Amiodarone prolongs the QT interval and the cardiac action potential. Despite being a class III antiarrhythmic, it has properties of all four Vaughan Williams classes. Its most important limitation in long-term use is:

• A Torsades de pointes due to QT prolongation — occurring more often than with sotalol
• B Pulmonary toxicity (interstitial pneumonitis/fibrosis) requiring regular monitoring of DLCO and chest imaging ✓
• C Irreversible hepatic failure occurring in >20% of patients on long-term therapy
• D Class IV calcium channel effects causing severe bradycardia necessitating permanent pacemaker in most patients

Explanation

Amiodarone's most important and potentially fatal long-term complication is pulmonary toxicity (incidence ~5–10%), which may manifest as interstitial pneumonitis progressing to fibrosis. Annual monitoring includes chest X-ray, HRCT if symptomatic, and DLCO (diffusing capacity). Paradoxically, despite prolonging QT, amiodarone rarely causes torsades de pointes (less than sotalol) — possibly because it simultaneously blocks IKr and IKs (preventing dispersion of refractoriness). Hepatotoxicity occurs but frank hepatic failure is uncommon (<1%). Bradycardia is manageable and does not usually necessitate permanent pacing.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.