Electrocardiographic changes in patients receiving neuroleptic medication

Abstract

The precise aetiology of sudden death in patients receiving neuroleptic medication is uncertain, but cardiac arrhythmias are a possible cause. We investigated the link between neuroleptic medication and electrocardiographic changes predictive of malignant cardiac arrhythmias. Electrocardiographs were performed on 111 patients receiving neuroleptic medication and on 42 unmedicated controls. Prolonged QTc intervals were more common in the patient sample, but QTc dispersion was not significantly increased. QTc interval prolongation was more likely in patients on doses above 2000 mg chlorpromazine equivalents daily (odds ratio 4.28, P < 0.02). Neuroleptic medication, especially at high doses, is associated with ECG changes that may herald more serious cardiac problems.

Cardiac side effects of psychiatric drugs

“…Data regarding the other typical agents are inconclusive, although several other studies have reported QT interval prolongation in patients receiving a variety of typical agents, even at conventional doses (Kitayama et al, 1999;Warner et al, 1996). A study of 65 patients taking antipsychotic drugs from the North East of England reported that only 2 (3%) of patients had a prolonged QT c interval .…”

Hidden Cardiac Lesions and Psychotropic Drugs as a Possible Cause of Sudden Death in Psychiatric Patients: A Report of 14 Cases and Review of the Literature

“…Arrhythmias are primarily a result of alterations in cardiocyte membrane ion transfers, which produce ECG changes; alterations include widening of QRS complexes, which can result in slowed intraventricular conduction, favouring the onset of reentry arrhythmias, ventricular tachycardia or fibrillation, changes in T waves, prolongation of the QT interval, and torsades de pointes (4,15,16).…”

Recent studies on ECG changes, antipsychotic use and sudden death in psychiatric patients

“…These effects are unrelated to brain receptor binding profiles. What these drugs have in common is an action to prolong cardiac repolarisation via blockade of the delayed rectifier potassium channel (l kr ) within the heart (Yap & Camm, 2000). The cloning of the humaǹ ether-a-go-go' (HERG) gene that encodes for this channel has resulted in studies confirming the specific l kr blocking potential of haloperidol, droperidol, pimozide and sertindole.…”

“…Although increasing antipsychotic dose has been linked to QT prolongation in psychiatric patients (Warner et al, 1996), other factors may operate, creating high-risk groups who develop QT prolongation and arrhythmias even at low doses. Old age, female gender and pre-existing ischaemic heart disease are all likely to increase risk.…”