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Defective cardiac ion channels: from mutations to clinical syndromes
Colleen E. Clancy, Robert S. Kass
Colleen E. Clancy, Robert S. Kass
Published October 15, 2002
Citation Information: J Clin Invest. 2002;110(8):1075-1077. https://doi.org/10.1172/JCI16945.
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Defective cardiac ion channels: from mutations to clinical syndromes

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Authors

Colleen E. Clancy, Robert S. Kass

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Figure 3

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Cellular electrical abnormalities and their relation to changes in the E...
Cellular electrical abnormalities and their relation to changes in the ECG. (Left) At fast pacing (heart) rates, mutation-induced changes in epicardial AP morphologies (thick line) cause dispersion of plateau potentials and a voltage gradient (∇Vm, arrow) (WT, thin line). This gradient will manifest on the ECG as ST segment elevation, indicative of BrS. (Middle) Mutations may prolong APD in M cells (thick line) compared to WT (thin line). The delay in repolarization (ΔAPD ∼ 60ms) is reflected as QT prolongation on the ECG, a hallmark of LQTs. (Right) A rightward shift in the Na+ channel activation curve is sufficient to reduce AP upstroke and slow cardiac impulse conduction (wide QRS segment) as observed in ICCD. WT, wild-type.

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