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SARAH E. BUSH, PHARM.D., is Clinical Specialist, Pharmacy Services, Greenville Hospital System, Greenville, SC; at the time of this study she was Pharmacy Practice Resident, Shands at the University of Florida (SUF), Gainesville. RANDY C. HATTON, PHARM.D., FCCP, BCPS, is Co-Director, Drug Information and Pharmacy Resource Center, SUF, and Clinical Professor, College of Pharmacy, University of Florida, Gainesville. ALMUT G. WINTERSTEIN, PH.D., is Associate Professor, Pharmaceutical Outcomes and Policy, Department of Healthcare Administration, College of Pharmacy, and Associate Professor, Department of Epidemiology and Biostatistics, College of Public Health and Health Professions, University of Florida. MARGARET R. THOMSON, PHARM.D., BCPS, is Clinical Specialist, Anticoagulation Services, Saint Thomas Hospital, Nashville, TN; at the time of writing she was Clinical Specialist, Cardiac Intensive Care Unit, Department of Pharmacy Services, SUF. GREGORY W. WOO, M.D., is Assistant Professor of Medicine, College of Medicine, University of Florida.

Address correspondence to Dr. Bush at Pharmacy Services, Greenville Hospital System, 701 Grove Road, Greenville, SC 29605 (sbush{at}ghs.org).

Purpose. The effects of concomitant amiodarone and haloperidol on Q-Tc interval prolongation were studied. Methods. All adult patients admitted to a 618-bed tertiary referral teaching hospital between January 1, 2005, and December 31, 2006, who received amiodarone and haloperidol concomitantly were included in this retrospective descriptive analysis. Data collected to assess patients’ risk of developing Q-T interval prolongation included age, sex, past medical history, and number of days of concomitant exposure. Data relevant for the assessment of cardiac effects were collected for the time period between 24 hours before and after the administration of haloperidol and included laboratory test values, use of other Q-T interval-prolonging drugs, heart rate, Q-Tc intervals, and clinical documentation of arrhythmia. To determine change in the Q-Tc interval, Q-T and R-R values were recorded using cardiac rhythm strips or electrocardiogram. Nurses’ and physicians’ records were reviewed to determine if an arrhythmia occurred. Descriptive statistics were used to analyze baseline patient information and Q-Tc interval data. Results. A total of 49 patients met inclusion criteria, yielding 381 distinct amiodarone–haloperidol exposures. During 138 (36.2%) of 381 haloperidol–amiodarone exposures, patients received at least one additional Q-T interval-prolonging drug. When amiodarone–haloperidol exposures were grouped by the number of concomitant Q-T prolonging drugs, no apparent association was detected between longer Q-Tc intervals and an increased number of concomitant Q-T interval-prolonging drugs. Conclusion. A small, potentially significant Q-Tc interval prolongation, but not ventricular arrhythmia, was observed in adult patients who received a concomitant administration of amiodarone and haloperidol at a tertiary referral teaching hospital. Index terms: Amiodarone; Antipsychotic agents; Cardiac drugs; Drug interactions; Electrocardiography; Haloperidol; Toxicity

 

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				J. G. Cherry, S. Bush, R. C. Hatton, and A. G. Winterstein Interpreting data about prolongation of the Q-Tc interval induced by amiodarone and haloperidol Am. J. Health Syst. Pharm., July 15, 2009; 66(14): 1254 - 1255. [Full Text] [PDF]