This is a moribund area with a history of failed drugs and bankrupt ideas. Ripe for More Work, in other words. Good therapeutic drugs have selectivity as well as specificity. Therefore any new antiarrhythmics will most likely target discreet macromolecules expressed in the heart.
Arrhythmias are electrophysiological events triggered by chemical signaling dysfunction.
Unsurprisingly I therefore favour the use of animal models of arrhythmogenesis and a bioassay approach. It's not just the drugs that elude. The identity of the relevant chemical mediators themselves is far from clear. Hopefully, however, 'a shot in the dark' would be an unfair description of my scientific approach. There has to be a question, and a sensible hypothesis with a feasible range of option for its testing.