title: QT is longer in drug-free patients with schizophrenia compared with age-matched healthy subjects.
abstract: The potassium voltage-gated channel KCNH2 is a well-known gene in which mutations induce familial QT interval prolongation. KCNH2 is suggested to be a risk gene for schizophrenia. Additionally, the disturbance of autonomic control, which affects the QT interval, is known in schizophrenia. Therefore, we speculate that schizophrenic patients have characteristic features in terms of the QT interval in addition to the effect of antipsychotic medication. The QT interval of patients with schizophrenia not receiving antipsychotics (n = 85) was compared with that of patients with schizophrenia receiving relatively large doses of antipsychotics (n = 85) and healthy volunteers (n = 85). The QT interval was corrected using four methods (Bazett, Fridericia, Framingham or Hodges method). In ANCOVA with age and heart rate as covariates, patients not receiving antipsychotic treatment had longer QT intervals than did the healthy volunteers, but antipsychotics prolonged the QT interval regardless of the correction method used (P<0.01). Schizophrenic patients with and without medication had a significantly higher mean heart rate than did the healthy volunteers, with no obvious sex-related differences in the QT interval. The QT interval prolongation may be manifestation of a certain biological feature of schizophrenia.
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Kumiko
authors.initials: K
authors.lastname: Fujii
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan; Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
authors.forename: Yuji
authors.initials: Y
authors.lastname: Ozeki
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Okayasu
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Takano
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Takahiro
authors.initials: T
authors.lastname: Shinozaki
authors.affiliation: Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Hori
authors.affiliation: Department of Health Care, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Masami
authors.initials: M
authors.lastname: Orui
authors.affiliation: Department of Cardiovascular and Respiratory Medicine, Shiga University School of Medical Science, Shiga, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Horie
authors.affiliation: Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kunugi
authors.affiliation: Department of Psychiatry, Dokkyo Medical University School of Medicine, Tochigi, Japan.
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Shimoda
mesh_terms: D000328:Adult; D014150:Antipsychotic Agents / Q000627:therapeutic use*; D016022:Case-Control Studies; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012559:Schizophrenia / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D014150:Antipsychotic Agents