Key result
CaMKII-dependent late Na+ current upregulation in HF prolongs action potentials and increases repolarization variability.
Why the study?
Underlying changes in inward currents in heart failure are often measured in nonphysiological conditions, leaving their behavior under physiological action potential clamp uncertain.
Does CaMKII-dependent upregulation of late Na+ current contribute to action potential prolongation and increased repolarization variability in failing rabbit ventricular myocytes?
Does CaMKII-dependent upregulation of late Na+ current contribute to action potential prolongation and increased repolarization variability in failing rabbit ventricular myocytes?
CaMKII-dependent upregulation of late Na+ current in heart failure significantly contributes to action potential prolongation and increased repolarization variability, which may increase arrhythmia propensity.
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Suggests CaMKII or late Na+ inhibition may reduce HF arrhythmia risk; leaves open translation from rabbit models.
Hegyi et al. (2019) studied Heart failure. Physiological action potential clamp and I NaL inhibition vs. Age-matched control was evaluated on Action potential duration, short-term variability of AP repolarization, and inward ionic currents. CaMKII-dependent upregulation of late Na+ current in heart failure significantly contributes to action potential prolongation and increased short-term variability of repolarization.