2017
DOI: 10.1177/0269881116684337
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Psychotropic drugs and ventricular repolarisation: The effects on QT interval, T-peak to T-end interval and QT dispersion

Abstract: Treatment with psychotropic drugs influences TpTe and QT dispersion. These parameters might be considered to better estimate the sudden cardiac death risk related to specific medications. Beyond antipsychotics and antidepressants, mood stabilisers determine significant effects on ventricular repolarisation.

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Cited by 28 publications
(28 citation statements)
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“…A prolonged QTc interval was observed in our study in 7.6% of the patients, but only one case had a QTc interval ⩾500 ms, which is the threshold considered to be a strong predictor of drug’s risk to cause torsades de pointes in both sexes. 30 This prevalence is consistent with the observed rates of QTc prolongation reported in the main studies performed in hospitalized psychiatric patients, with the majority of the values ranging between 2% and 17%, 10,23,25–27,3143 but up to 38% in some studies. 33,44 In somatic inpatients, the prevalence of QTc prolongation seems to be higher than in psychiatric inpatients, with rates varying between 22% and 35%.…”
Section: Discussionsupporting
confidence: 90%
“…A prolonged QTc interval was observed in our study in 7.6% of the patients, but only one case had a QTc interval ⩾500 ms, which is the threshold considered to be a strong predictor of drug’s risk to cause torsades de pointes in both sexes. 30 This prevalence is consistent with the observed rates of QTc prolongation reported in the main studies performed in hospitalized psychiatric patients, with the majority of the values ranging between 2% and 17%, 10,23,25–27,3143 but up to 38% in some studies. 33,44 In somatic inpatients, the prevalence of QTc prolongation seems to be higher than in psychiatric inpatients, with rates varying between 22% and 35%.…”
Section: Discussionsupporting
confidence: 90%
“…QTD and the QTD ratio (divided by cycle length and expressed as a percentage) in patients with acute myocardial infarction exhibiting ventricular fibrillation were significantly higher relative to those observed in patients with unstable angina [13]. It has been reported that methadone led to modest increases in QTD and TpTe [5,8]. The TpTe was associated with increased mortality (a cut-off value of 100 ms) [14].…”
Section: Effects Of Methadone On Cardiac Repolarizationmentioning
confidence: 92%
“…Similar to TpTe, the TpTe/QT ratio is considered as a crucial marker of TDR and a noninvasive arrhythmogenic index of sudden cardiac death [6]. A previous study reported that TpTe was prolonged by methadone [8]. However, it is important to note that most previous studies involved patients with opioid dependency but not cancer.…”
Section: Introductionmentioning
confidence: 99%
“…34 IGF-1 increases both the activity and the expression of hEAG channels through an AKT-dependent pathway, 195 and restoration of depressed hERG channel function is proposed as a mechanism for insulin treatment of abnormal QT prolongation and associated arrhythmias in diabetic rabbits. 196 Although some HDAC inhibitors have also been reported to inhibit hERG channel through complex transcriptional changes of genes required for ion channel trafficking, 197 there is no evidence that VPA (discussed above) prolongs the QT interval [198][199][200] and therefore, by inference, does not inhibit the hERG channel.…”
Section: Potential Use In Oncologymentioning
confidence: 99%