P. T. Pollak,1 P. A. Tourin2; 1University of Calgary, Calgary, AB, Canada, 2University of Alberta, Edmonton, AB, Canada

BACKGROUND: Amiodarone (Amio) is the most effective drug for atrial fibrillation, but pulmonary toxicity (APT) is a commonly cited concern. We analyzed serial pulmonary function tests (PFT) in patients taking Amio.

METHODS: 62 patients, mean age 64 y, monitored for > 24 mo, after loading with 600 - 1600 mg/d for 7-14 d, then maintained with 200-400 mg/d. Serum [Amio] and desethylamiodarone [DEA], were measured at 0, 0.5, 1, 2, 3, 4, 6, 9,12, 18, 24 mo. Forced Vital Capacity (FVC, L), Forced Expiratory Volume (FEV-1, L) and Diffusion Capacity for CO (DCO, mL/min/mmHg) were measured at each visit. Subclinical APT was defined as a 30% drop in pulmonary function for > 2 visits.

RESULTS: Mean [Amio] peaked at 1.84 ± 0.94 mg/L by 2 wk, then fell to 1.37 ± 0.65 mg/L by 3 mo. Mean [DEA], peaked at 1.25 ± 0.69 mg/L at 12 mo, then fell to 0.98 ± 0.46 mg/L by 30 mo. Mean FVC and FEV-1 did not change from baseline. Mean DCO fell from 19.7 ± 6.8 at baseline to 17.9 ± 6.9 at 3 mo and no further over time. Only 3 patients (4.8%) developed subclinical APT. All resolved without intervention and mean DCO recovered to > 70% of baseline by 24 mo.

CONCLUSION: FVC and FEV1 do not change with Amio exposure. DCO initially declines, suggesting a possible effect on lipid composition of lung surfactant. Lack of correlation with [Amio] suggests maximum lipid effect is reached at low [Amio] with no evidence of further effect over time at stable [Amio]. At several multiples of clinically useful concentrations, Amio causes toxicity in pulmonary cell cultures. Adjusting dosing to maintain [Amio] within a range of 1 - 2 mg/L should avoid toxicity while remaining effective. Routine PFT’s did not provide any predictive information, suggesting it only need be recorded at baseline and repeated as infrequently as q2 y and when there is a clinical change in pulmonary function.