Critical isthmus of slow conduction protected by anatomical and functional barriers. Inner and outer
loops complete the circuit by connecting both ends of the isthmus to produce a figure of 8 reentry.
Adjacent bystander sites are blind channels or alleys within the circuit that are passively activated
during tachycardia and are not essential to the reentrant circuit. The critical isthmus is an essential
component of the circuit and, therefore, the target of ablation.
LBBB morphology (terminal negative forces in
V1) = RV V or left septal VT
RBBB morphology (terminal positive forces in
V1) = LV VT
Superior axis: inferior wall origin
Inferior axis: anterior or OT origin
Positive precordial concordance: basal VT
near mitral valve
Negative precordial concordance: apical VT
Left fascicular VT: narrow and looks like
bifascicular block (RBBB+hemiblock)
In NSR: late potentials and pace mapping
in VT: entrainment mapping
Fractionated, low amplitude EGM recorded at
the end or after the QRS complex, reflect sites
of delayed activation due to slow conduction.
Because slow conduction is a prereq for reentry
targeting late potentials might interrupt the
critical isthmus. Late potentials however do not
differentiate sites critical to the tachycardia from
The VT morphology reflects the exit site, pacing
from the isthmus can produce a QRS
morphology identical to VT.
Short Stim-QRS + 100% PM = Exit site
Long Stim-QRS + 100% PM = central isthmus, adjacent bystander
Sinus PM cannot distinguish between a site essential to VT from a
Functional barriers during VT not present during sinus rhythm can
generate imperfect pacemaps despite stimulation from a site
integral to the tachycardia.
Pacing stimuli that penetrate the circuit and entrain give rise to
orthodromic and antidromic wavefronts. The antidromic wavefront
of the first resetting stimulus collides with tachycardia, while its
orthodromic counterpart advances the circuit. The last orthodromic
wavefront has no antidromic wavefront with which to collide and
completes one revolution around the circuit with continuation of
1-Paced QRS Morphology
Entrainment from inner loop, isthmus (entrance, central, exit) and
adjacent bystander sites cause ventricular activation from the exit
site so that the paced QRS morphology is identical to tachycardia
(entrainment with concealed fusion). Collision between
orthodromic and antidromic wavefronts occurs "upstream" within
the circuit, reulting in local fusion that is undetectable on 12 lead
ECG. Entrainment from outer loop and remote bystander sites
cause different paced QRS morphologies from T (entrainment
with manifest fusion).
The St-QRS interval is measured from the pacing stimulus to onset
of the QRS complex.
-Inner loop stimulation => very long (>70% VTCL).
-Entrance Stimulation => long (51-70% VTCL)
-Central isthmus stimulation => Intermediate (31-50% VTCL)
-Exit stimulation => short (< 30% VTCL)
-Outer loop and remote bystander stimulation => short cause
healthy tissue outside is directly depolarized
-Adjacent bystander => long (conduction time over the bystander
pathway plus the conduction time from its junction with the isthmus
to the exit site.
This is the activation time from the mapping site to the onset of the
QRS. It is very long for inner loop sites and becomes progressively
shorter as the mapping catheter heads towards the entrance,
central isthmus and exit sites. EGMs from the isthmus are
generally fractionated and low amplitude, and occur during
diastole resulting in early -(entrance), mid -(central), and late
-(exit) diastolic or presystolic potentials. A diastolic EGM is not
specific for the isthmus and can be recorded from a bystander site.
Inner loop and Isthmus sites (entrance to exit) demonstrate
matching St-QRS and EGM-QRS intervals (< 20 ms difference)
while bystander sites (adjacent, remote) do not (> 20 ms). The
St-QRS for a remote bystander site is close to 0.
Entrainment from a site integral to the circuit (isthmus, inner, and
outer loop) result in a PPI-TCL<30 ms while entrainment from
bystander sites (adjacent, remote) doesn't.
from exit site.
from outer loop.
from inner loop.
St-QRS (a+b) >
PPI=TCL + 2a
PPI=TCL + 2c
The optimal target site is the isthmus of slow conduction.
A pacing stimulus that fails to capture the ventricle but terminates
tachycardia (nonglobal capture) is specific for a critical component
of the reentrant circuit and should be targeted for ablation.
Entrainment from central isthmus below. Arrows denote mid-diastolic and
far-field potentials. PPI-TCL = 17 ms. St-QRS = 48% VTCL which puts it in
the intermediate range (central) and St-QRS = EGM-QRS
Scar <0.5 mV
Healthy myocardium > 1.5 mV
F-J (big curve) catheter
especially in DCM to reach
CFAE: do mitral block lines
RIPV -> MA
LAA -> MA
Check block by pacing and having latest signals on the other side of the line
ECG characteristics of epicardial
MDI .55: time from onset of QRS to first peak of QRS in precordial leads is a marker that it is a long initial interval >
55% of total QRS time suggests epicardial
QS in aVR & III
Daniels et al. Circulation 2006: 1659-1666
Catheter Insertion Retrograde Aortic
Figure of 6 in LAO and RAO
Flex and straighten for mapping
Induce and Entrain: Map
-Pacing entrainment confirms the presence of reentrant VT mechanism
-Perivalvular scar distribution is a hallmark of idiopathic NICM
-His bundle septal VT has a typical LBBB appearance
-QS in lead I : think of epicardial VT
HRS 12.2016 is the pacing site in or out of VT
The VT exhibited right bundle branch block morphology with right superior axis and V4 transition consistent with an inferoseptal and apical location within the scar.