Ioan Liuba, M.D., Anders Jönsson,
M.D., Håkan Walfridsson, M.D.
Department of Cardiology, Heartcenter,
University Hospital Linköping, Linköping, Sweden.
Address for correspondence: Ioan
Liuba, M.D., Department of Cardiology, Heartcenter, University Hospital Linköping,
Linköping, Sweden. Email: ioan.liuba@lio.se
Abstract
Incisional atrial tachycardias have been described most frequently in patients
with previous corrective surgery for congenital heart defects and mitral
valve disease. Less information is available on atrial tachycardias appearing
late after isolated aortic valve surgery. We report the case of a patient
who developed a left figure-8 tachycardia after undergoing aortic valve replacement.
During electrophysiologic study the entire cycle length of the tachycardia
was mapped within a low voltage area confined to the left anterior atrial
wall. However, during ablation a transmural lesion could not be attained.
The mapping and ablation strategy along with the mechanism of the tachycardia
are discussed.
Key words: atrial tachycardia; mapping; catheter ablation.
Case report
A 57-year-old
man with dilated cardiomyopathy and chronic heart failure, who had undergone
aortic valve replacement 26 years ago, was referred to our department for
a third attempt at radiofrequency (RF) catheter ablation of an atrial tachycardia.
According to reports, during the previous two electrophysiologic (EP) studies
both a typical atrial flutter and a left atrial reentrant tachycardia (cycle
length 190 ms) could be induced with burst pacing. Nevertheless, RF catheter
ablation had failed in both cases, either because it was not possible to
attain bidirectional block across the cavotricuspid isthmus (despite a large
number of RF applications), or due to transformation of left reentrant tachycardia
into atrial fibrillation during entrainment mapping and the impossibility
of reinducing the same tachycardia after DC cardioversion. The patient continued
to have frequent, prolonged episodes of palpitations despite several antiarrhythmic
drug trials. Twelve-lead ECG documented an atrial tachycardia with a p-p
interval of 240-280 ms and a variable degree of AV block as well as atrial
fibrillation. The patient underwent several successful DC cardioversions for
both arrhythmias. Transthoracic echocardiography revealed left atrial and
ventricular enlargement, left ventricular systolic and diastolic dysfunction,
and mild mitral and moderate tricuspid regurgitation.
At the time of
the third EP study, a decapolar catheter was placed in the coronary sinus
(CS) and a bipolar catheter was positioned in the right ventricle. An 8-French
deflectable quadripolar irrigated-tip catheter (Cordis-Webster, Thermocool,
F-curve) was used for mapping and ablation. Mapping was performed using the
Carto system (Carto; Biosense Inc). RF current was delivered through a Cordis
Stockert generator between the 4-mm tip of the catheter and an adhesive
patch on the posterior chest wall. Ablation was performed in temperature-controlled
mode with a target temperature of 50°C and a power limit of 50 W. Saline
was infused at a rate of 3 ml/min between ablations and 30 ml/min during RF
current delivery. After obtaining a right atrial activation map with an electroanatomical
reconstruction of the right atrium during proximal CS pacing, a regular tachycardia,
with ECG morphology similar to the clinically documented tachycardia, was
induced with burst pacing (Fig. 1). The CS electrograms were of low
amplitude, with electrograms in CS 9-10 starting 23 ms before electrograms
in CS 1-2.
Click here to enlarge
Fig. 1. Twelve-lead ECG and intracardiac
recordings during tachycardia. Note the positive p waves in lead V1. RF =
bipolar electrograms from the ablation catheter; CS = coronary sinus.
Click here to enlarge
Fig. 2. (A) Right anterior
oblique projection of the activation map of the left atrium during tachycardia.
Insets display local electrograms. The entire cycle length of the tachycardia
was mapped within a low voltage zone containing double- and fragmented potentials
(blue and yellow dots respectively) and electrically silent areas. We hypothesized
that the common channel is bordered by two lines of double potentials (parallel
white dotted lines) and a discrete scar (voltage 0.04 mV, medial gray area).
One loop revolves medially around a third, transverse, line of double potentials
(third white dotted line) and then propagates through a channel bordered
by this line and the ostium of the right inferior pulmonary vein. The second
loop revolves laterally through a channel bordered by the lateral line of
double potentials and a second, lower scar (voltage 0.03-0.05 mV, lower gray
area). Both groups of points exhibiting fragmented potentials, situated,
the first in the lateral channel, the second inferior to the transverse line
of block, have close activation times (-50 to -70 mV). The first component
of the isolated double potential point situated medially to the upper scar,
as well as points situated laterally to the lower scar, exhibit close activation
times also; nevertheless they are activated 20-40 ms later than the rest
of the fragmented potential points, thus further confirming the bifurcation
of the activation front at the exit from the common channel. The left superior
pulmonary vein (LSPV) and the right superior pulmonary veins (RSPV) are depicted
by red and dark gray tubular icons, respectively. Pink dots represent points
situated on the mitral annulus (MA). (B) Bipolar voltage map shows
that the entire circuit is confined to a larger low voltage area. (C)
Biosense propagation map depicting activation of the left atrium viewed
in a left anterior oblique projection.
