect** (K^+^ channel blockade) prolongs action potential duration and refractoriness → suppresses triggered activity 2. **Class II effect** (beta-blockade) reduces automaticity → compensates for beta-blocker intolerance 3. **Class I effect** (Na^+^ blockade) slows conduction → breaks micro-re-entrant circuits 4. **Class IV effect** (Ca^2+^ channel effects) → AV nodal slowing 5. **No negative inotropy** → safe in reduced ejection fraction (unlike Class IA/IC agents) **Mnemonic:** **ABCD of Amiodarone in Cardiomyopathy** = **A**ll-class action, **B**eta-like (compensates for beta-blocker intolerance), **C**onduction slowing, **D**oes not depress LV function.