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\begin{document}

\title{Stabilization of unstable reentrant atrial tachycardias via fractionated
continuous electrical activity ablation (CHAOS study).}



\author[1]{Eduardo Franco}%
\author[2]{Cristina Lozano}%
\author[3]{Roberto Matía}%
\author[4]{Antonio Hernandez-Madrid}%
\author[3]{Inmaculada Sánchez}%
\author[5]{Jose Zamorano}%
\author[6]{Javier Moreno}%
\affil[1]{Hospital Ramón y Cajal}%
\affil[2]{University Hospital Ramón y Cajal}%
\affil[3]{Ramón y Cajal Hospital}%
\affil[4]{Ramon y Cajal hospital}%
\affil[5]{Ramon y Cajal Hospital}%
\affil[6]{San Carlos University Hospital}%


\vspace{-1em}



  
  \date{May 22, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Introduction. Unstable reentrant atrial tachycardias (ATs) (i.e. those
with frequent circuit modification or conversion to atrial fibrillation)
are challenging to ablate. We have tested a strategy to achieve
arrhythmia stabilization into mappable stable ATs based on the detection
and ablation of rotors. Methods and Results. From May 2017 to December
2019, 97 consecutive patients with reentrant ATs were ablated. Of these,
18 (18.6\%) presented unstable circuits and were included. Mapping was
performed using conventional high-density mapping catheters (IntellaMap
ORION, PentaRay NAV or Advisor HD Grid). Rotors were subjectively
identified as fractionated continuous (or quasi-continuous) electrograms
on 1-2 adjacent bipoles of the mapping catheter, without dedicated
software. 13 patients (72\%) had detectable rotors (median 2 {[}1--3{]}
rotors per patient); focal ablation achieved conversion into stable AT
or sinus rhythm in 12 (92\%). In the other 6 patients, sites with
spatiotemporal dispersion (i.e. all the cycle length comprised within
the mapping catheter) plus non-continuous fractionation on single
bipoles were targeted. 17 sites with spatiotemporal dispersion were
detected and focally ablated. Globally, and excluding 1 patient with
spontaneous AT stabilization, ablation success to stabilize the AT was
achieved in 16/17 patients (94.1\%). One-year freedom from atrial
arrhythmias was similar between patients with unstable and stable ATs
(66.7\% Vs 65.8\%, p=0.946). Conclusion. Most unstable reentrant ATs
show detectable rotors, identified as sites with single-bipole
fractionated quasi-continuous signals, or spatiotemporal dispersion plus
non-continuous fractionation. Ablation of these sites is highly
effective to stabilize the AT or convert it into sinus rhythm.%
\end{abstract}%



\sloppy


\textbf{Stabilization of unstable reentrant atrial tachycardias via
fractionated continuous electrical activity ablation (CHAOS study).}

\textbf{Authors:} Eduardo Franco, MD, PhD,\textsuperscript{*} Cristina
Lozano Granero, MD,\textsuperscript{*} Roberto Mat\selectlanguage{ngerman}ía, MD,
PhD,\textsuperscript{*} Antonio Hernández-Madrid, MD,
PhD,\textsuperscript{*} Inmaculada Sánchez, MD,\selectlanguage{english}\textsuperscript{+} Jose
Luis Zamorano, MD, PhD,\textsuperscript{*} Javier Moreno, MD,
PhD\textsuperscript{*}.

\emph{\textsuperscript{*} Arrhythmia Unit. Cardiology Department.
University Hospital Ramon y Cajal. Madrid, Spain.}

\selectlanguage{english}\textsuperscript{+} \emph{Pediatric Cardiology Department. University
Hospital Ramon y Cajal. Madrid, Spain.}

\textbf{Corresponding author:} Eduardo Franco, MD, PhD.

Arrhythmia Unit. Cardiology Department. University Hospital Ramon y
Cajal.

Postal address: Carretera de Colmenar Viejo, Km 9.100. ZIP: 28034.
Madrid, Spain.

Tel: +34913369006. Fax: +34913368515. E-mail: efranco@academiamir.com

\textbf{Financial support} : none

\textbf{Disclosures} : Dr. Eduardo Franco has received consulting fees
from Biosense Webster. Dr. Javier Moreno has received consulting fees
from Boston Medical, Abbott Medical and Biosense Webster. The rest of
the authors declare no conflicts of interest.

\textbf{ABSTRACT}

\textbf{Introduction.} Unstable reentrant atrial tachycardias (ATs)
(i.e. those with frequent circuit modification or conversion to atrial
fibrillation) are challenging to ablate. We have tested a strategy to
achieve arrhythmia stabilization into mappable stable ATs based on the
detection and ablation of rotors.

\textbf{Methods and Results} . From May 2017 to December 2019, 97
consecutive patients with reentrant ATs were ablated. Of these, 18
(18.6\%) presented unstable circuits and were included. Mapping was
performed using conventional high-density mapping catheters (IntellaMap
ORION, PentaRay NAV or Advisor HD Grid). Rotors were subjectively
identified as fractionated continuous (or quasi-continuous) electrograms
on 1-2 adjacent bipoles of the mapping catheter, without dedicated
software. 13 patients (72\%) had detectable rotors (median 2 {[}1--3{]}
rotors per patient); focal ablation achieved conversion into stable AT
or sinus rhythm in 12 (92\%). In the other 6 patients, sites with
spatiotemporal dispersion (i.e. all the cycle length comprised within
the mapping catheter) plus non-continuous fractionation on single
bipoles were targeted. 17 sites with spatiotemporal dispersion were
detected and focally ablated. Globally, and excluding 1 patient with
spontaneous AT stabilization, ablation success to stabilize the AT was
achieved in 16/17 patients (94.1\%). One-year freedom from atrial
arrhythmias was similar between patients with unstable and stable ATs
(66.7\% Vs 65.8\%, p=0.946).

