Figure 3 Propagation map of both atria with marked circuit of the
peri-CS flutter. Blue spheres show exemplary areas with double signals
with one highly fractionated component, white ones exits in the right
and left atrium with a PPI equal to the tachycardia cycle length (CL).
PPI-CL from all decapolar catheter bipoles was <20msec. White
crosses represent sites with PPI-TCL>50msec.
Radiofrequency energy was delivered endocardial in LA at the area of
fractionated signals at the inferolateral exit of the CS using an
irrigated 3,5mm-tip ablation catheter (TactiCath SE, St Jude Medical)
with a power of 40 Watts and a cut-off temperature of 43◦C terminating
the tachycardia at the first application.
On completion of the procedure, bidirectional conduction block at the
roof line without further ablation was proven. Noninducibility of the
tachycardias was also confirmed by burst pacing down to a CL of 200msec.
Discussion
Atrial arrhythmias involving the musculature of the coronary sinus are
common after ablation for atrial fibrillation but also in patients
without prior procedures, mostly in the context of a perimitral flutter
with a critical isthmus in the LA. Less commonly, but with increasing
incidence after atrial ablation, a biatrial flutter that utilizes the CS
musculature is diagnosed. The increasing incidence may partly be due to
a better understanding of tachycardia mechanisms through high density
activation maps.
We here describe a rare type of biatrial flutter that utilizes the CS
musculature, the adjacent myocardium of the LA and the right atrium in
the CS orifice only. To the best of our knowledge, this type of
macroreentrant tachycardia has only been described once before. Maruyama
et al described a case of peri-coronary sinus flutter after ablation in
the proximal CS in the context of AVNRT ablation. The CS musculature was
activated from proximal to distal during the tachycardia exiting in the
inferolateral LA and reaching the CS orifice endocardially again. The
decapolar catheter showed double potentials in the coronary sinus with a
dull second component.
In our case, the decapolar catheter in coronary sinus with its larger
cylindric electrodes, despite the spacing of 2 mm, showed the
endocardial activity, epicardial CS sleeves activity was not detected.
This could also be due to anteroposterior position discrepancy (see
Figure 1). The HD-mapping catheter with the flat small electrodes,
though endocardial, was capable of showing signals of the CS
musculature. Hence, the signals on the linear catheter in the coronary
sinus should not be equated to the activity of the CS musculature, as
they can be far field signals of the numerous LA endocardial myocardial
cells. The amplitude of a bipolar electrogram depends on the electrode
size, the electrode spacing, the angle of incidence between the catheter
and tissue, and the orientation of the bipole relative to the wavefront
propagation. It has been previously shown in ventricular mapping that
the grid catheter with a smaller electrode area, increased electrode
density and orthogonal bipole orientations, was capable of detecting
activation at the same anatomic sites where a linear catheter failed to
record any activity.
A recent study showed that depending on the adjacent tissue EGMs
acquired from larger electrodes may be composed of far-field components
without near-field components.
Our case is the first case proving this unique form of peri-CS flutter
through extensive biatrial ultra high-density mapping with a multipolar
HD-mapping catheter. In our case there was no previous ablation within
or in vicinity of the coronary sinus.
Unawareness of the possibility of such a flutter circuit could lead to
underdiagnosis. Proof of participation of CS musculature in the
macroreentrant circuit is ordinarily used as equivalent to confirmation
of a perimitral flutter. Extensive activation and entrainment mapping
including the coronary sinus and the LA bottom is of substantial
importance to verify the exact tachycardia mechanism. The LA bottom,
despite the distance to the pulmonary veins and the often present
difficult anatomical conditions, should not be neglected.
Such a circuit could probably also coexist with a perimitral flutter as
a dual loop tachycardia. Especially if during a perimitral flutter
double signals with inverse activation sequences are detectable
throughout the coronary sinus, such as the cases of perimitral flutter
reported from Olgin et al and Jimenez et al.
Conclusion
The CS musculature with its connections to both atria can provide the
anatomic substrate for macroreentrant atrial tachycardias. The
peri-coronary sinus atrial flutter without utilizing a larger left
atrial or biatrial circuit, although rare, should be included in the
differential diagnosis of an atypical flutter. Awareness of the
existence of this type of atrial flutter is required to prevent
underdiagnosis. Despite the precision of the current electroanatomical
maps, basic electrophysiological maneuvers such as entrainment mapping
should be, if possible, part of every electrophysiological study of a
stable macroreentrant tachycardia. A multipolar HD-mapping catheter with
small flat electrodes can record crucial low voltage electrocardiograms.
This underlines the use of HD-mapping catheters and systems to directly
address the tachycardia pathomechanism and prevent needless ablation due
to misunderstanding of the tachycardia.