M. Yamaura et al., Abrupt loss of constant fusion during entrainment of ventricular tachycardia at a critical paced cycle length, JPN HEART J, 42(1), 2001, pp. 67-78
Sustained monomorphic ventricular tachycardia (VT) can be frequently entrai
ned and interrupted with rapid pacing and the mechanism of the pacing-induc
ed interruption is considered to be due to orthodromic block.
This study focused on the incidence of VT which was interrupted at a critic
al cycle length and was characterized by an abrupt loss of constant fusion
in the surface electrocardiogram (ECG), and the role of orthodromic block a
s the cause of such characteristic change and interruption of VT M as analy
zed.
Among 45 consecutive patients with symptomatic VT, rapid pacing was perform
ed in 43 VTs of 39 patients. The exit was mapped as the earliest site of th
e activation during VT and an electrode catheter was located at the site. R
apid pacing was performed at progressively shorter cycle lengths in steps o
f 10 msec until VT was interrupted and the timing of the orthodromic and di
rect capture was compared at the exit.
Abrupt loss of constant fusion was observed in 25 of 39 patients (64.1%). a
nd the loss was invariably associated with interruption of VT. When the tim
ings of the activation of the exit were compared, which were measured from
the preceding (n-1) stimulus as the time reference, the direct capture was
relatively delayed compared to that of the orthodromic capture. This findin
g suggests that orthodromic
In the remaining 13 patients (35.9%), the surface ECG showed a gradual tran
sition into the fully paced QRS morphology. The direct capture M as confirm
ed in the non-fused beats, but it was not necessarily associated with inter
ruption of VT. The interval from the stimulus to the entrained electrogram
at the exit showed a gradual prolongation until the exit was finally captur
ed directly from the pacing site.
The confirmation of constant fusion followed by abrupt loss in ECG can be a
reliable hallmark of orthodromic block as the cause of the interruption of
VT during transient entrainment at a critical paced cycle length.