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LONG-QT SYNDROME (LQTS) results from structural abnormalities in
the potassium channels of the heart, which predispose affected
persons to an accelerated heart rhythm (arrhythmia). This can lead
to sudden loss of consciousness and may cause sudden cardiac
death in teenagers and young adults who are faced with stressors
ranging from exercise to loud sounds.
LQTS is usually inherited as an autosomal dominant trait. In the
case of LQT1, which has been mapped to chromosome 11,
mutations lead to serious structural defects in the person's cardiac
potassium channels that do not allow proper transmission of the
electrical impulses throughout the heart. There also appear to be
other genes, tentatively located on chromosomes 3, 6 and 11
whose mutated products may contribute to, or cause, LQT
syndrome.
Beta blockers are used to treat the symptoms of the disease, and
appear to be effective in some symptomatic
patients. However, common sense therapies such as avoiding
strenuous physical exercise and other stressors are also effective.
Research on how the genes discussed above interact with each
other should encourage the development of new treatments for
long-QT syndrome.