The long QT syndrome (LQTS) was first described in 1957 in a family
in which several children with congenital bilateral neural deafness and QT
prolongation on electrocardiogram (ECG) experienced recurrent syncope and
sudden death, with a family pattern that suggested autosomal recessive inheritance
(Jervell and Lange-Nielsen syndrome).1 A similar
and much more common familial disorder with QT prolongation but without deafness
was described a few years later, with family patterns that suggested autosomal
dominant inheritance (Romano-Ward syndrome). These reports highlighted the
familial nature of this QT prolongation disorder, and subsequent studies identified
malignant ventricular arrhythmias as the cause of syncope and sudden death
in patients with LQTS. The molecular-genetic basis of LQTS was discovered
in the 1990s and, currently, mutations have been identified in 7 LQTS genes
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