Reversal of reentry and acceleration due to double-wave reentry: two mechanisms for failure to terminate tachycardias by rapid pacing.

OBJECTIVES

We sought to demonstrate mechanisms by which rapid pacing can cause conduction block without terminating reentry.

BACKGROUND

Rapid pacing can fail to terminate or can accelerate tachycardias in patients. Mechanisms for these responses are poorly understood.

METHODS

We studied reentry in the canine atrial tricuspid ring and a left ventricular ring in vitro in 12 preparations. Activations were recorded from 10 sites around the ring, and monophasic action potentials were recorded from critical sites of block. Rapid pacing at cycle lengths that intermittently caused conduction block was performed at multiple sites.

RESULTS

Action potential alternans contributed to block of an orthodromic impulse during rapid pacing. When pacing continued for two stimuli after orthodromic block, a second episode of block could reverse the direction of tachycardia. Continued pacing at this site was likely to produce block of an antidromic impulse, which may initiate double-wave reentry. Double-wave reentry could be sustained or nonsustained. Its cycle length was 56% to 77% of the single-wave cycle length. The ratio of double-wave cycle length to single-wave cycle length was inversely correlated with the relative excitable gap (p < 0.01). Double-wave reentry can be a mechanism for persistent cycle length alternation during tachycardia.

CONCLUSIONS

Successful termination of reentry by rapid pacing required block of an othrodromic impulse and stopping pacing within one stimulus after orthodromic block. Reversal of reentry makes the circuit resistant to termination from this site of pacing. Antidromic block can cause acceleration due to double-wave reentry when there is a substantial excitable gap.