148
Distinguishing Focal from Macroreentrant Atrial Tachycardias:
Has This Job Just Become Easier?
GEORGE D. VEENHUYZEN, M.D. and L. BRENT MITCHELL, M.D.
From the Libin Cardiovascular Institute of Alberta, Calgary Health Region, and University of Calgary, Calgary, Alberta, Canada
Editorial Comment
As they are currently understood, the mechanism of all
tachyarrhythmias can be attributed to enhanced normal auto-
maticity, abnormal automaticity, triggered activity, or reentry.
In the clinical arena, making this distinction has proven to be
difficult, if not impossible. Furthermore, prior to the era of
catheter ablation, making this distinction provided little clini-
cal benefit. To a team faced with the challenge of successfully
ablating an atrial tachycardia (AT), a more relevant distinc-
tion is between a focal and a macroreentrant AT. Indeed, in
2001, a Joint Expert Group from the Working Group of the
European Society of Cardiology and the North American So-
ciety of Pacing and Electrophysiology made for classification
of ATs recommended classifying ATs as focal ATs (due to au-
tomaticity, triggered, or microreentrant mechanisms) versus
macroreentrant ATs (due to macroreentrant mechanisms that
can be characterized with current clinical mapping systems)
in recognition that this distinction has clinical utility as it will
direct an ablation strategy.1 Focal ATs demonstrate centrifu-
gal activation of the atria away from a small area (usually
<2 cm), while macroreentrant ATs demonstrate a larger cir-
cuit that often involves conduction barriers such as valve an-
nuli or scars and areas of slow conduction. A focal AT is
mapped to its origin by finding progressively earlier activa-
tion sites, the earliest of which is targeted for ablation. In the
case of a macroreentrant AT, earliest activation has no mean-
ing, for a site with an earlier activation time in comparison
with the current site can always be found and the ablation
target is a critical isthmus bounded by nonconducting tissue
rather than the earliest site. Accordingly, a crucial first step
in the design of an ablation procedure for a patient with an
AT is to determine if the AT is focal or macroreentrant.
The presence of an isoelectric segment between P waves
on an electrocardiogram (ECG) recorded during AT favors
a focal AT, but false positive and false negative exceptions
are well appreciated, particularly in atria that are scarred.
Adenosine responsive ATs are more likely to be focal, but
microreentry, an increasingly recognized mechanism of fo-
cal ATs,2 represents important exceptions.3 The induction
and termination of AT by programmed stimulation is pos-
sible in both macroreentrant and focal ATs, when the latter
are due to microreentry or triggered activity. As a result of
these limitations, global mapping, using a three dimensional
electroanatomic mapping system, is often required to direct
J Cardiovasc Electrophysiol, Vol. 19, pp. 148-149, February 2008.
Address for correspondence: L. Brent Mitchell, M.D., Foothills Medical
Centre, 1403 29th Street NW, Calgary, Alberta, Canada T2N 2T9. Fax: 403-
944-2906; E-mail: brent.mitchell@calgaryhealthregion.ca
doi: 10.1111/j.1540-8167.2007.01027.x
an ablation strategy. Demonstration of a clear centrifugal ac-
tivation pattern and demonstration that atrial conduction time
does not account for the entire AT cycle length is helpful in
identifying focal ATs, but scars, including those created by
prior linear ablation, may force wavefronts traveling away
from focal sources into noncentrifugal patterns with intra-
atrial conduction times that approximate the AT cycle length.
Furthermore, the noncentrifugal patterns of macroreentrant
circuits, particularly those that are not common and well rec-
ognized, can be difficult to interpret. Clearly, it would be
desirable to determine if an AT was focal or macroreentrant
prior to investing the time and effort required to create a global
activation map.
