CAN AMIODARONE PULMONARY TOXICITY BE PREDICTED IN PATIENTS UNDERGOINGIMPLANTABLE CARDIOVERTER-DEFIBRILLATOR IMPLANTATION

Citation
Hr. Hawthorne et al., CAN AMIODARONE PULMONARY TOXICITY BE PREDICTED IN PATIENTS UNDERGOINGIMPLANTABLE CARDIOVERTER-DEFIBRILLATOR IMPLANTATION, PACE, 16(12), 1993, pp. 2241-2249
Citations number
40
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
16
Issue
12
Year of publication
1993
Pages
2241 - 2249
Database
ISI
SICI code
0147-8389(1993)16:12<2241:CAPTBP>2.0.ZU;2-M
Abstract
Implantable cardioverter defibrillator (ICD) implantation is rapidly b ecoming accepted as primary therapy for malignant ventricular arrhythm ias. Many patients undergoing ICD implantation are on concomitant anti arrhythmic drugs to decrease shock frequency, slow tachycardia rate, a nd suppress supraventricular arrhythmias. Amiodarone is a potent antia rrhythmic agent that is also frequently used in the treatment of patie nts with refractory ventricular arrhythmias. Ten to forty percent of p atients undergoing ICD implantation will also be taking amiodarone. It has been reported to cause pulmonary toxicity in about 5% of patients per year. Acute amiodarone toxicity presenting as adult respiratory d istress syndrome has been reported much less frequently. Although peri operative morbidity due to amiodarone has been described, the risk, pr edictability, and consequences of acute pulmonary toxicity from amioda rone in patients undergoing ICD implantation have not been previously described. We reviewed the records of 99 consecutive patients undergoi ng ICD implantation at our institution from October 1987 to April 1992 . Thirty-nine patients were taking 480 +/-230 mg of amiodarone (median 400 mg, lower 20th percentile 400 mg, upper 80th percentile 800 mg) f or 291 +/- 554 days prior to ICD implantation. Ten patients taking ami odarone developed acute pulmonary toxicity clinically manifesting as d iffuse pulmonary infiltrates on chest radiography and adult respirator y distress syndrome with hypoxia (arterial pO2 < 60 mmHg) without evid ence of pneumonia or elevated pulmonary capillary wedge pressure (PCW less-than-or-equal-to 15 mmHg). Of the 60 patients not taking amiodaro ne none developed adult respiratory distress syndrome. There was no re lationship between the clinical variables of age, type of anesthesia, ejection fraction, dose or duration of amiodarone use, number of intra operative ICD test shocks, operative time, or intraoperative FI(O2). C ompared to patients on amiodarone who did not develop toxicity, patien ts with amiodarone pulmonary toxicity had prolonged intensive care uni t stays (17.1 +/- 16.9 days vs 3.5 +/- 1.5 days, P < 0.001), as well a s prolonged ventilator dependence (9.1 +/- 18.7 days vs 0.9 +/- 1.1 da ys, P = 0.02). Acute amiodarone pulmonary toxicity resulted in a widel y variable clinical syndrome that occurred 1-5 days after surgery. In conclusion, pulmonary toxicity was not predicted by clinical or hemody namic variables, results in markedly prolonged ventilator dependence a nd intensive care unit stays, and may result in death.