\textbf{Conclusion} . Most unstable reentrant ATs show detectable
rotors, identified as sites with single-bipole fractionated
quasi-continuous signals, or spatiotemporal dispersion plus
non-continuous fractionation. Ablation of these sites is highly
effective to stabilize the AT or convert it into sinus rhythm.

\textbf{KEYWORDS}

Clinical: Catheter ablation -- atrial tachycardia; Clinical: Catheter
ablation -- atrial flutter; Rotor; High-density mapping.

\textbf{INTRODUCTION}

Reentrant atrial tachycardias (ATs), excluding cavotricuspid isthmus
(CTI)-dependent atrial flutter, can be challenging to map, especially
in\emph{unstable} circuits (i.e. those with frequent circuit
modification or conversion to atrial fibrillation (AF)). These cases,
which count for up to 15-20\%,\textsuperscript{1,2} are considered
non-mappable and ablation is frequently not attempted. Electrical
cardioversion and re-induction of the clinical AT can be tried, but
arrhythmia induction and stabilization is often difficult to achieve.
Class Ic antiarrhythmic agents can be used for this
purpose,\textsuperscript{3} but modification of atrial conduction
properties can lead to non-clinical ATs. Other strategy is to perform
substrate mapping and ablation in sinus rhythm.\textsuperscript{4}

Patients with unstable circuits have been excluded from most reentrant
AT ablation series, which have focused on mappable
circuits.\textsuperscript{1,2,5-9} These patients are frequently
considered untreatable with ablation, and this may lead to stopping
rhythm control and accepting the atrial arrhythmia is permanent. During
the last years, ablation strategies that try to terminate AF, the `most
unstable' atrial arrhythmia, via identification and ablation of AF
drivers (rotational or focal), have emerged.\textsuperscript{10} Another
approach is ablate areas with electrical spatiotemporal dispersion
(STD), as a surrogate of local rotational
activation.\textsuperscript{11} Given the known relationship between
atrial fibrillation and reentrant ATs,\textsuperscript{12} we
hypothesized that these strategies, specifically ablation of sites with
rotational activation (i.e. rotors), might as well be used to stabilize
or terminate unstable reentrant ATs.

The Conversion of Hardly mappable Atrial tachycardias via rOtor ablation
into Sinus rhythm (CHAOS) study was a prospective single-center study,
designed to test an ablation strategy in patients with unstable
reentrant ATs based on the ablation of rotors, which were subjectively
identified with conventional high-density mapping catheters as sites
with fractionated quasi-continuous electrograms (EGMs) on 1-2 adjacent
bipoles.

\textbf{METHODS}

The single-center CHAOS study prospectively included all patients
scheduled for reentrant AT ablation from May 2017 to December 2019,
excluding patients diagnosed with CTI-dependent atrial flutter, in which
the tachycardia circuit was deemed non-mappable due to continuous
circuit modification or conversion to atrial fibrillation. All patients
had pre-procedural documentation of reentrant AT on the surface ECG
based on: 1) the presence of continuous atrial activity on the surface
ECG, or: 2) in patients with focal AT pattern, the arrhythmia behavior
(stable cycle length without modification at onset or end) and patient
characteristics (diseased atria).\textsuperscript{13} Patients could
present to the ablation procedure in sinus rhythm, AT or AF.

Written informed consent was obtained before the procedures and patient
data were collected in a dedicated database. The study complied with the
Declaration of Helsinki and received prior approval by the ethics
committee of our institution.

\textbf{Procedures}

Procedures were preferably performed under general anesthesia, or
conscious sedation if general anesthesia was not available.
Antiarrhythmic medications were neither discontinued prior to ablation,
nor administered during the procedures. After achieving
echography-guided femoral vein access, a 24-pole diagnostic catheter
(Woven Orbiter, Boston Scientific Inc.) was placed around the tricuspid
annulus with its distal part into the coronary sinus. If the initial
rhythm was AT, entrainment from both right and left atria (via coronary
sinus) was used to define AT origin. If the patient was in sinus rhythm,
atrial programmed stimulation with ramps was first used to induce AT. If
the left atrium (LA) was intended to map, transseptal puncture with a
conventional long sheath (SL1, Abbott Medical Inc., Chicago, IL) was
performed and intravenous heparin was administered to achieve a target
activated clotting time of 350-400 seconds. Steerable sheaths (Agilis,
Abbott Medical Inc.) were only used to improve catheter manipulation in
selected difficult cases.

Patients were included if AF was induced, or conversion from AT to AF
(or continuous AT circuit changes, considered equivalent to AF) happened
during the procedure, and no spontaneous re-conversion to a stable AT
occurred during the following 15 minutes. Also, patients with AF as
initial rhythm were included.

\textbf{Mapping protocol and rotor identification}

Mapping was performed using conventional high-density electroanatomical
mapping catheters (IntellaMap ORION, Boston Scientific Inc.; PentaRay
NAV, Biosense Webster Inc.; or Advisor HD Grid, Abbott Medical, Inc.)
and their respective mapping system (Rhythmia, Carto3 or Ensite
Precision). Bipolar voltage maps were created, with the threshold for
dense scar set bellow 0.03 mV in all navigation systems, in order to
allow annotation of low-voltage signals.

