RESUMEN
Citalopram is a selective serotonin reuptake inhibitor with a favorable cardiac-safety profile. Corrected QT interval (QTc) prolongation and cardiac arrhythmias have not been previously reported in association with citalopram use except in the presence of overdose, abnormal electrolyte values, or renal or liver failure. Herein, we report the case of a 40-year-old woman with mental depression who presented with a prolonged QTc interval and torsades de pointes after the initiation of citalopram at therapeutic doses. The QTc interval improved when citalopram therapy was discontinued. We recommend that clinicians investigate the family history for sudden deaths and perform baseline electrocardiography before prescribing citalopram. We also recommend routine electrocardiographic testing during citalopram therapy, and that patients with long QT syndrome avoid taking citalopram.
Asunto(s)
Antidepresivos de Segunda Generación/efectos adversos , Citalopram/efectos adversos , Depresión/tratamiento farmacológico , Sistema de Conducción Cardíaco/efectos de los fármacos , Inhibidores Selectivos de la Recaptación de Serotonina/efectos adversos , Torsades de Pointes/inducido químicamente , Adulto , Antidepresivos Tricíclicos/uso terapéutico , Sustitución de Medicamentos , Electrocardiografía , Femenino , Sistema de Conducción Cardíaco/fisiopatología , Humanos , Mianserina/análogos & derivados , Mianserina/uso terapéutico , Mirtazapina , Valor Predictivo de las Pruebas , Factores de Tiempo , Torsades de Pointes/diagnóstico , Torsades de Pointes/fisiopatologíaRESUMEN
Elevated catecholamine levels are a well-recognized cause of various types of cardiomyopathy. Causes of catecholamine elevation include tumors, toxins, drugs, emotional stress, and sepsis. Milnacipran is a dual and equipotent inhibitor of norepinephrine and serotonin uptake. It is frequently prescribed as therapy for fibromyalgia, and the drug has a good safety profile. Herein, we report the case of a 42-year-old woman with undefined connective-tissue disease and fibromyalgia who developed a severe and reversible cardiomyopathy while taking recommended doses of milnacipran. The cardiomyopathy was associated with a hyperadrenergic state manifested by tachycardia, hypertension, and elevated plasma catecholamine levels. The discontinuation of milnacipran and the initiation of anti-failure therapy resulted in complete resolution of the cardiomyopathy in 6 months. To our knowledge, this is the first report of milnacipran as a possible cause of catecholamine-induced cardiomyopathy.