September 5, 2013Circulation Arrhythmia and ElectrophysiologyOpen Access

Selective Targeting of Gain-of-Function KCNQ1 Mutations Predisposing to Atrial Fibrillation

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Population

Heterologous expression systems and cultured adult rabbit left atrial myocytes

Comparison

HMR-1556 (IKs selective blocker) vs Wild-type KCNQ1 channels and cells expressing…

Design

Preclinical

Authors

CCCourtney CampbellMayo Clinic in Arizona JCJonathan D. CampbellNational Health Council CTChristopher H. ThompsonNorthwestern University

Discussion

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Implication

Supports proof-of-principle for genotype-specific IKs blockade in KCNQ1-AF; hypothesis-generating pending human studies.

Structured PICO

Population

Heterologous expression systems (coexpression of KCNQ1-WT or familial atrial fibrillation mutations KCNQ1-S140G/KCNQ1-V141M with KCNE1) and cultured adult rabbit left atrial myocytes

Intervention

HMR-1556 (IKs selective blocker)

Comparator

Wild-type (WT) KCNQ1 channels and cells expressing WT-IKs

Outcome

Electrophysiological properties including potassium current sensitivity to HMR-1556 and action potential durationsurrogate

Gain-of-function KCNQ1 mutations predisposing to atrial fibrillation show enhanced sensitivity to the IKs blocker HMR-1556, providing proof of principle for genotype-specific targeted therapy.

Cite This Study

Campbell et al. (2013) studied this question.

synapsesocial.com/papers/6a768eb0f6749a0058ec1780 https://doi.org/10.1161/circep.113.000439

Topics

Atrial fibrillation Persistent AF management

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Selective Targeting of Gain-of-Function KCNQ1 Mutations Predisposing to Atrial Fibrillation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Selective Targeting of Gain-of-Function KCNQ1 Mutations Predisposing to Atrial Fibrillation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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