The molecular basis of long QT syndrome and prospects for therapy

Qing Wang, Neil E. Bowles, Jeffrey A. Towbin

Research output: Contribution to journalReview article

23 Citations (Scopus)

Abstract

Long QT syndrome (LQT) is a cardiac disorder that causes sudden death from ventricular tachyarrhythmias, specifically torsade de pointes. Two types of LQT have been reported, autosomal-dominant LQT (Romano-Ward syndrome) and autosomal-recessive LQT (Jervell and Lange-Nielsen syndrome); Jervell and Lange-Nielsen syndrome is also associated with deafness. Four LQT genes have been identified for autosomal-dominant LQT: K+ channel genes KVLQT1 on chromosome 11p15.5, HERG on 7q35-36 and minK on 21q22, and the cardiac Na+ channel gene SCN5A on chromosome 3p21-24. Two genes, KVLQT1 and minK, have been identified for Jervell and Lange-Nielsen syndrome. Genetic testing and gene-specific therapies are available for some LQT patients.

Original languageEnglish (US)
Pages (from-to)382-388
Number of pages7
JournalMolecular Medicine Today
Volume4
Issue number9
DOIs
StatePublished - Sep 1 1998

Fingerprint

Long QT Syndrome
Jervell-Lange Nielsen Syndrome
Mink
Therapeutics
Genes
Romano-Ward Syndrome
Chromosomes
Torsades de Pointes
Genetic Testing
Deafness
Sudden Death
Tachycardia
Genetic Therapy
Cause of Death

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Genetics

Cite this

The molecular basis of long QT syndrome and prospects for therapy. / Wang, Qing; Bowles, Neil E.; Towbin, Jeffrey A.

In: Molecular Medicine Today, Vol. 4, No. 9, 01.09.1998, p. 382-388.

Research output: Contribution to journalReview article

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