Acceleration of typical atrial flutter due to double-wave reentry induced by programmed electrical stimulation

Acceleration of reentrant tachycardia induced by programmed electrical stimulation is a well-documented phenomenon, but the mechanisms remain poorly understood.

Twelve patients with typical atrial flutter were studied. Activation sequence of the underlying reentrant circuit was recorded by multiple multipolar electrodes placed in the right atrium. In five patients, 27 episodes of atrial flutter acceleration were induced by single extrastimuli delivered in the isthmus between the tricuspid annulus and eustachian ridge (TA-ER isthmus) and one by rapid overdrive atrial pacing. Analyses of the activation sequences, intracardiac electrograms, and 12-lead surface ECG P-wave morphology indicated that the acceleration was caused by two successive activation wave fronts circulating in the same direction along the same reentrant circuit (double-wave reentry, DWR). DWR was induced only within a narrow range of coupling interval, from 2 to 45 ms beyond the effective refractory period, and was associated with unidirectional antidromic block of the paced impulse. Patients with DWR had a shorter effective refractory period (138.8+/-13.4 versus 163.8+/-12.2 ms, P<.015) and larger excitable gap (124.0+/-22.6 versus 83.2+/-13.2 ms, P<.009) compared with patients without inducible DWR. All of the DWR episodes were transient. Most (78.6%) terminated after one of the double wave fronts was blocked in the TA-ER isthmus.

DWR is one of the mechanisms responsible for programmed electrical stimulation-induced atrial flutter acceleration in human subjects. Its induction requires a sufficient excitable gap and antidromic unidirectional block of the paced impulse in the TA-ER isthmus. In addition, the TA-ER isthmus is the usual site of DWR termination.