For patients with AT as initial rhythm, or AT induced from sinus rhythm,
and posterior destabilization, mapping was initiated within the right
atrium (RA) or LA, depending on the suspected origin of the AT according
to initial entrainment. If destabilization occurred before or during
entrainment, mapping was started within the atrium in which initial
disorganization of electrical signals during AT presumably led to AF.
For patients with AF as initial rhythm, mapping was initiated in the
atrium with faster cycle length according to the Orbiter catheter
signals. If rotors were identified in the initially mapped atrium, rotor
ablation was performed; if rotors were not present, or rotor ablation
was not successful to convert AF into AT or sinus rhythm, the other
atrium was then mapped for rotor identification.

Rotors were subjectively identified as fractionated continuous (or
quasi-continuous) bipolar EGMs on 1-2 adjacent bipoles of the mapping
catheter, using a digital recorder (Bard LabSystem Pro) at 200 mm/s
speed (Figure 1, panel A). Filters for bipolar signals were set at 30
and 250 Hz, with notch filter. When such EGMs were identified, the
mapping catheter was kept still for 10 seconds to confirm temporal
stability of the rotor, which was then annotated with a manual marker
deployed on an electroanatomical bipolar voltage map. After mapping was
complete, the mapping catheter was repositioned in sites with rotors to
confirm temporal permanence before ablation. Temporally unstable rotors
were neither annotated nor targeted for ablation.

If rotors were absent in both atria, or rotor ablation was unsuccessful
to stabilize or terminate AF, sites with STD (i.e. all the AF cycle
length comprised within the different bipoles of the mapping catheters)
plus non-continuous fragmentation on single bipoles, arbitrarily defined
as continuous bipolar EGMs with \textgreater{}4 deflections and total
duration \textgreater{}70 ms, were manually annotated and targeted for
ablation (Figure 1, panel B). At least 10 seconds of temporal stability
was also required for these sites.

\textbf{Ablation protocol}

Radiofrequency ablation was performed using open-tip irrigated catheters
(IntellaNav MIFI, Boston Scientific Inc.; Thermocool SmartTouch,
Biosense Webster Inc.; TactiCath, Abbott Medical Inc.; or TactiCath,
Sensor Enabled, Abbott Medical Inc.). A power of 30-35 W was used for
posterior wall lesions, 35-40 W for anterior or free wall lesions, and
25-30 W inside the coronary sinus.

First, focal ablation of the identified rotors were performed with 1-4
adjacent lesions. If rotor ablation was unsuccessful, sites with STD
were targeted using the same focal approach.

\emph{Rotor ablation success} was defined, for each patient, as
conversion to sinus rhythm or a stable AT using the aforementioned
strategy. If rotors were present within the pulmonary veins antra,
circumferential pulmonary vein isolation of that vein or pair of veins
was performed including the rotor within the line. If rotor ablation was
performed \textless{}1 cm from a scar or another radiofrequency
application, an ablation line between them was performed. If rotor
ablation was not successful, electrical cardioversion and empirical
pulmonary vein isolation plus CTI ablation was performed.

All stable ATs were mapped using local activation time mapping,
propagation mapping and entrainment, and subsequently ablated (focal
ablation for small reentries or focal ATs; lines for macroreentries). In
the case of conversion to another AT, the new AT was mapped and ablated.
After conversion to sinus rhythm, bidirectional block at the ablation
lines was checked with differential pacing or with activation mapping,
and absence of capture at focal ablation sites was tested. If the
patient had undergone previous ablation procedures, bidirectional block
of the previously performed lines was checked, and ablation was
performed if gaps were present. Pulmonary vein isolation was not
performed in all patients, but it was routinely completed in those with
previously documented atrial fibrillation.

Finally, programmed atrial stimulation was used to test arrhythmia
inducibility; if other sustained ATs were induced, they were mapped and
ablated. \emph{Procedural success} was defined as the successful
ablation of all inducible ATs, without requiring electrical
cardioversion, with final sinus rhythm and non-inducibility at the end
of the procedure.

\textbf{Follow-up}

Patients were followed up with clinical visits and 24-hour Holter
monitoring at 3, 6 and 12 months. Any arrhythmia lasting
\textgreater{}30 seconds, according to patients' symptoms or documented
on Holter monitoring, was considered a recurrence. A blanking period of
3 months, in which recurrences were mostly treated with electrical
cardioversion, was considered. After the 3-month blanking period,
paroxysmal and well tolerated short episodes of tachycardia were managed
with medication or a wait-and-see strategy. Persistent or bad tolerated
episodes were treated with repeat ablation, electrical cardioversion or
atrioventricular node ablation and pacemaker implant, depending on the
presumed risk of posterior recurrences according to the grade of atrial
disease.

In patients taking rhythm control drugs before the procedure, these were
kept during the blanking period, and afterwards discontinued if no
recurrences had occurred; these drugs might be continued up to 3
additional months (until the 6-month follow-up visit) at the discretion
of the attending physician.

\textbf{Statistical analysis}

Categorical variables are described as number (percentage) and were
compared with the \selectlanguage{greek}χ\selectlanguage{english}\textsuperscript{2} or the Fisher's exact tests, as
appropriate. Continuous variables are described as mean \selectlanguage{ngerman}± SD for
variables with normal distributions or as median {[}interquartile
range{]} for variables not normally distributed. The Kolmogorov-Smirnov
test was used to assess normality in continuous variables. Comparisons
among normal continuous variables were made using Student's t tests
(normal variables) or Mann-Whitney U tests (for variables not normally
distributed). Bilateral p values \textless{}0.05 were considered
statistically significant. For survival analysis (recurrence of atrial
arrhythmias), the Kaplan-Meier method was used. Statistical analysis was
performed using SPSS Statistics Base version 22.0 package (IBM Inc.,
Armonk, NY).

