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Chest, Vol 93, 254-263, Copyright © 1988 by American College of Chest Physicians
ARTICLES |
GD Adams, R Kehoe, M Lesch and J Glassroth
Department of Medicine (Section of Pulmonary Medicine), Northwestern University Medical School, Chicago.
Problems with pulmonary toxicity have emerged as a potentially limiting factor for amiodarone use. We prospectively studied 33 subjects treated with amiodarone for refractory arrhythmias. Serial clinical, radiographic and pulmonary function tests were correlated with the dose and duration of amiodarone treatment to define: a) prevalence of lung toxicity, b) subgroups of patients at particular risk for toxicity, c) potential interaction between amiodarone dose and toxicity. Considering all subjects, no significant change in lung volumes or airflow indices were noted; carbon monoxide diffusing capacity (DCO) underwent a mean reduction of 20.3 percent during treatment. Symptoms of possible pulmonary toxicity occurred in 27.3 percent of subjects. No type or degree of pretreatment cardiopulmonary dysfunction predicted lung toxicity. However, maintenance dose was correlated with toxicity; patients treated with doses of less than or equal to 400 mg per day from the start of treatment had insignificant reductions in DCO and did not develop symptoms.
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