Abstract
Drug-induced torsade de pointes arrhythmia (TdP) is frequently seen in patients. This proarrhythmia is not restricted to anti-arrhythmics but includes a variety of drugs. A genetic predisposition is an attractive explanation for this clinical problem. In this review, we: 1) explain the arrhythmogenic mechanisms of TdP, 2) provide data for a genetic cause based upon mutations in the long QT or in cytochrome genes responsible for drug metabolism, and 3) present pathology-based electrical remodeling as an alternative explanation. It can be concluded that the current evidence for a genetic basis for drug-induced TdP is weak.
MeSH terms
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Animals
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Anti-Arrhythmia Agents / adverse effects
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Anti-Arrhythmia Agents / metabolism
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Arrhythmias, Cardiac / chemically induced
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Arrhythmias, Cardiac / genetics
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Arrhythmias, Cardiac / physiopathology*
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Cytochrome P-450 Enzyme System / genetics
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Cytochrome P-450 Enzyme System / metabolism
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Dogs
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Electrocardiography
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Long QT Syndrome / chemically induced
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Long QT Syndrome / genetics
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Long QT Syndrome / physiopathology
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Mutation
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Sulfonamides / adverse effects
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Sulfonamides / metabolism
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Torsades de Pointes / chemically induced
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Torsades de Pointes / genetics
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Torsades de Pointes / physiopathology
Substances
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Anti-Arrhythmia Agents
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Sulfonamides
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ibutilide
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Cytochrome P-450 Enzyme System