Key result
IKr inhibition via LQT2 mutation or sotalol administration resulted in a significantly flatter T-amplitude/RR slope compared to LQT1 carriers and healthy individuals (P < 0.05).
Why the study?
Does T-amplitude adaptation to heart rate characterize IKr inhibition in congenital and acquired long QT syndrome?
Population
111 individuals, including 49 LQT1 carriers, 25 LQT2 carriers, and 37 healthy individuals
Comparison
Sotalol 160 mg and 320 mg administered to… vs Healthy individuals off drugs and LQT1 carriers
Design
Cross-sectional
Authors
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May flag IKr inhibition in LQT2 and sotalol-treated patients; hypothesis-generating for ECG marker validation in prospective studies.
Observational (n=111)
Does T-amplitude adaptation to heart rate characterize IKr inhibition in congenital and acquired long QT syndrome?
Absolute Event Rate: 0.31% vs 0.55%
p-value: p=< 0.05
Impaired adaptation of T-amplitude to changing heart rate is a distinct electrocardiographic marker of IKr inhibition, present in both LQT2 carriers and sotalol-induced QT prolongation.
Couderc et al. (2007) conducted an observational in Congenital and acquired long QT syndrome (n=111). IKr inhibition (LQT2 mutation or sotalol) vs. LQT1 carriers and healthy individuals off drugs was evaluated on T-amplitude/RR slope (p=< 0.05). IKr inhibition via LQT2 mutation or sotalol administration resulted in a significantly flatter T-amplitude/RR slope compared to LQT1 carriers and healthy individuals (P < 0.05).
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