\textbf{RESULTS}

From May 2017 to December 2019, 97 patients were scheduled for reentrant
AT ablation, excluding CTI-dependent atrial flutter. Of these, 18
patients (18.6\%) presented non-mappable circuits and were included
(Table 1). 7 Patients (39\%) were \textgreater{}75 years of age and 4
patients (22\%) were \textgreater{}80 years of age. 7 Patients (39\%)
had severe LA dilation. Mean procedural time was 265 ± 67 minutes and
mean fluoroscopy use, expressed as dose-product area (PDA), was 28499 ±
10212 mGy · cm\textsuperscript{2}. Of note, only 5 patients were on
rhythm control drugs (flecainide, n = 2; propafenone, n = 1; sotalol, n
= 1; and amiodarone, n = 1) before the index procedure.

Included patients (with non-mappable circuits) had less enlarged left
atria than those with mappable circuits.

\textbf{Mapping and rotor ablation}

Among the 18 included patients, 14 (77.7\%) presented to the ablation
procedure in sinus rhythm; in 12 patients, an AT was induced but was
considered not mappable due to conversion to AF (n = 10) or continuous
circuit modification (n = 2); in the other 2 patients, programmed atrial
stimulation directly induced AF. 3 Patients (16.7\%) presented in AT; in
2 of them, conversion to AF during mapping occurred; in the other
patient, after successful ablation of the index AT, programmed atrial
stimulation induced AF. 1 Patient (5.6\%) presented in AF.

Mapping was performed with PentaRay NAV catheter (Carto3) in 5 patients
(28\%), with IntellaMap ORION (Rhythmia) in 11 patients (61\%), and with
Advisor HD Grid (Ensite Precision) in 2 patients (11\%). Contact
force-sensing catheters were used for ablation in 6 patients (33.3\%).
In 9 patients (50\%), rotor mapping and ablation was performed only in
the LA; in 1 patient, only in the RA; in the other 8 patients (44.4\%),
both atria were mapped. Detailed rotor mapping and ablation approach is
showed in Figure 2.

Rotors, defined as sites with fractionated quasi-continuous signals on
1-2 adjacent bipoles of the mapping catheter, were found in 13 patients
(72\%) (median 2 {[}1--3{]} rotors per patient) (Figure 3); all detected
rotors showed temporal permanence after mapping and were target of
ablation. Focal rotor ablation was effective in 12 of these patients
(92\%); in the other patient, after unsuccessful rotor ablation, 2 sites
with STD and non-continuous fragmentation were detected and successfully
ablated to stabilize AF into reentrant AT. In 1 patient without
detectable rotors, spontaneous stabilization of AF into reentrant AT
happened during mapping, and AT ablation could be successfully
performed. In the other 4 patients without rotors, sites with STD and
non-continuous fragmentation were detected (2, 3, 4 and 6 sites in each
patient) (Figure 4); ablation of these sites resulted in arrhythmia
stabilization into AT in 3 patients (75\%); the other patient received
electrical cardioversion. Figure 5 shows location of the detected rotors
and sites with STD and non-continuous fragmentation; globally 44\% were
related with the pulmonary veins antra.

\textbf{Ablation and procedural success}

Globally, and excluding the patient in which spontaneous conversion of
AF into AT occurred, ablation of rotors or sites with STD was effective
in 16/17 patients (\emph{rotor ablation success} : 94.1\%); in 6
patients, conversion to sinus rhythm occurred, whereas in the other 10
patients, ablation resulted in stable AT. Table 2 shows details about
the ATs induced in each patient and the ablation strategy performed; 19
macroreentries and 10 microreentries were found; 5 focal ATs appeared.
Considering previous ablations and the index procedure, 11 patients
(61\%) had pulmonary vein isolation, and 15 patients (83\%) had CTI
ablation.

\emph{Procedural success} was achieved in 16/18 patients (88.9\%). The 2
patients with failed procedure were: the one in which rotor ablation was
not effective and electrical cardioversion was needed (empirical
pulmonary vein isolation plus CTI ablation was performed); and a patient
with successful rotor ablation and subsequent ablation of 2 reentrant
ATs, but inducibility of another AT that was not ablated afterwards (it
was terminated with entrainment maneuvers and no re-inducibility was
attempted). There were no procedural complications. In patients with
mappable reentrant ATs, the rate of procedural success (92.4\%; p =
0.639) and procedural complications (11.4\%; p = 0.200) were similar.

\textbf{Clinical results}

After a mean follow-up of 19.3 ± 15.3 months, and excluding a 3-month
blanking period, mean survival free from atrial arrhythmias was 22.1 ±
3.5 months (95\%CI: 15.4--28.9 months). Clinical and procedural
variables of patients with and without recurrences of atrial arrhythmias
are shown in Table 3. No statistical comparisons were made due to the
limited sample size.

5 Patients had arrhythmia recurrences \emph{during} the blanking period;
in 3 of them, electrical cardioversion was performed, with 1 recurrence
after the blanking period; in the other 2 patients, rhythm control
strategy was abandoned, and atrioventricular node ablation plus
pacemaker implant was needed. 8 Patients had arrhythmia
recurrences\emph{after} the blanking period (including the 2 patients in
whom rhythm control was stopped): 5 with AT and 3 with AF; 3 reablation
procedures were performed; 2 showed a different reentrant AT, and 1
showed a gap-related AT. Of the 15 patients with follow-up
\textgreater{}1 year, 10 (66.7\%) were free from atrial arrhythmias at a
12-month follow-up.

