<jats:p> <jats:italic>Background</jats:italic> Disease-associated electrophysiological alterations may contribute to the increased predisposition to arrhythmias of the hypertrophied or failing myocardium. An I <jats:sub>f</jats:sub> -like current is expressed in rat left ventricular myocytes (LVMs), its amplitude being linearly related to the severity of cardiac hypertrophy. Here, we report the occurrence and electrophysiological properties of I <jats:sub>f</jats:sub> in human LVMs. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> LVMs were isolated from hearts of three male patients undergoing cardiac transplantation for terminal heart failure due to ischemic dilated cardiomyopathy. The patch-clamp technique was used to record I <jats:sub>f</jats:sub> , ie, a barium-insensitive, cesium-sensitive, time-dependent increasing inward current elicited on hyperpolarization. Membrane capacitance was 244±27 pF (n=25). I <jats:sub>f</jats:sub> occurred in all cells tested; its density measured at −120 mV was 2.1±0.3 pA/pF. Activation curves of I <jats:sub>f</jats:sub> (n=24) were fitted by a Boltzmann function; the threshold was −55 mV; midpoint, −70.9±2.1 mV; slope, −5.4±0.3 mV; and maximal specific conductance, 19.6±2.5 pS/pF. I <jats:sub>f</jats:sub> blockade by extracellular cesium was voltage dependent. Reducing extracellular potassium concentration from 25 to 5.4 mmol/L caused a shift of the reversal potential from −12.7±0.5 to −24.8±2.1 mV and a 64% decrease of current conductance. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> I <jats:sub>f</jats:sub> is present in human LVMs. Its electrophysiological characteristics resemble those previously described in hypertrophied rat LVMs and suggest that I <jats:sub>f</jats:sub> could be an arrhythmogenic mechanism in patients with severe heart failure. </jats:p>