This review summarizes the molecular mechanisms underlying susceptibility to arrhythmias in long QT syndrome, including the role of DNA single nucleotide polymorphisms.
This review provides an overview of the molecular basis of long QT syndrome and its association with other primary electrical diseases of the heart.
Recent studies of the molecular basis of the long QT syndrome (LQTS) have advanced our understanding of the mechanisms responsible for the abnormal prolongation of ventricular repolarization and revealed associations between LQTS and other primary electrical diseases of the heart such as Brugada syndrome. The role of DNA single nucleotide polymorphisms in acquired LQTS and differences between the Romano-Ward and Jervell-Lange-Nielsen forms of congenital LQTS are gradually coming into focus. In this brief review, our goal is to summarize the molecular mechanisms proposed to underlie the susceptibility to arrhythmias in LQTS and discuss the direction of current and future research.
Dumaine et al. (Tue,) conducted a review in Long QT syndrome. This review summarizes the molecular mechanisms underlying susceptibility to arrhythmias in long QT syndrome, including the role of DNA single nucleotide polymorphisms.
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