Mean survival free from atrial arrhythmias in patients with ablation of
mappable reentrant ATs during the same period (24.9 ± 2.1 months;
95\%CI: 20.7--29.2 months) was similar (p = 0.740) (Figure 6), as well
as one-year freedom from atrial arrhythmias (65.8\%, p = 0.946).

\textbf{DISCUSSION}

We have tested an ablation strategy for unstable reentrant ATs based on
focal rotor ablation. To our knowledge, this is the first study that
uses driver ablation in patients with reentrant ATs in order to
stabilize unstable circuits. Most patients showed rotors or sites with
STD plus non-continuous fractionation that could be ablated to achieve
AT stabilization or termination with high success.

Ablation of reentrant ATs, excluding CTI-dependent atrial flutter, has
shown limited one-year freedom from atrial arrhythmias in recent reports
(51\%-77\%).\textsuperscript{1,5-7} Moreover, acute procedural success,
defined as AT termination into sinus rhythm or conversion to another AT,
is not achieved in approximately 10-15\% of
cases.\textsuperscript{1,5-7} We have obtained, in a cohort of patients
classically excluded from other series and considered as especially
complex, similar rates of procedural success (88.9\%) and one-year
freedom from atrial arrhythmias (66.7\%). In patients with mappable
reentrant ATs ablated in the same period of time in our Centre, results
were also comparable. Interestingly, included patients had less dilated
atria than these patients with mappable reentrant ATs; maybe, in more
enlarged atrium, with more dense-scarred tissue and less conduction
speed, reentrant circuits are more prone to stabilize.

Rotor identification has to date been based mostly on the use of
dedicated catheters and/or software that imply additional costs and time
consumption during ablation procedures.\textsuperscript{14-17} On the
contrary, STD analysis as a tool to find rotational activity can be
performed with conventional high-density mapping catheters and is
subjectively performed by operators according to visually detectable
electrical patterns which show very high (94.3\%) interobserver
concordance.\textsuperscript{11} Of these patterns, the most specific is
the finding of a fractionated continuous signal in a single bipole of
the mapping catheter, present in almost all regions with dispersion and
in almost no regions without dispersion.\textsuperscript{11} We
hypothesize that fractionated continuous (or quasi-continuous) activity
should be visualized within the majority of rotor cores on bipolar
signals, as true functional microreentries (Figure 1, panel A); in fact,
fragmentation to consider `conventional' anatomical microreentry has
been defined as that comprising \textgreater{}75\% of the tachycardia
cycle length.\textsuperscript{9,18} In peripheral regions, however, we
believe that spatiotemporal distribution of signals (i.e. all the AF
cycle length comprised within the different bipoles of the mapping
catheter), which may exhibit some fractionation but not on a continuous
manner, could be the most frequent pattern. Besides, finding the rotor
pivoting point (i.e. core) would allow focal ablation, which should be
sufficient to stop rotational activity without the need of performing
more extensive ablation of all the rotor `region'. For these reasons, we
decided to use the finding of fractionated quasi-continuous signals on a
limited number of adjacent bipoles of the mapping catheter as our
definition of rotor. This definition, whether representing or not the
true core of rotors, allowed focal ablation with high efficacy in our
series.

Another pattern, electrical STD plus non-continuous fragmentation on
single bipoles, was used as the marker of rotational activity for
patients in which the former pattern could not be found. We hypothesize
that, if the rotor core slightly travels with a rotational pattern,
fractionated but not continuous activity could be visualized with single
bipoles of the mapping catheter located within the travelling trajectory
of the rotor core (Figure 1, panel B).

In patients with AF, conversion rates with driver ablation ranges
between one third\textsuperscript{19} and two thirds of cases in most
reports\textsuperscript{17}, with a pooled success rate of 39.6\% in a
recent meta-analysis,\textsuperscript{10} although higher efficacies up
to 95\% have been reported.\textsuperscript{11} The high conversion rate
observed in our series could be related to the nature of the arrhythmia;
in the continuum between stable reentrant AT and AF, unstable reentrant
ATs might exhibit atrial conduction properties less prone to chaotic
conduction than AF, and, hence, easier to stabilize through ablation.
Also, the mean number of rotors we found in our cohort (2.0 ± 1.23
rotors per patient) is in the low range of reported data on AF driver
ablation (which ranges from 1.8 ± 1.23 to 5 ± 1.5 drivers per
patient)\textsuperscript{11,20}, although no clear relationship between
the number of drivers and ablation success to convert AF seems to
exist.\textsuperscript{10} The main location of rotors was the pulmonary
vein antra (42\%), which is a common place for AF drivers. In a study
that specifically addressed locations where AF termination was achieved
in a cohort of AF patients\textsuperscript{16}, 27.5\% of terminations
occurred ablating within the pulmonary vein antra, and in 91\% of these
locations a rotor was detected.

Another reason that may justify our rotor ablation success rate is a
higher short-term spatiotemporal stability of rotors in the context of
unstable AT than in AF. Although this affirmation is hypothetical, all
rotors that were found through initial mapping in our cohort persisted
in the same location when mapping was complete several minutes
afterwards. The 10-seconds criterion to determine temporal stability of
rotors in our series was arbitrarily set between reported time criteria,
which ranges between 2.5 s and 30 s in most
series.\textsuperscript{11,21} However, spatiotemporal stability of
drivers in the medium or long term in AF patients has not been
demonstrated,\textsuperscript{22} which might account at least partially
(along with atrial disease progression) for arrhythmia recurrences after
driver ablation both in AF and unstable AT patients. Indeed, 37.5\% of
recurrences in our cohort were AF instead of AT.

