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  <record>
   <ref-type name="Journal Article">17</ref-type>
   <contributors>
    <authors/>
   </contributors>
   <titles>
    <title></title>
   </titles>
   <dates>
    <year>2022</year>
    <pub-dates>
     <date>2023-01-09</date>
    </pub-dates>
   </dates>
   <doi>10.3390/ijms232415786</doi>
   <abstract>Antipsychotics (AP) induced prolongation of the QT interval in patients with schizophrenia&#13;
(Sch) is an actual interdisciplinary problem as it increases the risk of sudden death syndrome. Long&#13;
QT syndrome (LQTS) as a cardiac adverse drug reaction is a multifactorial symptomatic disorder,&#13;
the development of which is influenced by modifying factors (APs’ dose, duration of APs therapy,&#13;
APs polytherapy, and monotherapy, etc.) and non-modifying factors (genetic predisposition, gender,&#13;
age, etc.). The genetic predisposition to AP-induced LQTS may be due to several causes, including&#13;
causal mutations in the genes responsible for monoheme forms of LQTS, single nucleotide variants&#13;
(SNVs) of the candidate genes encoding voltage-dependent ion channels expressed both in the brain&#13;
and in the heart, and SNVs of candidate genes encoding key enzymes of APs metabolism. This&#13;
narrative review summarizes the results of genetic studies on AP-induced LQTS and proposes a&#13;
new personalized approach to assessing the risk of its development (low, moderate, high). We&#13;
recommend implementation in protocols of primary diagnosis of AP-induced LQTS and medication&#13;
dispensary additional observations of the risk category of patients receiving APs, deoxyribonucleic&#13;
acid profiling, regular electrocardiogram monitoring, and regular therapeutic drug monitoring of the&#13;
blood APs levels.</abstract>
   <urls>
    <web-urls>
     <url>https://repo.bashgmu.ru/publication/3885</url>
    </web-urls>
    <pdf-urls>
     <url>https://repo.bashgmu.ru/files/4061</url>
    </pdf-urls>
   </urls>
  </record>
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