Discussion:
Although current guidelines recommend pacemaker implant in patients with
severe symptomatic bradyarrhythmias, there is evidence that some of
these disorders are related to functional imbalance in cardiac autonomic
nervous system with a predominant excess of vagal tone(10). Cardiac parasympathetic drive occurs through
efferent signals from vagal fibers, connected to postganglionic cells
within atrial walls or in para-cardiac ganglia, mainly by decreasing
automatism, excitability and conductivity. Cardiac modulation of
parasympathetic GP abolishes the influence of excessive parasympathetic
autonomic influence (4). Even though GP are located in
epicardial fat pads, the extensive network of intramural atrial micro
ganglia(2,7,12) renders endocardial ablation
effective. Various reports (4,5,7,12) have shown that
modulation of cardiac parasympathetic system supports this approach as
an alternative strategy for these patients, particularly at younger ages
for whom pacemaker implant is unwanted due to its potential lifelong
complications. Similarly, in patients with vagally related AF in whom
increased parasympathetic tone has an important role in initiation and
perpetuation of AF episodes, modulation of parasympathetic drive in
addition to PVI seems to confer increased arrhythmia free survival(2,13).
The exclusion of sinus and AV node intrinsic disease can be done
non-invasively with Holter monitoring and exercise treadmill test.
Maintained circadian variation of HR and normal chronotropic response to
exercise are excellent surrogates of normal intrinsic sinus and AV node
function. Previous studies have found comparable accuracy of Holter
monitoring and treadmill exercise test with intrinsic HR measurements
after pharmacological autonomic blockade. On the other hand,
interpreting the measurement of baseline sinus node recovery time (SNRT)
performed at electrophysiological study is difficult, as pacing
suppression can be a normal phenomenon even in patients with normal
sinus node function and because of existent overlap in recovery times
between patients with normal and abnormal sinus node function.
Additionally, it has sensitivity of only 70% (14).
Furthermore, performing SNRT without pharmacological blockade is
misleading and do no reflect the intrinsic properties of sinus and AV
node and that is the reason why we didn“t performed SNRT.
In our study we included patients with suspected parasympathetic driven
bradyarrhythmias, that showed adequate chronotropic response on
non-invasive evaluation which otherwise would have indication for
pacemaker implant due to the severity of the clinical symptoms or the
rhythm disorder. Our results show that modulation of parasympathetic
cardiac system is effective in treating functional bradyarrhythmias. It
has shown good results in immediate period after ablation with increase
in HR, in shortening of AH intervals and WBCL and on follow up, as none
of the patients had recurrence of symptoms or severe bradyarrhythmias.
So far, targeting GP for parasympathetic modulation has been quite
challenging. Most of previous studies have used complicated
methodologies requiring appropriate specific systems for identification
of GP site, leading to extensive ablation in the atria and predisposing
patients to iatrogenic atrial arrhythmias (15).
Previous works (3,5,8,9,16,17) have shown that GP
ablation can be achieved either using high frequency stimulation (HFS)
(from epicardial or endocardial sides) to identify the GP or with an
anatomical approach at known GP sites. Some works(3,9,12,18) have posteriorly shown that the
sensitivity of HFS is low (21-71%) for the identification of GP sites
and for assessment of the success of ablation. It is increasingly
supported in the literature, the superiority of the anatomical approach
over the HFS methodology due do the inconsistent parasympathetic
response of the later. Besides, it allows avoidance of additional
dedicated catheters and generators to perform HFS and spares the awake
patient the unpleasant procedure (7,17,19). Our work
pursued a simplified methodology to perform parasympathetic modulation,
using only an anatomical approach with 3D electroanatomic mapping and
geometry reconstruction. With this method the GP described location was
easily accessible, as was precise delivery of radiofrequency lesions
with homogenization of the created scars and reducing potential
additional procedure complications, without compromising success.
Likewise, endpoints of the procedure are not standardized and there is
no current consensus on endpoints for successful procedures. The most
used assessment of parasympathetic modulation by achieving a blunted HR
response with atropine administration after ablation has low value
because of the increase in sympathetic tone (8,19).
So, in our study the endpoint of ablation was only anatomical deployment
of lesion in pre specified sites and with pre specified settings,
irrespective of any change in electrophysiological parameters.
Anatomic and physiological studies demonstrate that parasympathetic
drive is predominantly located in the GP between the right superior
pulmonary vein and right atria (which has most influence in cardiac
parasympathetic innervation) and that the group of fibers located
between the inferior vena cava and the right and left atria plays a
major role in AV nodal innervation (4). Increasing
clinical evidence, have also shown that the most important modification
of parasympathetic autonomic response during ablation occurs by
targeting the right GP and some authors additionally claim predominant
modulation from the right atria side of GP, namely during ablation of
the right side of the interatrial septum along the coronary sinus ostium(1,5,20). We used a simple and consistent method for
GP ablation aiming at just the right GP with anatomical endpoints. Our
results have shown that this strategy is feasible and effective, with
less scar creation. In our patients, approaching the right GP alone
seemed to be enough leading to abolishment of vagal cardiac tone, with
significant shortening of RR and AH intervals and WBCL acutely. Also, we
report a significant increase in minimal and mean heart rate 30 days
after parasympathetic modulation, rendering patients asymptomatic with
persistent effect in the medium-term. This data demonstrates that in the
absence of standardized hard endpoints for GP ablation, an anatomic
endpoint as surrogate of parasympathetic modulation and for
simplification of the procedure purposes, with creation of a lesion
subset in pre specified anatomic areas is enough.