\textbf{Study limitations}

The main limitation of this study is the limited sample size, due to the
fact that it was a single-center study and patients with non-mappable
reentrant ATs scheduled for ablation are not frequent. Also, as this was
an observational study, no comparisons were made with other ablation
strategies (e.g. substrate ablation), which may have been also
effective.

\textbf{CONCLUSION}

Most non-mappable reentrant ATs show detectable rotors, identified as
sites with single-bipole fractionated quasi-continuous signals, or STD
with non-continuous fractionation. Ablation of these sites is highly
effective to stabilize the AT or convert it into sinus rhythm.

\textbf{REFERENCES}

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7. Winkle RA, Moskovitz R, Mead RH, Engel G, Kong MH, Fleming W,
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8. Takigawa M, Derval N, Frontera A, Martin R, Yamashita S, Cheniti G,
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9. Strisciuglio T, Vandersickel N, Lorenzo G, Van Nieuwenhuyse E, El
Haddad M, De Pooter J, Kyriakopoulou M, Almorad A, Lycke M,
Vandekerckhove Y, Tavernier R, Duytschaever M, Knecht S. Prospective
evaluation of entrainment mapping as an adjunct to new-generation
high-density activation mapping systems of left atrial
tachycardias.\emph{Heart Rhythm} . 2020;17:211-219.

10. Baykaner T, Rogers AJ, Meckler GL, Zaman J, Navara R, Rodrigo M,
Alhusseini M, Kowalewski CAB, Viswanathan MN, Narayan SM, Clopton P,
Wang PJ, Heidenreich PA. Clinical implications of ablation of drivers
for atrial fibrillation: a systematic review and
meta-analysis.\emph{Circ Arrhythm Electrophysiol} . 2018;11:e006119.

11. Seitz J, Bars C, Théodore G, Beurtheret S, Lellouche N, Bremondy M,
Ferracci A, Faure J, Penaranda G, Yamazaki M, Avula UM, Curel L, Siame
S, Berenfeld O, Pisapia A, Kalifa J. AF ablation guided by
spatiotemporal electrogram dispersion without pulmonary vein isolation:
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12. Waldo AL, Feld GK. Inter-relationships of atrial fibrillation and
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13. 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
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American Society of Pacing and Electrophysiology. \emph{J Cardiovasc
Electrophysiol.} 2001;12:852-866.

14. Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel WJ, Miller
JM. Treatment of atrial fibrillation by the ablation of localized
sources: CONFIRM (Conventional Ablation for Atrial Fibrillation With or
Without Focal Impulse and Rotor Modulation) trial. \emph{J Am Coll
Cardiol} . 2012;60:628-636.

15. Calvo D, Rubín J, Pérez D, Morís C. Ablation of rotor domains
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fibrillation. \emph{Circ Arrhythm Electrophysiol} . 2017;10:e005740.

16. Navara R, Leef G, Shenasa F, Kowalewski C, Rogers AJ, Meckler G,
Zaman JAB, Baykaner T, Park S, Turakhia MP, Zei P, Viswanathan M, Wang
PJ, Narayan SM. Independent mapping methods reveal rotational activation
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2018;29:687-695.

17. Quintanilla JG, Alfonso-Almazán JM, Pérez-Castellano N, Pandit SV,
Jalife J, Pérez-Villacastín J, Filgueiras-Rama D. Instantaneous
amplitude and frequency modulations detect the footprint of rotational
activity and reveal stable driver regions as targets for persistent
atrial fibrillation ablation. \emph{Circ Res} . 2019;125:609-627.

18. La\selectlanguage{polish}ţ\selectlanguage{english}cu DG, Bun SS, Viera F, Delassi T, El Jamili M, Al Amoura A,
Saoudi N. Selection of critical isthmus in scar-related atrial
tachycardia using a new automated ultrahigh resolution mapping
system.\emph{Circ Arrhythm Electrophysiol.} 2017;10:e004510.

19. Atienza F, Almendral J, Ormaetxe JM, Moya A, Mart\selectlanguage{ngerman}ínez-Alday JD,
Hernández-Madrid A, Castellanos E, Arribas F, Arias MÁ, Tercedor L,
Peinado R, Arcocha MF, Ortiz M, Martínez-Alzamora N, Arenal A,
Fernández-Avilés F, Jalife J; RADAR-AF Investigators. Comparison of
radiofrequency catheter ablation of drivers and circumferential
pulmonary vein isolation in atrial fibrillation: a noninferiority
randomized multicenter RADAR-AF trial. \emph{J Am Coll Cardiol} .
2014;64:2455-2467.

20. Steinberg JS, Shah Y, Bhatt A, Sichrovsky T, Arshad A, Hansinger E,
Musat D. Focal impulse and rotor modulation: acute procedural
observations and extended clinical follow-up. \emph{Heart Rhythm} .
2017;14:192--197.

21. Honarbakhsh S, Schilling RJ, Finlay M, Keating E, Hunter RJ.
Prospective STAR-guided ablation in persistent atrial fibrillation using
sequential mapping with multipolar catheters. \emph{Circ Arrhythm
Electrophysiol} . 2020;13:e008824.

