Why the study?
Does a specific I(Kr) chemical activator normalize action potential duration in human cardiomyocytes from patients with LQT1?
Population
Cultured differentiated human cardiomyocytes from healthy controls and patients with Long QT syndrome type 1
Comparison
Specific chemical activator for I causing a… vs I chemical activator of primary effects in…
Design
Preclinical
Key result
An I(Kr) chemical activator that reduces voltage sensitivity of inactivation caused dose-dependent shortening of action potential durations and normalized action potentials in LQT1 cells.
Authors
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Should not yet change LQT1 practice; leaves open I(Kr) activation as a therapeutic target pending human validation.
Does a specific I(Kr) chemical activator normalize action potential duration in human cardiomyocytes from patients with LQT1?
Pharmacological elevation of I(Kr) by reducing voltage sensitivity of inactivation can normalize action potential duration in LQT1 cardiomyocytes, providing a theoretical and experimental basis for novel LQTS therapies.
Zhang et al. (2012) studied Long QT syndrome type 1 (LQT1). I(Kr) chemical activator causing a right shift of V(1/2) for inactivation vs. I(Kr) chemical activator slowing channel deactivation was evaluated on Action potential duration. An I(Kr) chemical activator that reduces voltage sensitivity of inactivation caused dose-dependent shortening of action potential durations and normalized action potentials in LQT1 cells.