A Difficult Case of Atrial Tachycardia
Meruka Hazari MD, Deepak Saluja MD
Rutgers- Robert Wood Johnson Medical School.
A 60-year-old male with a history of prior ablation of typical cavotricuspid isthmus-dependent atrial flutter presented to us with recurrent palpitations. The surface 12-lead EKG was consistent with atrial tachycardia, for which an ablation was planned. The patient was found to have multiple marcroreentrant left atrial tachycardias utilizing areas of scar as substrate. Isthmuses of tissue with fractionated electrograms associated with scar were targeted for ablation.
Corresponding Address : Deepak Saluja, M.D.Department of CardiologyRutgers- Robert Wood Johnson Medical SchoolOne Robert Wood Johnson PlaceMEB 583New Brunswick, NJ 08903
While well known in patients with prior ablation or cardiac surgery, left atrial tachycardias in patients without previous surgery or ablation are much less common. The available literature suggests that spontaneous scarring in characteristic areas of the left atrium produces the substrate for marcroreentry, which commonly involves the mitral valve and right-sided pulmonary veins. These rhythms can be successfully ablated by targeting isthmuses of slow conduction created either between adjacent areas of scar or between an area of scar and an anatomical barrier. We describe the electrophysiological findings and results of ablation in a patient with scar-related macroreentrant left atrial tachycardias without prior surgery or ablation.
A 64 year-old man with a history of hyperlipidemia and coronary artery disease with a previous stent to the right coronary artery for angina, and a prior ablation for typical cavotricuspid isthmus-dependent atrial flutter presented with intermittent palpitations. An echocardiogram showed an ejection fraction of 60% with normal valvular function, a normally sized left atrium (LA), and no wall motion abnormalities. A 12-lead EKG of the presenting rhythm (Fig. 1) showed an atrial tachycardia (AT) with an atrial cycle length of approximately 220ms.
The patient presented to the electrophysiology laboratory in sinus rhythm. An AT with a cycle length and morphology similar to that shown in Fig 1 was induced. The earliest activation on the decapolar coronary sinus (CS) catheter was seen in CS 3-4 (Fig 2A). Ablation and circular mapping catheters were delivered to the LA via double transseptal punctures. Examination of the endocardial LA revealed large areas of decreased voltage (<0.5mV) on the anterior, septal, and posterior aspects of the LA, as well as on the roof (Fig. 3A,B and C).
Twelve-lead EKG of clinical tachycardia
An activation map of the initial tachycardia (AT1) suggested a double-loop pattern of reentry with an isthmus of tissue between two areas of dense scar near the posterior right-sided pulmonary vein carina acting as the common pathway (see Fig 4A and Propagation video #1). Ablation lesions were applied connecting areas of scar surrounding the circuit (Fig 3C, arrows), first resulting in variable exit block (Fig 5B), then complete isolation of the circuit with resumption of sinus rhythm in the body of the atrium (Fig 5C). Ablation of fractionated EGMs in the common isthmus (Fig 3C, asterisk) resulted in termination of the isolated tachycardia (Fig 5C).
Burst pacing from the CS initiated a second tachycardia (AT2) with left to right CS activation (Fig 2B). Entrainment demonstrated that two separate CS bipoles were included in the circuit (Fig 6A and B), and an electroanatomic activation map confirmed the diagnosis of perimitral flutter (Fig 4B and Propagation Video #2). An ablation line was created from pre-existing scar in the anterior LA to the mitral valve (Fig 3A), resulting in termination of AT2.
Burst pacing from the CS initiated a third tachycardia (AT3). The CS activation sequence of AT3 was reminiscent of perimitral flutter, and may have been mistaken for a recurrence of AT2. However, placement of the ablation catheter distal to the distal CS electrode indicated nonlinear activation of the CS, which is inconsistent with perimitral activation (Fig 2C). Furthermore, entrainment of the proximal CS was inconsistent with its participation in the circuit (Fig 6C). An activation map was created (Fig 4C and Propagation Video #3), showing AT3 to be a reentrant circuit rotating around the anterior scar and breaking through the previously created mitral line. Additional ablation in the region of the anterior mitral line resulted in termination of the tachycardia.
The CS activation sequences of AT1 (A), AT2 (B) and AT3 (C) are shown. In 2B, the ablation catheter (ABL) is located anterior to the CS os. In 2C, ABL D is located just distal to the distal CS electrode
No other tachycardias were inducible, and the patient has remained free of palpitations in two years of follow-up.
Voltage maps of the LA shown in modified AP (A), right lateral (B), and PA (C) views. AT1 was a double-loop reentry centered around the isthmus of tissue in between two scars near the posterior carina of the two right sided pulmonary veins (asterisk). Ablation (performed at the site of the black arrows) connecting adjacent regions of scar resulted in isolation of tachycardia with resumption of sinus rhythm in the main body of the atrium. EGMs at the site of the asterisk were fractionated, and ablation there resulted in termination of tachycardia. See text
We describe a case of multiple left atrial reentrant circuits
associated with endocardial scarring in a patient with no prior
ablation or surgery and an apparently structurally normal heart.
