Drug-Induced Torsade de Pointes: From Molecular Biology to Bedside

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A progressively increasing number of cardiac and noncardiac drugs prolong the ventricular action potential duration(QT interval of the electrocardiogram)and cause a distinctive polymorphic ventricular tachycardia termed torsades de pointes(TdP)that can degenerate into ventricular fibrillation and sudden cardiac death.Drugs prolong the QT interval and cause TdP by blocking cardiac K<SUP>+</SUP> channels in general and selectively blocking the rapidly activating delayed rectifier channel I<SUB>Kr</SUB>.Coassembly of HERG(human−ether−ago−go−related gene)α−subunits and MiRP1(MinK−related peptide 1)β−subunits recapitulate the behavior of native human I<SUB>Kr</SUB> and mutations of HERG and MiRP1 decrease the repolarizing current, delay ventricular repolarization and prolong the QT.Thus, drug−induced QT prolongation and TdP might represent an iatrogenic reproduction of the congenital LQTS.In patients with silent forms of the congenital LQTS associated with mutations in I<SUB>Kr</SUB>, arrhythmic symptoms developed almost exclusively after exposure to QT−prolonging drugs.This review centers on the possible cellular mechanisms underlying drug−induced QT prolongation and TdP, the description of specific drugs and risk factors facilitating the development of TdP, and the recommendations for preventing and treating this potentially fatal arrhythmia.

収録刊行物

  • The Japanese journal of pharmacology

    The Japanese journal of pharmacology 83(1), 1-19, 2000-05-01

    公益社団法人 日本薬理学会

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被引用文献:  14件中 1-14件 を表示

各種コード

  • NII論文ID(NAID)
    10008184072
  • NII書誌ID(NCID)
    AA00691188
  • 本文言語コード
    ENG
  • 資料種別
    REV
  • ISSN
    00215198
  • NDL 記事登録ID
    5399678
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  CJP引用  NDL  J-STAGE 
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