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Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

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Serial pulmonary function tests in patients treated with low-dose amiodarone.

C S Ulrik¹, V Backer, J Aldershvile

¹Laboratory of Respiratory Physiology, Rigshospitalet, Copenhagen, Denmark.

American Heart Journal

|June 1, 1992

Summary

Low-dose amiodarone therapy for arrhythmias can cause pulmonary toxicity. Higher cumulative doses of amiodarone are linked to reduced lung diffusion capacity (TLCO), even in asymptomatic patients.

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Area of Science:

Cardiology
Pulmonology
Pharmacology

Background:

Pulmonary toxicity is a significant concern limiting amiodarone use.
Low-dose amiodarone is prescribed for refractory tachyarrhythmias.

Purpose of the Study:

To investigate the impact of low-dose amiodarone on pulmonary function.
To identify factors associated with amiodarone-induced pulmonary toxicity.

Main Methods:

Prospective study of 24 patients on low-dose amiodarone (≤400 mg/day).
Serial pulmonary function tests (PFTs) were conducted.
PFT results were correlated with amiodarone dosage, serum concentration, cumulative dose, and treatment duration.

Main Results:

A mean reduction of 12.9% in total lung diffusion capacity (TLCO) was observed in 22/24 patients.
Decreased TLCO significantly correlated with higher cumulative amiodarone doses.
No correlation found between TLCO reduction and daily dose, duration, serum levels, or baseline PFTs.
29% of patients developed asymptomatic pulmonary toxicity (TLCO decrease ≥20%).

Conclusions:

Long-term, low-dose amiodarone treatment is associated with significant reductions in TLCO.
Cumulative amiodarone dose is a key predictor of pulmonary function decline.
Pre-existing pulmonary abnormalities do not predict subclinical toxicity development.