During an AT, the presence of electrocardiographic P wave
fusion or evidence of fusion among atrial electrograms dur-
ing transient entrainment establishes reentry as the AT mech-
anism. Local postentrainment pacing intervals (PPIs) within
20 ms of the AT cycle length indicate pacing sites that are
within the reentrant circuit. When two or more such sites can
be found that are separated by more than 2 cm, the mech-
anism of the AT can be assumed to be macroreentrant. Un-
fortunately, entrainment pacing may terminate or transform
the AT, and the identification of PPIs within 20 ms of the
AT cycle length at two sites separated by more than 2 cm
can also be time consuming. Furthermore, the identification
of entrainment with fusion is often difficult because P waves
may be obscured by QRS complexes and/or T waves. Of-
ten, fusion cannot be demonstrated and transient entrainment
is implied (rather than proven) when the AT resumes after
pacing. In this situation, one cannot differentiate between
macroreentry, microreentry, and overdrive suppression fol-
lowed by resumption of an automatic AT.
Recently, variation in the AT cycle length of greater than
15% has been suggested as a reliable marker of a focal AT.4
However, in that study, a regular AT could be either focal or
macroreentrant. Furthermore, although probably quite rare,
macroreentrant ATs can display considerable variation in the
cycle length.5 Thus, the rapid electrophysiologic differentia-
tion of a focal from a macroreentrant AT remains a challenge.
In this edition of the Journal, Colombowala et al.6 ex-
amined 14 focal and 17 macroreentrant ATs (using global
electroanatomical mapping as the gold-standard for AT
mechanism) in 29 patients. Atrial overdrive pacing from the
proximal coronary sinus was performed, and the absolute dif-
ference between the PPI after pacing at a cycle length that
was 10 ms shorter than the AT cycle length and the PPI af-
ter pacing at a cycle length that was 30 ms shorter than the
AT cycle length was calculated as the PPI variability (PPIV).
Using this derivation set, the observation was made that the
PPIV was significantly shorter for macroreentrant ATs (6.0
2.5 ms) than for focal ATs (56.5 20.6 ms) and a clinical
prediction rule was derived, wherein a low PPIV (<10 ms)
identified macroreentrant ATs with a sensitivity of 94% and

a specificity of 100% while a high PPIV (>30 ms) identified
focal ATs with a sensitivity of 93% and a specificity of 100%.
Although there was no overlap of the PPIV values of the two
groups, 2 patients had PPIV between 10 and 30 ms, and 8
patients had PPIV values that were within 5 ms of the cutoff
values.
Because the PPI reflects the time required for the stimu-
lated wavefront to travel to a reentrant circuit, revolve once
around the circuit, and travel back to the pacing site, it is un-
derstandable that, in the absence of rate-dependent conduc-
tion slowing, the PPIV should approach zero (e.g., consistent
PPIs should be obtained). It is also understandable that, be-
cause overdrive pacing at faster rates should overdrive sup-
press a focal automatic AT more than pacing at slower rates
as long as inputs at faster rates are still able to penetrate the
focus, the PPIV should be some positive value. However,
focal ATs may be reentrant and macroreentrant circuits can
contain tissue with decremental conduction properties. It is
not clear how many of the 14 focal ATs included in the study
of Colombowala et al. were due to microreentry, but the dis-
cussion relates that some were and, nevertheless, displayed a
low PPIV. The authors speculate that microreentrant circuits
are more likely to display decremental conduction because of
smaller excitable gaps and, correspondingly, overdrive pac-
ing inputs have a greater likelihood of encountering tissue in
its relative refractory period. Perhaps this also explains why
focal microreentrant ATs tend to have more variable AT cycle
lengths as well.4
It is opportune at this juncture to note how powerful a
tool overdrive pacing is proving to be in the electrophysiol-
ogy laboratory. The PPI may prove clinically useful mapping
focal ATs as well as macroreentrant ATs.7 Atrial and ven-
tricular overdrive pacing can help to distinguish atrial tachy-
cardia from atrioventricular (AV) node dependent tachycar-
dias,8,9 and ventricular overdrive pacing can also distinguish
AV nodal reentry from AV reentry.10 In addition, the value
of overdrive pacing in the evaluation of macroreentrant atrial
and ventricular tachycardias is well established.11,12 Virtu-
ally every catheter ablation procedure stands to benefit from
this versatile and richly informative pacing maneuver. Nev-
ertheless, despite its promise, overdrive pacing still has lim-
itations, as discussed above. For these reasons and because
of the small number of ATs studied by Colombowala et al.,
one should apply these authors prediction rule cautiously
with recognition that exceptions can occur. Furthermore, like
every good clinical prediction rule, the predictive values of
PPIV should be prospectively and externally validated. In the
meantime, teams faced with the task of successfully ablating
Veenhuyzen and Mitchell Editorial Comment 149
an AT will undoubtedly utilize the observations of Colom-
bowala et al. to determine, for themselves, whether the job
of differentiating a focal AT from a macroreentrant AT has,
indeed, become a little easier.
