Introduction
Key Teaching Points
•
Left atrial propagation can occur via nonuniform 3-D activation patterns in refractory
cases of atrial flutter with prior endocardial block.
•
The Bachmann bundle is an important anatomic structure that may be resistant to transmural
ablation and can function as an epicardial bridge across the anterior wall of the
left atrium.
•
Epicardial mapping can provide mechanistic evidence for the challenges in creating
durable transmural anterior block across the mitral isthmus.
The left atrium is typically perceived as a thin-walled chamber without anatomic impediments
to creating transmural ablation lesions. However, nontransmural lesions are a common
cause of recurrent mitral annular atrial flutter (MAFL),
1
representing ablation gaps in 3-D (depth). Percutaneous epicardial mapping in the
region of the Bachmann bundle (BB) may provide mechanistic evidence for the difficulties
associated with creating durable anterior block for MAFL. We report a case of MAFL
with epicardial bridging over a previously blocked endocardial anterior linear lesion
set.
Case report
A 67-year-old man presented with atrial flutter recurrence despite 3 prior procedures
of pulmonary vein isolation with linear ablations. Spontaneous MAFL was detected in
the previous procedure with failed mitral isthmus (MI) line ablation and finally terminated
with additional ablation along the anterior wall. Only a unidirectional block of an
inferolateral MI line was confirmed (proximal-to-distal coronary sinus activation
with lateral pacing). However, atrial flutter recurred within 2 weeks.
Owing to multiple failed endocardial attempts, a minimally invasive maze procedure
was offered, but the patient preferred an adjunctive percutaneous epicardial approach.
Our approach to epicardial mapping for refractory atrial fibrillation has been previously
described.
1
Briefly, epicardial access was obtained prior to systemic heparinization and a steerable
sheath was used to facilitate mapping of the posterior wall and sulcus between the
left atrial appendage and left superior pulmonary vein. Activation mapping was performed
of the clinical atrial flutter (tachycardia cycle length 360 ms), which indicated
clockwise MAFL.
However, the prior endocardial anterior line appeared blocked with extensive low-voltage
scar (<0.1 mV) and low-voltage zone (<0.5 mV) without discrete electrograms (EGM).
A discontinuous activation pattern of endocardial activation was observed, with an
incomplete leak at the roof and focal activation distal to the anterior line with
propagation back towards it (Figure 1). Therefore, an epicardial breakthrough was
suspected. Of note, there were split potentials within the coronary sinus and the
epicardial lateral isthmus over a previously performed inferior mitral line. Additional
advancement of a decapolar catheter (DecaNav, Biosense Webster, Diamond Bar, CA) through
the epicardial aspect of the left-sided ridge resulted in direct recordings of the
roof and anterior wall over the region of the BB. High-density mapping (4338 points)
exhibited a long, local, fractionated EGM (103 ms) recorded over the epicardial anterior
wall on the distal decapolar catheter, which bridged the flutter propagation during
the endocardial activation gap (Figure 2, also shown in Supplementary Video).
Figure 1
A 3-dimensional activation map of the left atrial endocardium revealed discontinuous
activation with endocardial block, a leak near the roof, and then sudden breakthrough
at the anterolateral wall by the left atrial appendage. Endocardial activation consisting
of far-field electrograms (EGM) within the anterior mitral line corresponds with continuous
near-field local epicardial activation over the region of the Bachmann bundle.
Figure 2
A 3-dimensional activation map shows epicardial geometry overlying the region of the
Bachmann bundle (BB), at the site of discontinuous endocardial activation. A long
fractionated local epicardial electrogram was recorded on decapolar 3,4 over the region
of the BB, which was captured by overdrive pacing fulfilling classical entrainment
criteria with concealed intracardiac fusion. CS = coronary sinus; LAA = left atrial
appendage; LSPV = left superior pulmonary vein; MV = mitral valve; RA = right atrium;
RSPV = right superior pulmonary vein; SVC = superior vena cava. Anatomic image courtesy
of Angel Cabrera, MD, PhD, with permission.
Overdrive pacing was performed from the fractionated EGM on decapolar 3,4 was captured
by pacing with 350 ms (1 mA and 1.0 ms), which demonstrated entrainment with concealed
intracardiac fusion, proving that the epicardial BB was “in” the flutter circuit (Figure 2).
Ablation targeting the fragmented epicardial EGM prolonged the cycle length immediately,
with subsequent flutter termination to sinus rhythm lateral to this site (40 W, 17–20
mL/min). Additional endocardial ablation was performed directly across these successful
sites to optimize transmurality. The patient was noninducible for atrial flutter as
the procedural endpoint. At 2-month follow-up, the patient has remained free of recurrence.
Discussion
The functional relevance of epicardial structures like the vein of Marshall
2
and septopulmonary bundle
3
have been recently described in refractory left atrial flutter. MAFL is commonly encountered
after atrial fibrillation ablation and terminated by creating linear lesion sets across
the MI, although epicardial structures like the vein of Marshall and coronary sinus
may serve as a barrier for MI ablation transmurality.
2
,
4
,
5
While an anterior line is predominantly performed targeting thinner atrial myocardium,
the thickness of epicardial structures in the region of BB is a barrier to achieving
completely transmural lesions.
BB is a primary interatrial connection that spans from the superior vena cava to the
left atrial appendage along the epicardial left atrial superior anterior wall. Piorkowski
and colleagues
6
demonstrated the requirement for epicardial ablation to achieve anterior block in
78% of cases as well as localized epicardial reentry within abnormal BB fibers. However,
simultaneous epi-endo mapping with nonuniform activation between the 2 surfaces during
macroreentry was not reported. The creation of biatrial reentry over BB with endocardial
block has been previously described.
7
Miyazawa and colleagues
8
reported an MAFL across the endocardial anterior scar, while with indirect evidence
indicating a detouring circuit conducting at the epicardial anterior wall. In our
case, the refractory MAFL in the presence of endocardial anterior line block with
focal distal breakthrough led to a suspected epicardial breakthrough. Direct epicardial
recordings over the Bachmann bundle region exhibited a fragmented EGM with concealed
entrainment, indicating a slowly conducting activation bridge over the BB region during
MAFL. In this regard, the case highlights the difficulties associated with creating
durable anterior block across the MI, and highlights complex 3-D activation in refractory
cases of atrial flutter bridged by epicardial structures. We can only conclude that
the recorded EGM is in the region of the BB, as precise correlation would require
direct visualization and/or pathologic confirmation.
Conclusions
The BB consists of epicardial fibers that serve as an important barrier to achieving
transmural conduction block across the anterior wall and is fully accessible via a
percutaneous epicardial approach. Activation and entrainment mapping were consistent
with critical participation of epicardial activation over the region of the BB to
sustain refractory MAFL. Discontinuous endocardial activation patterns signify the
presence of epicardial bridging, which highlights the need to consider 3-D activation
in refractory cases of atrial flutter with prior endocardial block. To the best of
our knowledge, this is the first report of simultaneous epicardial and endocardial
mapping during refractory left atrial macroreentry that provides direct evidence of
epicardial bridging across the BB region as the mechanism of discontinuous endocardial
activation.