Cardiac action potentials are simulated using the algorithm of O'Hara-Rudy (2011) as this model is recognised by the CiPA initiative as one of the most relevant for the human situation at the time being in order to test drug cardiac adverse effects such as early afterdepolarization


Except mentionned, equations, constants (extracellular ionic concentrations, cell geometry, channel conductance), initial conditions for state variables and scaling factors (appiied to various ionic fluxes or to the conductance of various channels allowing the testing of differences among endo-,mid- and epicardial myocytes) were used as described in the ORd algorithm.  At the time being, the kinetics and the state dependence  of drug binding on the various channels were not taken into account




This site describes the in silico effects of various ions, cardiac currents or drugs on the cardiac action potential (AP). 

This AP is described by various parameters such as resting membrane potential (RMP), AP amplitude (APA), maximal rate od AP rise (Vmax), AP duration at 40, 60 or 90 % of APA (APD40, 60 or 90) and difference between APD90 and APD40 or 60 <=> estimation of triangulation (T40 or 60). 

From these parameters, various cardiac markers are calculated or observed such as early afterdepolarization (EAD), transmural dispersion of repolarisation (TDR), reverse use dependence (RUD), APD prolongation or shortening, triangulation,  Vmax increase or decrease or Vmin (minimal rate of AP decrease at EAD take-off voltage).

see definitions