Ziprasidone induced symptomatic bradycardia: a case report

Correspondence Ziprasidone induced symptomatic bradycardia: a case report DOI: 10.3109/00048674.2011.585456 Vikas Menon, Shivanand Kattimani, Sugaparaneetharan Ayyanar, Department of Psychiatry, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry-605006, India A 25 year old male was admitted with symptoms of psychoses for 6 months duration. Physical examination showed a resting pulse rate of 84/min, BP was 120/80 mmHg. Systemic examination was unremarkable. Routine blood counts, biochemistry and metabolic screening including liver and renal function tests were within normal limits. As he developed side effects to oral risperidone (weight gain) and oral haloperidol (extrapyramidal symptoms) in sequential trials, oral ziprasidone was initiated. Initially the patient showed good response and was discharged on 80 mg ziprasidone. After 2 weeks he had to be readmitted for symptomatic worsening and ziprasidone was increased to 100 mg. The following day he complained of light-headedness and inability to stand/walk. On examination, his pulse rate was 58/min and BP was 100/60 mmHg. ECG showed a QTc interval of 402 ms. Since the bradycardia was temporally related to the increase in dose, we decided to stop ziprasidone treatment. Currently with oral aripiprazole his symptoms are well controlled. This case, wherein tolerability issues with various antipsychotics prompted a search for an agent with lesser

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extrapyramidal symptoms and better metabolic profile, is in our experience an increasingly common one. As per the Naranjo Adverse Drug Reaction Probability scale [1] the association of bradycardia with ziprasidone is classified as probable. Such a reaction has been reported with various atypical agents [2,3]. Snarr et al. have recently reported a similar case with oral ziprasidone [4]. The mechanisms postulated for antipsychotic-induced bradycardia include a possible action on ventricular myocyte K⫹ channels for risperidone [2]. Other probable mechanisms may include 5-HT1A mediated preganglionic mechanisms and autonomic nervous system modulations [5]. Further studies on the role of 5-HT1A receptor and effect of antipsychotics on the electrophysiology of the heart would be in order. We hope this case will alert clinicians to look specifically for bradycardia while using oral ziprasidone. References 1. Naranjo CA, Busto U, Sellers EM et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981; 30:239–245. 2. Goyal RS, Goyal SB. Symptomatic bradyarrythmia secondary to risperidone [letter]. Am J Psychiatry 2003; 160:2243. 3. Chen CC, Tsai JH, Yang P, Chung W. Bradyarrhythmic shock associated with olanzapine [letter]. Aust N Z J Psychiatry 2007; 41:89. 4. Snarr SB, Phan SV, Garner A, VandenBerg MA, Barth SK. Symptomatic bradycardia with oral aripiprazole and oral ziprasidone. Ann Pharmacother 2010; 44:760–763. 5. Jordan D. Vagal control of the heart: central serotonergic (5-HT) mechanisms. Exp Physiol 2005; 90:175–181.