22. Jarman JW, Wong T, Kojodjojo P, Spohr H, Davies JE, Roughton M,
Francis DP, Kanagaratnam P, Markides V, Davies DW, Peters NS.
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and persistent atrial fibrillation in the human left atrium. \emph{Circ
Arrhythm Electrophysiol} . 2012;5:650-658.

\textbf{FIGURES}

\textbf{FIGURE 1}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1.} Schematic rationale of rotor detection using a
hypothetical 12-pole mapping catheter. (A) A stable rotor would
theoretically show fractionated quasi-continuous electrograms on the
bipoles placed on the rotor core (6-7), as the mapping area of that
bipoles would detect electrical activity during almost all the cycle
length. Other bipoles may (or may not) show some degree of
fractionation. Red arrow represents rotor spiral wavefront. (B) If the
rotor core meanders around the neighboring tissue, the fractionation
would move between different bipoles through time, resulting in
non-continuous fractionation. Red arrow represents meandering of the
rotor core.

\textbf{FIGURE 2}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2.} Detailed mapping and ablation approach. AF = atrial
fibrillation; AT = atrial tachycardia.

* Unstable AT is defined as having continuous circuit modification.

+ Spatiotemporal dispersion mapping was biatrial in all patients but 1,
in which after failed rotor ablation in the LA, sites with
spatiotemporal dispersion were successfully targeted in the LA before
considering RA rotor mapping.

\textbf{FIGURE 3}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 3} . Representative examples of rotors (dotted lines).
Upper panel and middle panel: IntellaMap ORION catheter; rotors detected
in a single bipole. Lower panel: Advisor HD Grid catheter; rotor
detected in 2 adjacent bipoles (D1-D2 and D2-D3). Note the low voltage
of electrical signals in the middle and lower panel. Paper speed: 200
mm/s. ORB = Woven Orbiter catheter; blue bipoles around tricuspid
annulus and green bipoles into the coronary sinus.

\textbf{FIGURE 4}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

\textbf{Figure 4} . Representative examples of sites with spatiotemporal
dispersion and non-continuous fractionation (dotted lines). Arrows
represent hypothetical trajectory of a meandering rotor core. Upper
panel: IntellaMap ORION catheter. Middle panel: PentaRay NAV catheter
(PR). Lower panel: Advisor HD Grid catheter. Paper speed: 200 mm/s. ORB
= Woven Orbiter catheter; blue bipoles around tricuspid annulus and
green bipoles into the coronary sinus.

\textbf{FIGURE 5}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

\textbf{Figure 5.} Location of rotors (pink dots) and sites with
spatiotemporal dispersion and non-continuous fragmented EGMs (green
dots). 11 Rotors (42\%) were related to the antra of the pulmonary
veins, especially the anterior aspect of the right superior pulmonary
vein (n = 6) and the ridge between the left atrial appendage and the
left superior pulmonary vein (n = 4). CS = coronary sinus; FO = foramen
ovale; IVC = inferior vena cava; LIPV = left inferior pulmonary vein;
LSPV = left superior pulmonary vein; RIPV = right inferior pulmonary
vein; RSPV = right superior pulmonary vein; SVC = superior vena cava.

\textbf{FIGURE 6}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

\textbf{Figure 6.} Estimated survival free from atrial arrhythmias,
excluding a 3-month blanking period, in included patients and patients
with ablation of mappable reentrant ATs during the same period. AT =
atrial tachycardia.

\textbf{TABLES}

\textbf{Table 1.} Comparison between clinical variables of the included
patients and patients with mappable reentrant ATs scheduled for ablation
in our Center during the inclusion period.\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
Included patients (non-mappable ATs) (n = 18)\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
Other patients (mappable ATs) (n = 79)\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
p\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Age (years)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
72.1 \selectlanguage{ngerman}± 8.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
70.5 \selectlanguage{ngerman}± 9.0\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.514\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Females (\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
9 (50\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
45 (57\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.610\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Left ventricular ejection fraction (\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
58 {[}54--61{]}\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
64 {[}55--71{]}\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textbf{0.023}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Indexed left atrial volume (ml/m\textsuperscript{2})\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
36.6 \selectlanguage{ngerman}± 11.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
45.8 \selectlanguage{ngerman}± 17.4\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textbf{0.038}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Significant structural cardiopathy\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
9 (50\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
43 (54\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.797\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Previous atrial fibrillation\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
11 (61\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
38 (48\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.435\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Prior ablation procedures - Pulmonary vein isolation - CTI ablation -
Other reentrant AT ablation\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
11 (61\%) 5 (28\%) 6 (33\%) 3 (17\%)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
35 (44\%) 18 (23\%) 19 (24\%) 7 (9\%)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
0.296\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Prior cardiac surgery\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4 (22\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
22 (39\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.772\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

Data are shown as mean \selectlanguage{ngerman}± SD, median {[}interquartile range{]} or number
(percentage), when appropriate. AT = atrial tachycardia. CTI =
Cavotricuspid isthmus.

