Amiodarone toxicity

Amiodarone has the properties of class I, II, III, IV drugs.

Because of it extensive toxicity profile of amiodarone it should not be considered 1st line agent for rhythm control for AF in patients whom an alternative antiarrhythmic agent can be safely used.

Adverse effects are dose dependent and may occur in up to 75% of patients treated at high doses for 5 years.

Pulmonary toxicity. Dry cough, dyspnea, pulmonary infiltrates, rales. CXR and PFT at baseline and q12 months or when patients complain of shortness of breath. Interstitial infiltrates on the CXR and decreased diffusing capacity raise concern of amiodarone pulmonary toxicity.

Photosensitivity is a common reaction, and in some patients, a violaceous skin discoloration develops in sun-exposed areas. The blue-gray discoloration may not resolve completely with discontinuation of therapy.

Thyroid dysfunction is a common adverse effect. Hypothyroidism or hyperthyroidism have been reported. TSH at baseline and monitored q6 months. If hypothyroidism develops, concurrent treatment with levothyroxine may allow continued amiodarone use.

Corneal microdeposits, detectable on slit-lamp exam on virtually all patients. Do not interfere with vision and are not an indication for discontinuation of drug. Optic neuritis and blindness is rare.

ECG changes. Prolonged PR intervals and bradycardia. High-grade AV block in patients with preexisting conduction abnormalities. Prolongation of QT intervals. TdP is rare.

Liver dysfunction usually manifests in an asymptomatic and transient rise in transaminases. AST and ALT q6 months. If increase is x 3 times, d/c amiodarone.

Drug interaction. Raises blood level of digoxin, warfarin, and phenytoin. Reduce the dose of amiodarone by 50%.

Risk of hypothyroidism, hyperthyroidism, pulmonary fibrosis, hepatitis is low if dose is 100-200 mg/d.