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PGY-III Resident Creighton–Nebraska Psychiatry Residency Program 3528 Dodge Street Omaha, Nebraska 68131-8200 fax 402/345-8815 sriramrr{at}rocketmail.com
Staff Psychiatrist Omaha Veterans Affairs Medical Center Assistant Professor of Psychiatry University of Nebraska Medical Center Omaha
Assistant Professor of Psychiatry and Associate Director of Residency Training School of Medicine Creighton University Staff Psychiatrist Omaha Veterans Affairs Medical Center
Professor of Psychiatry and Vice Chair for Research School of Medicine Creighton University Associate Chief Department of Mental Health and Behavioral Sciences Omaha Veterans Affairs Medical Center
Published Online, June 1, 2004. www.theannals.com, DOI 10.1345/aph.1E020
Case Report. A 48-year-old white man presented with depressed mood, loss of interest, decreased energy, decreased concentration, fatigue, decreased appetite, loss of libido, and insomnia. These symptoms started approximately 4 months after he began taking sotalol 80 mg twice daily. There were no signs or symptoms of drug toxicity such as orthopnea, fluid retention, or confusion. Laboratory tests, including thyroid function tests, were normal. No new psychosocial stressors were identified. There was no comorbid anxiety disorder. Approximately one year earlier, the patient became depressed while on amiodarone therapy, which resolved with amiodarone discontinuation. There was no history of psychiatric treatment or illicit drug use, as well as prescription or herbal medications abuse.
The patient's medical history was significant for myocardial infarction, coronary artery bypass surgery, monomorphic ventricular tachycardia, anticardiolipin antibody syndrome, hyperlipidemia, hypertension, and right upper extremity neuropathy. Approximately 2 years ago, he received an implantable cardioverter-defibrillator (ICD). His medications at the time of assessment included sotalol, warfarin, ramipril, loratadine, aspirin, methadone, and alprazolam. Alprazolam was prescribed to control occasional nocturnal jerky movements of his right hand. Although the man became depressed on sotalol therapy, the drug was continued as the ICD was not controlling the arrhythmia. Subsequently, citalopram was initiated; however, his depressive symptoms persisted.
Discussion. Sotalol is a class III antiarrhythmic drug that, in addition to increasing action potential duration by blocking potassium channels, also antagonizes ß-adrenergic receptors. Amiodarone is also a class III antiarrhythmic. Both drugs are efficacious in ventricular and supraventricular tachyarrhythmias. The suggested mechanisms for ß-blocker–induced depression include inhibitory effects on central nervous system ß and serotonin receptors. Although lipophilic ß-blockers have been suggested to cause more depression, in the above case, sotalol, a lipophobic agent, probably caused the depression.
The development of depression in patients on amiodarone and sotalol therapy suggests that a common pathway may be involved in causing depression. Both amiodarone and sotalol attenuate adrenergic stimulation and have antisympathetic actions. It has been suggested that depression may be caused by deregulation of the noradrenergic system.3 This might explain the depression related to sotalol therapy in our patient.
Use of the Naranjo probability scale indicated a possible relationship between depression and sotalol therapy in this patient.4 At the time of assessment, the patient was taking depressants such as alprazolam and methadone (for treatment of upper extremity neuropathy). There is also some evidence that an ICD can cause anxiety and depression.5 However, since the ICD, alprazolam, and methadone were initiated 2 years prior to the development of depression, it is unlikely that they contributed to the current episode.
Although this case report does not offer conclusive evidence, clinicians should be aware of this possible adverse effect with sotalol therapy until better data become available.
References
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