The in vivo response of ouabain-induced arrhythmias to pacing: acceleration instead of termination.

In vitro, arrhythmias that result from triggered activity based on delayed afterdepolarizations can be reproducibly terminated by pacing. We studied the effect of similar pacing protocols on ouabain-induced ventricular tachycardia (VT) in the intact canine heart. The experiments were performed in 17 conscious dogs that had surgically induced atrioventricular block. The pacing protocol included 1, 2, or 20 stimuli and also continuous stimulation during 15, 60, and 120 seconds with interstimulus intervals varying between 500 and 200 msec. A total of 331 stimulation trains were given. The cycle length of the ouabain-induced VT was compared before and after pacing. The mean R-R interval of the induced VT was 380 +/- 80 msec. Termination was only observed in 3% of the pacing experiments and was not reproducible. The common response to pacing was a shortening in cycle length of VT that resulted in R-R intervals of 300 +/- 50 msec (p less than or equal to 0.001). Acceleration was dependent on duration of stimulation. A decrease in the interstimulus interval resulted in shortening of both the first postpacing interval and the cycle length of VT after pacing. These concordant relations were independent of the pacing modes. In conclusion, pacing of ouabain-induced VT in the intact heart rarely results in termination of the arrhythmia. Acceleration of VT is the rule. This finding may be of help in differentiating triggered activity that results from delayed afterdepolarizations from other arrhythmogenic mechanisms.