Omecamtiv mecarbil (OM), an activator of cardiac myosin, strongly affects 
contractile characteristics of the ventricles and, to a much lesser extent, the 
characteristics of atrial contraction. We compared the molecular mechanism of 
action of OM on the interaction of atrial and ventricular myosin with actin 
using an optical trap and an in vitro motility assay. In concentrations up to 
0.5 μM, OM did not affect the step size of a myosin molecule but reduced it at a 
higher OM level. OM substantially prolonged the interaction of both isoforms of 
myosin with actin. However, the interaction characteristics of ventricular 
myosin with actin were more sensitive to OM than those of atrial myosin. Our 
results, obtained at the level of isolated proteins, can explain why the impact 
of OM in therapeutic concentrations on the contractile function of the atrium is 
less significant as compared to those of the ventricle.