| Action potential morphology |
(Britton et al., 2017; Coppini et al., 2013; Jost et al., 2013) |
| Calcium transient time to peak, duration, and amplitude |
(Coppini et al., 2013) |
| I-V relationship and steady-state inactivation of L-type calcium current |
(Magyar et al., 2000) |
| Sodium blockade is negatively inotropic |
(Gottlieb et al., 1990; Tucker et al., 1982; Legrand et al., 1983; Bhattacharyya and Vassalle, 1982). |
| L-type calcium current blockade shortens the action potential |
(O'Hara et al., 2011) |
| Early depolarisation formation under hERG block |
(Guo et al., 2011) |
| Alternans formation at rapid pacing |
(Koller et al., 2005) |
| Conduction velocity of ca. 65 m/s |
(Taggart et al., 2000) |
| Validation |
|---|
| Action potential accommodation |
(Franz et al., 1988) |
| S1-S2 restitution |
(O'Hara et al., 2011) |
| Drug blocks and action potential duration |
(Dutta et al., 2017a; O'Hara et al., 2011) |
| Hyperkalemia promotes postrepolarisation refractoriness |
(Coronel et al., 2012) |
| Hypertrophic cardiomyopathy phenotype |
(Coppini et al., 2013) |
| Drug safety prediction using populations of models |
(Passini et al., 2017) |
| Physiological QRS and QT intervals in ECG |
(Engblom et al., 2005; van Oosterom et al., 2000; Bousseljot et al., 1995; Goldberger et al., 2000) |