References
1. Saoudi N, Cosio F, Waldo A, Chen S-A, Iesaka Y, Lesh M, Saksena S,
Salerno J, Schoels W: Classification of atrial flutter and regular atrial
tachycardia according to electrophysiologic mechanism and anatomic
basis: A statement from a Joint Expert Group from the Working Group
of the European Society of Cardiology and the North American So-
ciety of Pacing and Electrophysiology. J Cardiovasc Electrophysiol
2001;12:852-866.
2. Sanders P, Hocini M, Jas P, Hsu L-F, Takahashi Y, Rotter M, Scavee C,
Pasquie J-L, Sacher F, Rostock T, Nalliah CJ, Clementy J, Hassaguerre
M: Characterization of focal atrial tachycardia using high-density map-
ping. J Am Coll Cardiol 2005;46:2088-2099.
3. Markowitz SM, Nemirovsky D, Stein KM, Mittal S, Iwai S, Shah BK,
Dobesh DP, Lerman BB: Adenosine-insensitive focal atrial tachycardia:
Evidence for de novo micro-re-entry in the human atrium. J Am Coll
Cardiol 2007;49:1324-1333.
4. Knecht S, Matsuo S, Lim K-T, Lim K-T, Kodali S, Arantes L, ONeill
MD, Nicolas D, Hocini M, Jas P, Klein G, Clementy J, Hassaguerre M:
Focal vs. macroreentrant atrial tachycardia after prior ablation: Value
of cycle length variability. Heart Rhythm 2007;4 (Suppl S):S238.
5. ONeill MD, Hocini M, Matsuo S, Hassaguerre M: Twin perimitral
flutters with alternating tachycardia cycle lengths. J Cardiovasc Elec-
trophysiol 2007;18:455-456.
6. Colombowala IK, Massumi A, Rasekh A, Saeed M, Cheng J, Fakhri
B, Shuraih M, Razavi M: Variability in post-pacing intervals predicts
global atrial activation pattern during tachycardia. J Cardiovasc Elec-
trophysiol 2008;19:142-147.
7. Mohamed U, Skanes AC, Gula L, Leong-Sit P, Krahn AD, Yee R,
Subbiah R, Klein GJ: A novel pacing maneuver to localize focal atrial
tachycardia. J Cardiovasc Electrophysiol 2007;18:1-6.
8. Knight BP, Zivin A, Souza J, Flemming M, Pelosi F, Goyal R, Ching
M, Strickberger A, Morady F: A technique for the rapid diagnosis of
atrial tachycardia. J Am Coll Cardiol 1999;33:775-781.
9. Maruyama M, Kobayashi Y, Miyauchi Y, Ino T, Atarashi H, Katoh
T, Mizuno K: The VA relationship after differential atrial overdrive
pacing: A novel tool for the diagnosis of atrial tachycardia in the elec-
trophysiologic laboratory. J Cardiovasc Electrophysiol 2007;18:1127-
1133.
10. Michaud GF, Tada H, Chough S, Baker R, Wasmer K, Sticherling
C, Pelosi F Jr, Knight BP, Strickberger SA, Morady F: Differentia-
tion of atypical atrioventricular node re-entrant tachycardia from ortho-
dromic reciprocating tachycardia using a septal accessory pathway by
the response to ventricular pacing. J Am Coll Cardiol 2001;38:1163-
1167.
11. Miyazaki H, Stevenson WG, Stephenson K, Soejima K, Epstein LM:
Entrainment mapping for rapid distinction of left and right atrial tachy-
cardias. Heart Rhythm 2006;3:516-523.
12. Stevenson WG, Friedman PL, Sager PT, Saxon LA, Kocovic D,
Harada T, Wiener L, Khan H: Exploring postinfarction reentrant ven-
tricular tachycardia with entrainment mapping. J Am Coll Cardiol
1997;29:1180-1189.