Block of cardiac I_Na is a pharmacological intervention in the treatment of atrial fibrillation (AF). Since electrical remodelling of I_Na in AF could alter drug effects we have investigated I_Na characteristics in human atrial myocytes isolated from right atrial appendages from patients in sinus rhythm (SR) and chronic atrial fibrillation (AF). I_Na was measured at 22 °C with 5 mM intra- and extracellular [Na⁺] and activated following a 1 s conditioning pulse at –110 mV from a holding potential of –80 mV, 0.5 Hz. Membrane capacity was 94,5±1,7 pF in SR and (n=343/77) and 106,8±2,7 pF in AF (n= 158/35, p < 0.0001). Maximum current density was significantly lower in AF, the maximum at a test potential of –25 mV amounted to 30.1±1.2 pA/pF in SR (n=77/28) and 25.3±1.4 in AF (n=31/18, p=0.0261). Voltage-dependence of activation and steady-state inactivation were almost identical in SR and AF, V_0.5 of activation was –31,7±0,8 mV in SR and –31,2±1,5 mV in AF, V_0.5 of steady-state inactivation was –81,2±0,5 mV in SR and –81,7±0,7 mV in AF. Recovery from inactivation was biphasic, 90% of I_Na recovered with a fast time constant t_fast of 7,0±0,9 ms (SR) and 5,0±0,2 ms (AF) and 10% with a t_slow of 124,2±4,9 ms and 82,6±7,3 ms. An ultra slow component became apparent after 30 s of rest at –110 mV, I_Na amplitude increased by 25% of the steady-state value at 0.5 Hz of regular stimulation with a 1 s prepulse to –110 mV.

In atrial trabeculae dV/dt_max was not different between SR and AF (SR, 213±6 V/s, n=164; AF 219 ± 7 V/s, n=122) possibly due to the slightly more negative resting membrane potential in AF (SR –73,4 ± 0,36 mV, n=140; AF –76,2 ± 0,4, n=106).

Conclusion: In contrast to earlier reports (Bosch et al. 1999), I_Na characteristics of human atrial myocytes are not significantly different between SR and AF supporting the first investigations by Sakakibara et al. 1992.