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.