Onset dynamics of reentrant tachycardia and rate-dependent conduction changes in canine ventricular muscle: Effects of Na+ and Ca2+ channel blockade

To show that cycle-length (CL) prolongation occurring at the onset of reent rant tachycardias may be associated with an increase in conduction time (CT ), and to investigate the involvement of Na+ and Ca2+ channel activity, ree ntrant activity was induced by programmed stimulation in thin ventricular m uscle slices with a central cryothermal lesion, as documented with 7 to 12 bipolar recordings. We studied the course of the CL measured in successive tachycardia beats, as well as the course of conduction times after abrupt t ransition from a pacing CL of 1,000 to 400 ms (pacing paradigm). The majori ty of the tachycardias displayed a dynamic behavior in which CL increased p rogressively, with an exponential rate constant of 37 +/- 35 bears (mean +/ - SD), stabilizing at 325 +/- 67 ms after a total increase of 17 +/- 17 ms. In the pacing paradigm, CT was prolonged from 68 +/- 21 ms to 79 +/- 24 ms according to a biphasic course consisting of an abrupt increase in the fir st response to 400 ms, followed up by an exponential increase, stabilizing with a rate constant of 18 +/- 23 beats. Lidocaine 5 x 10(-5) mol/L induced an increase in steady-state CT, which was not further modified by adding v erapamil 10-5 mol/L. However, verapamil prolonged the rate constant of the exponential course by 60 +/- 40 beats. Thus, the onset dynamics of reentran t tachycardias share common features with the dynamic behavior of CT in the pacing paradigm, in which both Na+ channel activity and Ca2+-modulated cel lular coupling appear to be involved.