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Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome
Colleen E. Clancy, … , Michihiro Tateyama, Robert S. Kass
Colleen E. Clancy, … , Michihiro Tateyama, Robert S. Kass
Published November 1, 2002
Citation Information: J Clin Invest. 2002;110(9):1251-1262. https://doi.org/10.1172/JCI15928.
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Article Cardiology

Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome

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Abstract

Research Article

Authors

Colleen E. Clancy, Michihiro Tateyama, Robert S. Kass

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Figure 5

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Bursting properties of WT and Y1795C mutant channels. (a) Experimental r...
Bursting properties of WT and Y1795C mutant channels. (a) Experimental records of WT (left) and Y1795C (right) channels in a bursting mode. Arrows are included to indicate beginning (left arrow) and termination (right arrow) of channel bursting. Single-channel traces were elicited by depolarization (–30 mV, 100 milliseconds) from a holding potential of –120 mV. Shown are successive sweeps for each construct. (b) Influence of the Y1795C mutation on the latency to burst. The latency to burst was determined by the time to the left-hand arrows shown in a after initiation of pulses. The plots show histograms of the latency to burst (bin size = 20 seconds, see Methods) for WT (left) and Y1795C (right) channels. A single exponential function was fitted to the histogram for Y1795C channels, resulting in the following time constant for burst latency: τin = 280 seconds. A fit was not possible for WT channels (see Methods). (c) Burst mode dwell time was measured as the time between arrows in a. The plots show histograms of burst dwell times (bin size = 500 milliseconds, see Methods) for WT (left) and Y1795C (right) channels. Double exponential functions were fit to these histograms (see text and Table 2 for values).

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