To prevent lethal arrhythmias, patients at risk receive implantable cardioverter-defibrillators. These devices convert tachycardias to a normal rhythm using high frequency antitachycardia pacing (ATP). One of the suggested ATP mechanisms involves paced-induced-drift of rotating waves, followed by their collision with the boundary of excitable tissue. This study provides direct experimental evidence of this mechanism. We employed monolayers of neonatal rat cardiomyocytes, in which rotating waves of activity were initiated by premature stimuli and propagating wave patterns were observed using calcium-sensitive indicator Fluo-4. The interaction of the spiral tip with a paced wave was then monitored at a high spatial resolution. In the course of experiments we observed spiral wave pinning to local heterogeneities within the myocyte layer. High frequency pacing led, in a majority of cases, to successful termination of spiral activity. Our data show that: i) stable spiral waves in cardiac monolayers tend to be pinned to local heterogeneities or areas of altered conduction, ii) overdrive pacing can shift a rotating wave from its original site, iii) the wavebreak, formed as a result of interaction between the spiral tip and a paced wavefront, moves by a paced-induced drift mechanism to an area where it may become unstable or collide with a boundary. The data were complimented by numerical simulations, with which experimentally observed behavior was further analyzed.