We investigated the cellular and molecular mechanisms underlying arrhythmias in heart
failure. A genetically engineered mouse lacking the expression of the muscle LIM protein
(MLP−/−) was used in this study as a model of heart failure. We used electrocardiography
and patch clamp techniques to examine the electrophysiological properties of MLP−/−
hearts. We found that MLP−/− myocytes had smaller Na+ currents with altered voltage
dependencies of activation and inactivation and slower rates of inactivation than control …