The whimsies of Chiara’s ECG

A plausible explanation

QT interval prolongation, well-known for antipsychotics (http:www.aritmo-project.org), has less evidences in regard to antidepressants.¹ Among antidepressants, monoamine oxidase inhibitors and tricyclics can cause the block of the tardive repolarizing IKr rapid current, prolonging the QT. Higher selectivity of selective serotonin reuptake inhibitors seems to guarantee a safer cardiovascular profile, however dose-dependent QT prolongation has been registered for citalopram and escitalopram;² besides, for fluvoxamine as for other antidepressants, the risk is higher in polytherapy that use antipsychotics and antidepressants.³ The drug inhibits in vitro the hERG potassium channel with consequent reduction of the IKr current.^4,5 The data sheets of medical products containing fluvoxamine do not list QT interval prolongation among the side effects and the active principle does not even appear in the list of drugs that can cause QT prolongation, published by Credible Meds Arizona AZCERT Group. The Italian National Network for Pharmacovigilance collected some reports of cardiologic problems under fluvoxamine therapy, but the case here discussed represents the first report of QT interval prolongation caused by this drug. In literature only two cases of QT prolongation have been reported. The first one concerns a 55 years old woman under neurological and fluvoxamine (150 mg/day) polytherapy; the other case reports increased heart rate and QTc (490 msec) in a 13 years old patient after 4 months of fluvoxamine therapy (75 mg/day).^6,7 Like in our case, the patient was young, with no pre-existent cardiac pathologies and did not use other drugs. For Chiara, however, other relevant aspects need to be considered: there is no concomitant use of other substances and this fact allows us to exclude any possible pharmacological interactions, the administered dose is lower than the one described in literature (50 mg/day), the absence of induced vomit exclude altered drug consumption and the QT prolongation is registered after 4 days of therapy only. Surely, the patient presents some well-known predisposing factors for QT prolongation, that might have contributed, such has female sex, hypokaliemia and hypomagnesiemia,^1,8 most likely derived from the eating disorder which affects the patient,⁹ but none of those had influenced her health state before the intake of fluvoxamine. It should be noted, however, that K and Mg levels are slightly out of range. In the reported case, then, the most suspected cause for the adverse reaction seems to be fluvoxamine. An evaluation of electrocardiographic parameters and cardiovascular risk factors might therefore be conducted both in asymptomatic patients under antidepressant treatment – in order to exclude eventual cardiologic damages due to the ongoing therapy – and in patients who are about to start an antidepressant treatment, in order to choose the most suitable drug based on the risk/benefit report.¹⁰