Ventricular tachycardia (VT) is considered to be the most common precursor of ventricular fibrillation (VF). However, the mechanisms underlying the transition from VT to VF remain unclear. Here, we investigated whether and how perfusion of the heart with verapamil, a blocker of L-type calcium channels, changed the macro-dynamics of the heart between VT and VF. The experiments were performed with Langendorff perfused isolated rat hearts, in which left ventricular pressure and left ventricular cardiomyogram were measured. Sustained VT or VF was induced by burst pacing of the left ventricular muscles. During sustained VF, verapamil perfusion resulted in the conversion of VF to VT. A cross-correlation analysis between left ventricular cardiomyogram and left ventricular pressure revealed that the correlation coefficient was small during VF, but became larger during VT. This study showed that inactivation of L-type Ca(2+) channels occurred during verapamil-induced conversion of pacing-induced sustained VF to VT, and characterized the changes in macro-dynamics of the heart associated with the transition.