The long QT syndromes: genetic basis and clinical implications.

@article{Chiang2000TheLQ,
  title={The long QT syndromes: genetic basis and clinical implications.},
  author={Chern-en Chiang and Dan M. Roden},
  journal={Journal of the American College of Cardiology},
  year={2000},
  volume={36 1},
  pages={1-12}
}
It is becoming clear that mutations in the KVLQT1, human "ether-a-go-go" related gene, cardiac voltage-dependent sodium channel gene, minK and MiRP1 genes, respectively, are responsible for the LQT1, LQT2, LQT3, LQT5 and LQT6 variants of the Romano-Ward syndrome, characterized by autosomal dominant transmission and no deafness. The much rarer Jervell-Lange-Nielsen syndrome (with marked QT prolongation and sensorineural deafness) arises when a child inherits mutant KVLQT1 or minK alleles from… CONTINUE READING

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The much rarer Jervell - Lange - Nielsen syndrome ( with marked QT prolongation and sensorineural deafness ) arises when a child inherits mutant KVLQT1 or minK alleles from both parents .
The much rarer Jervell - Lange - Nielsen syndrome ( with marked QT prolongation and sensorineural deafness ) arises when a child inherits mutant KVLQT1 or minK alleles from both parents .
The much rarer Jervell - Lange - Nielsen syndrome ( with marked QT prolongation and sensorineural deafness ) arises when a child inherits mutant KVLQT1 or minK alleles from both parents .
The much rarer Jervell - Lange - Nielsen syndrome ( with marked QT prolongation and sensorineural deafness ) arises when a child inherits mutant KVLQT1 or minK alleles from both parents .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
Polymorphic ventricular tachycardia ( torsade de pointes ) is thought to be initiated by early after - depolarizations in the Purkinje system and maintained by reentry in the myocardium .
It is becoming clear that mutations in the KVLQT1 , human " ether - a - go - go " related gene , cardiac voltage - dependent sodium channel gene , minK and MiRP1 genes , respectively , are responsible for the LQT1 , LQT2 , LQT3 , LQT5 and LQT6 variants of the Romano - Ward syndrome , characterized by autosomal dominant transmission and no deafness .
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