Long QT Syndrome pathophysiology: Difference between revisions
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The two most common types of LQTS are genetic and drug-induced. Genetic LQTS can arise from mutation to one of several genes. These mutations tend to prolong the duration of the [[ventricular action potential]] (APD), thus lengthening the QT interval. LQTS can be inherited in an [[autosomal dominant]] or an [[autosomal recessive]] fashion. The autosomal recessive forms of LQTS tend to have a more severe[[phenotype]], with some variants having associated [[syndactyly]] (LQT8) or congenital neural deafness (LQT1). A number of specific genes loci have been identified that are associated with LQTS. | |||
==References== | ==References== | ||
Revision as of 04:53, 24 August 2012
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Long QT Syndrome Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Long QT Syndrome pathophysiology On the Web |
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American Roentgen Ray Society Images of Long QT Syndrome pathophysiology |
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Risk calculators and risk factors for Long QT Syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Pathophysiology
Genetics
The two most common types of LQTS are genetic and drug-induced. Genetic LQTS can arise from mutation to one of several genes. These mutations tend to prolong the duration of the ventricular action potential (APD), thus lengthening the QT interval. LQTS can be inherited in an autosomal dominant or an autosomal recessive fashion. The autosomal recessive forms of LQTS tend to have a more severephenotype, with some variants having associated syndactyly (LQT8) or congenital neural deafness (LQT1). A number of specific genes loci have been identified that are associated with LQTS.