Discussion
While VVS in young patients represents a management challenge, recurrent
VVS post-CNA poses an even greater dilemma. Repeat CNA has not yet been
reported in the nascent literature on this novel approach; the present
case is the first such report to our knowledge.
The first interesting aspect of the present case was the inability to
pharmacologically suppress vagal tone in pre-procedural testing, despite
both her ILR data and clinical recurrence demonstrating its return (see
Figs 1 and 2). This “reinnervation” phenomenon has been previously
described in AF populations treated via GP ablation, including the same
HRV trend back to pre-procedural values (8). However, AF suppression in
these patients remained durable despite recovery of GP inputs. The
underlying mechanism is not well understood; indeed, our present patient
was autonomically denervated, after which her ILR data exhibited gradual
reinnervation (Fig 2). Unlike the AF cohorts, however, she suffered
clinical relapse.
As such, one might expect to find at least one endocardial site behaving
similarly to her GP in the initial procedure, perhaps suggesting that
ablation had been incomplete, or that some GP connections had been
missed. Yet after she failed to generate a tachycardic response to
serial doses of atropine, she could not reproduce her junctional
responses to HFS at GP sites. The significance of this finding is not
entirely clear, although one explanation is that her reinnervation
process may have been characterized by a “re-growth” of injured vagal
inputs, perhaps with altered functional properties, or possibly a
scenario where alternative plexi gradually took over cardiac vagal
function. Yet during the RF phase of the procedure, in which her GP were
largely targeted anatomically due to lack of a response to HFS, it was
notable that two of her GP (posterior RA and right anterior GP)
exhibited accelerated sinus rates in response to RF. During her first
procedure, all five GP had clearly accelerated.
One limitation of our present report is that current protocols favoring
atropine administration for vagal testing may be fallible, and one
practice favors administration of atropine 1-2 days in advance of the
procedure. Given her lack of chronotropic response to atropine on this
second CNA, it is not clear that advance administration would have
changed the responses, nor is it clear that the absent junctional
responses to HFS at previously-responsive GP were simply blunted
pharmacologically, by the same rationale. One promising albeit primitive
alternative to atropine testing is extracardiac vagal stimulation
(ECVS), performed by applying high-amplitude, high-frequency pulses from
within the lumen of the right internal jugular vein to achieve transient
asystole or atrioventricular block. A report from a Brazilian group
found GP-ablated patients significantly less responsive to the maneuver
at the end of the procedure than a control group, suggesting significant
vagal denervation (9). It is of course theoretically possible that, had
our present patient been tested either at the end of her first CNA or
the beginning of her second, ECVS might have revealed some lingering
vagal inputs, perhaps at the GP which produced HR increases on second
CNA, although this is only speculative.
A second limitation in the present case may have been simply related to
patient selection, the optimal approach to which is widely acknowledged
to be an enigma in CNA. Early work in a post-CNA population with
recurrent syncope found nocturnal deceleration capacity, calculated from
interval differences in R waves from signal-averaged ECGs, to be
predictive of recurrent VVS in post-CNA patients (6).
The pace of progress in CNA is encouraging; however, larger prospective
studies are needed to better understand the post-CNA population with
recurrent VVS.