September 21, 1998Circulation ResearchOpen Access

Inhibition of Cardiac Delayed Rectifier K ⁺ Current by Overexpression of the Long-QT Syndrome HERG G628S Mutation in Transgenic Mice

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Structured PICO

Population

Transgenic mice expressing high myocardial levels of LQT2-associated HERG mutation (G628S) (n=80) and wild-type mice

Intervention

Overexpression of the long-QT syndrome HERG G628S mutation

Comparator

Wild-type mice

Outcome

Cardiac delayed rectifier K+ current (IKr), action potential duration, and ECG intervals (including QT duration)surrogate

The HERG G628S mutation exerts a dominant negative effect on endogenous IKr in vivo, causing prolonged repolarization in isolated myocytes but not QT prolongation in intact mice.

Discussion

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Implication

Isolated myocyte APD changes may not predict ECG findings in intact animals; leaves open compensatory mechanisms in repolarization reserve.

Cite This Study

Babij et al. (1998) studied this question.

synapsesocial.com/papers/6a0f9dcad03631df9ce9ccdf https://doi.org/10.1161/01.res.83.6.668

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Implication

Isolated myocyte APD changes may not predict ECG findings in intact animals; leaves open compensatory mechanisms in repolarization reserve.