Discussion
Tachycardias
with figure-8 activation pattern have been described both in the right and
left atrium, most frequently in patients who have undergone surgery for
congenital heart defects and valve disease1,2,3,4,5,6,7. As with other incisional
tachycardias, the electrophysiological substrate is provided by the presence
of areas of low voltage and depressed conductivity, electrically silent zones
and lines of block that are attributable to an insufficient myocardial protection
of cardioplegia, atriotomies and cannulating sites3,4,8. In the
right atrium the loops are often disposed around the tricuspid annulus and
lateral atriotomies, while in the left atrium the geometry seems more variable,
with loops rotating around mitral annulus, electrically unexcitable areas,
or the ostia of the pulmonary veins1,2,4,5.
It is conceivable
that a figure-8 activation pattern may be encountered in both reentrant and
focal tachycardias9. The latter
scenario supposes the existence of a discharging focus inside a protected
isthmus having a zone of slow conduction at one of its extremities. Entrainment
is therefore of particular interest in such tachycardias since its demonstration
may relatively simply differentiate between a reentrant and a focal mechanism.
Furthermore, a post-pacing interval equal to tachycardia cycle length indicates
a site within the reentry circuit while supplementary demonstration of a
short stimulus-to-P wave interval points out the exit of the protected isthmus.
However, one of the main shortcomings of entrainment mapping is the possibility
of interrupting or transforming the tachycardia during rapid pacing. This
aspect is of particular concern in patients with left atrial tachycardias4. Therefore, some authors prefer to delineate
the circuit by performing a high-density activation mapping of the entire
cavity avoiding thus entrainment1,2,3. In this case, the reentrant nature
of the tachycardia as well as the configuration of the circuit are finally
proven by successfully interrupting the loops during ablation (Mines’ test).
RF current may be delivered either in the common isthmus or separately for
each of the two loops (in the latter case, sometimes with an instantaneous
ECG transformation of the tachycardia after the interruption of the first
loop)1.
We have found
in the literature 5 patients with atrial tachycardias and a remote history
of isolated aortic valve replacement2,,5,6,7. All had macroreentrant tachycardias
(4 in the left atrium, 1 in the right atrium) and 1 presented a concomitant
focal tachycardia. Among patients with left tachycardias, data regarding
activation map and/or ablation were available only in two cases. In the first
case, described by Jais et al.2, although no complete electro-anatomical
map was obtained, the tachycardia was successfully ablated by drawing a line
between the ostium of the right superior pulmonary vein and the mitral annulus.
In the second case, reported by Ouyang et al.5, mapping revealed a figure-8 activation
pattern with one loop situated in the anterior left atrial wall and the other
one in the roof of the same atrium. Curative ablation was performed at the
shared channel identified by activation and entrainment mapping.
In this report
we describe a figure-8 tachycardia originating in the left anterior atrial
wall in another patient with previous aortic valve replacement. The full
cycle length of the tachycardia was mapped inside a low voltage zone containing
electrically silent areas and multiple sites exhibiting double- or
fragmented potentials. This fact suggests a severely affected anatomical substrate.
In order to avoid terminating or transforming the tachycardia, as reported
during the previous two EP studies in this patient, we did not perform entrainment.
Ablation targeted what was regarded as the common and medial channels (including
the possible channel between the medial scar and the transverse line of double
potentials) and, presumably, in order to avoid other secondary circuits,
it should have been continued in the lateral channel as well. Tachycardia
interruption along with its noninducibility after severance of these channels
would have supported our hypothesis concerning the electrophysiological mechanism
and the configuration of the circuit. However the instability and difficult
maneuverability of the catheter, probably explained by the anatomical position
of the targeted area, precluded a transmural ablation. Additional factors
contributing to this outcome might be the structural changes of the anatomical
substrate and the fact that we targeted first the common and medial channels.
Shah et al.1.
noted that
in the case of right figure-8 tachycardias, catheter stability in the region
of the shared isthmus may be problematic.
This report confirms
that patients with previous aortic valve replacement may have areas with
abnormal electrophysiology in the left atrium that favor complex atrial tachycardias.
Participation of the left anterior atrial wall in such tachycardias (as showed
in the patient presented by Ouyang et al. and in this report) may be related
to mechanical trauma during surgery (due to the proximity of this region
to aortic root) as well as to intra- and postoperative atrial ischemia. In
cases of figure-8 activation patterns, confirmation of the tachycardia mechanism
and geometry of the circuit requires detailed activation mapping combined
with entrainment and/or a successful ablation strategy (defined as modification/interruption
of the tachycardia due to a transmural lesion with impossibility of reinitiating
the same tachycardia).
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