Literature on the study of atrial tachyarrhythmia is hampered by
heterogeneity in terminology. Traditionally, organized non-sinus
atrial tachyarrhythmias have been classified as either atrial flutter or
atrial tachycardia (AT) based upon the surface EKG characteristics
of an upper atrial rate cutoff of 240-250/min and an isoelectric
baseline between atrial deflections as defining AT.5 However, this
classification is insensitive to mechanism, which has become more
precisely understood as mapping technology has advanced. In
practice, many electrophysiologists utilize the term atrial flutter to
describe a macroreentrant circuit, and atrial tachycardia to describe
a focal mechanism. This classification is insensitive to rate, and
presupposes a knowledge of the tachycardia mechanism, which may
be apparent only after invasive study. We will use the term atrial
tachycardia to generally describe an organized atrial tachyarrhythmia
of non-sinus origin, and atrial macroreentrant tachycardia (AMRT)
to describe an atrial rhythm due to a reentry circuit of measurable
size with fixed and/or functional barriers.
Left atrial tachycardia (LAT) is commonly seen after atrial
fibrillation ablation, occurring with a frequency of 3-30%.2 Areas
of incomplete prior ablation frequently provide regions of slow
conduction that may used as substrates for reentry.2-4 However, LAT
occurring in a naïve and structurally normal heart is less common.
Focal LAT has been described as occurring in between 9 to 37% of all focal tachycardias,5 but left AMRT may be less common than that,
occurring in 2.6% of all organized atypical reentrant tachycardias
described in one series,6 and comprising only 10% of all patients
referred for any type of LAT ablation in another.7
The available literature suggests that in these patients, macroreentry
is associated with regions of atrial scarring, particularly in the
anterior, superior, and posterior aspects of the LA near the rightsided
pulmonary veins, which can encompass a significant portion of the atrial mass (on average 25%8). Narrow isthmuses of tissue
between adjacent areas of scar or between an area of scar and an
anatomic barrier (such as the mitral annulus) frequently demonstrate
fractionated, long-duration electrograms, which create the substrate
for reentry, and can be successfully targeted by ablation.7,8 Acute
success rates for ablation are as high as 82%,6 although recurrence
rates may be as high as 20-45% in medium-term follow-up.6-8 The
arrhythmias seen commonly involve either the right-sided pulmonary
veins and/or the mitral valve, with double-loop reentry implicated in
a substantial number of cases.6,7
The diagnosis of left AMRT may not be suspected prior to invasive
study, since patients do not have common risk factors for left-sided
arrhythmias. A left-sided origin may be suggested on the surface
EKG by the presence of an upright or isoelectric p-wave in V1,7 but
focal mechanism is frequently suspected, since isoelectric intervals
between p-waves corresponding to long-duration fractionated
EGMs are commonly encountered.7,8
The case we describe parallels many of the features typically found
in these patients. We induced three tachycardias associated with scars
in the anterior, superior, and posterior aspects of the LA. The ability
to map the entire the cycle length, the demonstration of critical
isthmuses of conduction, and the response to entrainment suggest
these rhythms were reentrant.
Ablation between regions of adjacent scar was used first to isolate,
then to terminate, AT1, which was a double-loop reentry circuit near
the posterior right-sided venous carina. AT2 was a perimitral flutter
passing through an area of fractionation between the anterior scar
and the mitral annulus. Ablation through this area, connecting the
scar with the valve annulus, terminated tachycardia. AT3 rotated
around an anterior scar and passed through the same isthmus of
tissue utilized in AT2. Although these features were present in the
atrium at baseline, AT3 was induced after ablation was performed
in this region, and as such we cannot rule out an iatrogenic etiology.
Rapidly distinguishing between distinct arrhythmias that may
appear similar in the limited number of fixed bipoles available in
a typical study is key for the electrophysiologist ablating multiple
ATs. Failing to recognize arrhythmia transformation can result in inaccurate activation maps and prolonged procedure times. Strategic
sampling of activation and entrainment points can, in some cases, be
used to rapidly guide AT mapping.
Activation maps of AT1 (A), AT2 (B), and AT3 (C)
A) AT1 is shown, with 1:1 conduction out of the circuit to the rest of the atrium. Ablation connecting areas of scar around the circuit resulted in variable block (B), then isolation of the circuit from the remainder of the atrium, which converted to sinus rhythm (C). Ablation of fractionated signal tissue in the common isthmus of the circuit resulted in termination of the isolated tachycardia (C). The circular mapping catheter (Lasso 1-20) is positioned in the right upper pulmonary vein
Entrainment of AT2 from CS 5-6 (A) and distal CS (B) at an S1 of 210ms demonstrates post-pacing intervals of 227ms and 225ms, respectively. The tachycardia cycle length of AT2 was 220ms. C) Entrainment of AT3 from proximal CS at an S1 of 220ms demonstrates a post-pacing interval of 273ms. The cycle length of AT3 was 232ms
In our patient, the CS activation and cycle lengths of AT2 and
AT3 were similar (Fig 2B and 2C). In the case of AT2, performing
entrainment from two different CS locations (Fig 6A and B) rapidly
suggested a perimitral circuit, which could then be confirmed with
activation mapping. Similarly, in the case of AT3, placing the mapping
catheter distal to the distal CS electrode rapidly demonstrated
nonlinear CS activation, and entrainment from the proximal CS
(Fig 6C) confirmed that a recurrence of perimitral flutter could be
ruled-out, allowing the focus to shift to mapping a new arrhythmia.
This case also demonstrates the utility of fully assessing scar burden,
when present, in patients with multiple tachycardias, as scars may be
implicated in either the genesis of the arrhythmia and/or be targeted