Figure 5

Impact of WT/T309I dysfunctional channels on action potential (AP) configuration in a human ventricular cell model. (A) APs (upper panels) and I_Ks (lower panels) at steady-state stimulation at the cycle length (CL) 1000 ms in control conditions and during β-adrenergic stimulation; APD₉₀—AP duration at 90%-repolarization. (B) APs (upper panels) and I_Ks (lower panels) at extrastimulation within the vulnerable period of AP in the WT/T309I model during β-adrenergic stimulation—CL suddenly shortened from 1000 to 268 ms. (C) Intracellular Ca²⁺ concentration at the end of stimulation cycle ([Ca²⁺]_i,end; left upper panel), APs (right upper and middle panels) and intracellular Ca²⁺ transients ([Ca²⁺]_i; lower panel) after change of CL from 1000 to 500 ms and contemporary start of β-adrenergic stimulation (for sequence of changes, note the time axes in all graphs); arrows—stimuli at CL 500 ms, *delayed afterdepolarization (DAD) or AP activated by DAD. All graphs were prepared using the software Origin, version 8.5.1.