\textbf{Table 2.} Detailed procedural results in each patient.\selectlanguage{english}
\begin{longtable}[]{@{}llllll@{}}
\toprule
\begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
Patient number\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
Number of rotors\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
Effect of rotor ablation\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
Number of sites with STD *\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
Effect of STD ablation\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
ATs ablated and other performed ablations (apart from focal ablation of
rotors and sites with STD).\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
- Small reentry in the posterior LA wall.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
0 +\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
- Small reentry in the RSPV + right superior PVI.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Typical atrial flutter. - Right superior PVI.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
4\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Typical atrial flutter. - Focal AT in the posterior LA wall.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
5\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Perimitral flutter: ASL. - Typical atrial flutter. - SVC isolation +
line between SVC and IVC to connect rotor ablation sites.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
6\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Small reentry in the LA roof. - Perimitral flutter: MAL. - Typical
atrial flutter.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
7\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Macroreentry around the left pulmonary veins. - Macroreentry around
the right pulmonary veins.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
8\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
5\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- PVI (rotors within the RSPV and LSPV antra). - Focal AT in the crista
terminalis.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
9\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Small reentry in posteroseptal mitral annulus. - Perimitral flutter:
MAL. - Focal AT from proximal coronary sinus. - PVI (gaps from previous
procedure). - Prophylactic ASL. - CTI ablation (gap from previous
procedure).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
10\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Typical atrial flutter. - Macroreentry around the left pulmonary
veins. - Right inferior PVI (gap from previous procedure).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
11\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
4\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
No effect\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Right PVI (sites with SPT within the RSPV antrum). Left pulmonary
veins were spontaneously isolated. - Line from anterior mitral annulus
to scar in the anterior LA wall including site with SPT. - Empirical CTI
ablation after electrical cardioversion.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
12\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Right PVI (rotor within the RSPV antrum). - Small reentry in the
posterior LA roof.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
13\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
No effect\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Macroreentry around the right pulmonary veins. - Line from anterior
mitral annulus to scar in the anterior LA wall including rotor. - Small
reentry in the interatrial septum. - Macroreentry around the left
pulmonary veins.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
14\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
6\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- PVI (sites with SPT within the LIPV and RIPV antra). - Roof line (site
with SPT in the LA roof). - Small reentry in anterior mitral annulus. -
Small reentry in anteroseptal LA wall. - ASL to connect small-reentry
focal ablations. - Prophylactic CTI ablation.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
15\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- ASL to connect 2 focal rotors ablations (PVI performed in previous
procedure). - Prophylactic CTI ablation.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
16\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
SR\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Perimitral flutter: ASL. - Small reentry in anterior LA wall. - Left
PVI (gaps from previous procedure). - Typical atrial flutter.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
17\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- Right PVI (rotor within RSPV antrum). - Small reentry in LSPV: focal
ablation. - Macroreentry around the left pulmonary veins: left PVI. -
Perimitral flutter: ASL. - AVNRT.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
18\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
3\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
AT\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
- PVI (sites with SPT within the LIPV and RIPV antra, and in the ridge).
- Reentry around posterior LA wall scar. - Perimitral flutter: ASL. -
Focal AT from the vein of Marshall. - Focal AT from the anterior LA
wall. - Prophylactic posterior LA box.\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

ASL = anteroseptal line (line between mitral annulus and right superior
pulmonary vein); AT = atrial tachycardia; AVNRT = atrioventricular nodal
reentrant tachycardia; CTI = cavotricuspid isthmus; IVC = inferior vena
cava; LA = left atrium; LIPV = left inferior pulmonary vein; LSPV = left
superior pulmonary vein; MAL = modified anterior line (line between
mitral annulus and left superior pulmonary vein); PVI = pulmonary vein
isolation; RIPV = right inferior pulmonary vein; RSPV = right superior
pulmonary vein; STD = spatiotemporal dispersion; SVC = superior vena
cava.

* Sites with spatiotemporal dispersion plus non-continuous fractionation
were only mapped if no rotors were present or if rotor ablation was
ineffective.

+ Spontaneous conversion from AF to stable AT occurred after rotor
mapping in the left atrium was completed (no rotors were found).

\textbf{Table 3.} Clinical and procedural variables of patients with and
without recurrences of atrial arrhythmias.\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
& Patients without recurrences (n = 10) & Patients with recurrences (n =
8)\tabularnewline
\midrule
\endhead
Age (years) & 71.1 \selectlanguage{ngerman}± 11.2 & 73.2 \selectlanguage{ngerman}± 5.3\tabularnewline
Females (\%) & 4 (40\%) & 5 (63\%)\tabularnewline
Left ventricular ejection fraction (\%) & 56 {[}42--60{]} & 60
{[}55--66{]}\tabularnewline
Indexed left atrial volume (ml/m\textsuperscript{2}) & 33.6 \selectlanguage{ngerman}± 10.6 &
40.2 \selectlanguage{ngerman}± 13.0\tabularnewline
Significant structural cardiopathy & 5 (50\%) & 4 (50\%)\tabularnewline
Previous atrial fibrillation & 6 (60\%) & 5 (63\%)\tabularnewline
Prior ablation procedures & 9 (90\%) & 2 (25\%)\tabularnewline
Prior cardiac surgery & 2 (20\%) & 2 (25\%)\tabularnewline
Procedural time (min) & 260 \selectlanguage{ngerman}± 66 & 267 \selectlanguage{ngerman}± 72\tabularnewline
Presence of rotors & 7 (70\%) & 6 (75\%)\tabularnewline
Use of contact force-sensing ablation catheters & 3 (30\%) & 3
(37\%)\tabularnewline
Pulmonary vein isolation * & 7 (70\%) & 4 (50\%)\tabularnewline
Cavotricuspid isthmus ablation * & 8 (80\%) & 7 (88\%)\tabularnewline
\bottomrule
\end{longtable}

Data are shown as mean \selectlanguage{ngerman}± SD, median {[}interquartile range{]} or number
(percentage), when appropriate. No statistical comparisons between
patients with or without recurrences were made because of the limited
sample size.

* Performed during the index or previous procedures.

\selectlanguage{english}
\FloatBarrier
\end{document}

