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Thalidomide-Induced Sinus Bradycardia

PharmD Student, Thomas J Long School of Pharmacy, University of the Pacific, Stockton, CA

Susan S Yu, BS

PharmD Student, Thomas J Long School of Pharmacy, University of the Pacific

Audrey J Lee, PharmD BCPS

Associate Professor of Pharmacy Practice, Thomas J Long School of Pharmacy, University of the Pacific; Clinical Specialist, Internal Medicine, VA Medical Center, San Francisco, CA

Teresa B Chiao, PharmD

Drug Information Clinical Specialist, VA Medical Center, San Francisco; Adjunct Faculty, Thomas J Long School of Pharmacy, University of the Pacific

Reprints: Audrey J Lee PharmD BCPS, Pharmacy Department (119), VA Medical Center, San Francisco, CA 94121-1545, FAX 415/750-2055, E-mail audrey.lee{at}med.va.gov

OBJECTIVE: To report a case of thalidomide-induced sinus bradycardia in an elderly man.

CASE SUMMARY: A 72-year-old white man, with transfusion-dependent refractory anemia with ringed sideroblasts and hypertension treated with atenolol, was started on thalidomide 100 mg at bedtime. During the dose titration period (maximum dose 400 mg/d), his heart rate decreased from a baseline of 63 beats/min to as low as 44 beats/min with positive electrocardiogram findings of sinus bradycardia. After discontinuation of atenolol, the patient's heart rate increased to 68 beats/min, but symptoms of bradycardia persisted. Due to the patient's continued dizziness and lightheadedness, thalidomide was discontinued. In the 3 months following discontinuation of thalidomide, the patient's heart rate increased to an average of 74 beats/min.

DISCUSSION: Clinical trials and postmarketing surveillance suggest that the incidence of thalidomide-induced bradycardia is low. The mechanism of this effect is unknown. Concurrent medications affecting the heart rate may also increase the risk of thalidomide-induced bradycardia. Following titration of thalidomide to a maximum dose of 400 mg/d, our patient's heart rate decreased markedly, resulting in intermittent symptoms of lightheadedness and dizziness. He may have been at higher risk of thalidomide-induced bradycardia because of concurrent administration of atenolol. An objective causality assessment revealed that the adverse event was probable.

CONCLUSIONS: Despite the low incidence of thalidomide-induced bradycardia, it appears to be an important adverse effect, particularly in patients with comorbidities or concurrent medications that decrease heart rate. Therefore, providers should monitor these patients closely for signs and symptoms of bradycardia during the administration of thalidomide.

Key Words: bradycardia, thalidomide

Published Online, May 30, 2003. www.theannals.com, DOI 10.1345/aph.1D003

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