Augmented and slowed late Na⁺ current (I_NaL) was implicated in action potential duration variability, early afterdepolarizations, and abnormal Ca²⁺ handling in human and canine failing myocardium. Objective was to study I_NaL modulation by cytosolic Ca²⁺ ([Ca²⁺]_i) in normal and failing ventricular myocytes. Methods: Chronic heart failure was produced in 10 dogs by intracoronary microembolizations, 6 normal dogs served as a control. I_NaL fine structure was measured by whole-cell patch-clamp in ventricular myocytes and approximated by a sum of fast and slow exponentials produced by burst and late scattered modes of Na⁺ channel gating, respectively. Results: I_NaL greatly enhanced as [Ca²⁺]_i increased from "Ca²⁺ free" to 1µM: its maximum density increased, decay of both exponentials slowed, and steady-state-inactivation curve (SSI) shifted towards more positive potentials. Testing inhibition of CaMKII and CaM revealed similarities and differences of I_NaL modulation in failing vs. normal myocytes. Similarities: 1) CaMKII slows I_NaL decay and decreases the amplitude of fast exponential; 2) Ca²⁺shifts SSI rightward. Differences: 1) slowing I_NaL by CaMKII is greater; 2) CaM shifts SSI leftward; 3) Ca²⁺ increases the amplitude of slow exponential. Conclusions: Ca²⁺/CaM/CaMKII signaling increases I_NaL and Na⁺ influx in both normal and failing myocytes by slowing kinetics and shifting SSI. This Na⁺ influx provides a novel Ca²⁺ positive feedback mechanism (via Na⁺/Ca²⁺exchanger), enhancing contractions at higher beating rates, but worsening cardiomyocytes contractile and electrical performance in conditions of poor Ca²⁺ handling in heart failure.