June 1, 2000Journal of Cardiovascular Electrophysiology
Evidence for a Cardiac Ion Channel Mutation Underlying Drug‐Induced QT Prolongation and Life‐Threatening Arrhythmias
Key result
Mutational analysis of a patient with cisapride-induced cardiac arrest revealed a heterozygous KvLQT1 mutation, demonstrating that drug-induced QT prolongation may depend on a genetic substrate.
Why the study?
Does a genetic mutation in LQTS-related genes underlie drug-induced QT prolongation and life-threatening arrhythmias?
Population
An elderly female patient with documented cardiac arrest related to cisapride and transiently prolonged QT…
Comparison
Mutational analysis of known LQTS-related genes… vs Wild-type (WT) KvLQT1 gene/channel.
Design
Case_report
Authors
Discussion
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Implication
Should not yet change prescribing or testing practices; leaves open whether LQTS mutations underlie select drug-induced events.
Study Design
Type
Case Report (n=3)
Structured PICO
Does a genetic mutation in LQTS-related genes underlie drug-induced QT prolongation and life-threatening arrhythmias?
P
Population
An elderly female patient with documented cardiac arrest related to cisapride and transiently prolonged QT interval, her two adult asymptomatic sons, and Xenopus oocytes used as an in vitro expression system.
I
Intervention
Mutational analysis of known LQTS-related genes and in vitro expression of mutated KvLQT1 protein.
C
Comparator
Wild-type (WT) KvLQT1 gene/channel.
O
Outcome
Identification of genetic mutation and in vitro cellular phenotype (loss of current).surrogate
This study provides evidence that some cases of drug-induced QT prolongation and arrhythmias depend on a genetic substrate, specifically mutations in LQTS-related genes like KvLQT1.
Cite This Study
Napolitano et al. (2000) conducted a case report in Drug-induced QT prolongation and life-threatening arrhythmias (n=3). Mutational analysis of LQTS-related genes was evaluated on Identification of genetic mutation and in vitro cellular phenotype. Mutational analysis of a patient with cisapride-induced cardiac arrest revealed a heterozygous KvLQT1 mutation, demonstrating that drug-induced QT prolongation may depend on a genetic substrate.