Key result
Targeted disruption of KCNE1 in murine hearts prolonged epicardial action potential duration (57.1 vs 36.1 ms, P<0.001) and induced spontaneous ventricular tachycardia.
Why the study?
Does nifedipine suppress arrhythmogenic features in KCNE1-/- murine hearts modelling long QT syndrome 5?
Does nifedipine suppress arrhythmogenic features in KCNE1-/- murine hearts modelling long QT syndrome 5?
Absolute Event Rate: 57.1% vs 36.1%
p-value: p=<0.001
In a murine model of long QT syndrome 5, arrhythmogenic features caused by reduced outward K+ currents can be abolished by antagonizing inward L-type Ca2+ currents with nifedipine.
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Nifedipine abolishes VT in KCNE1-/- LQT5 mice; leaves open whether L-type Ca2+ blockade prevents arrhythmias in patients.
Thomas et al. (2006) studied Long QT syndrome 5 (n=10). Targeted disruption of KCNE1 (KCNE1-/-) vs. Wild-type (WT) hearts was evaluated on Epicardial action potential duration at 90% repolarization (APD90) (p=<0.001). Targeted disruption of KCNE1 in murine hearts prolonged epicardial action potential duration (57.1 vs 36.1 ms, P<0.001) and induced spontaneous ventricular tachycardia.
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