Discussion
One of the main findings of this study was that 2.8% of patients
developed acute onset of periaortic VT after SAVR retrospectively.
Previous studies have reported the electrophysiological characteristics
of VTs after AVR; however, the incidence rate of periaortic VTs after
AVR remains unclear (6,7). Although one of the major limitations of this
study is that we could not distinguish between the periaortic VTs
related to AVR and an idiopathic outflow/summit VT which shows
outflow/septal LGE unrelated to the aortic valve (8), the incidence of
such idiopathic OTVTs in the general population was reported to be 13.85
per 1000,000 patients (0.001385%); therefore, the incidence of
periaortic VTs after SAVR (2.8%) in this retrospective cohort is
apparently high (9). (Central illustration)
As for the timing of the periaortic VTs after AVR, a bimodal pattern has
been reported; they either occur immediately postoperatively or years
later (6,7,10,11). The periaortic VTs in this study occurred 12.3±6.7
years after SAVR, which is in agreement with the results of previous
studies. The high incidence of periaortic VTs after over 12 years raises
a concern of causality.
The periaortic region could be an arrhythmic substrate for scar-related
ventricular tachycardia, even with and without structural heart diseases
(8,12,13). Sabastiaan R.D. Piers et al. reported that two typical scar
patterns including anteroseptal scar in nonischemic cardiomyopathy with
contrast-enhanced MRI (13). From the high incidence of periaortic VT
after SAVR and spatial distribution of the basal anteroseptal scars
detected with cardiac MRI in this study, the periaortic scars appear to
be influenced by chronic mechanical stimulation to the arrhythmic
sensitive basal anteroseptal region by the artificial valve over a long
time. In our study, patients in the periaortic VT group also had
significantly wider IVSd than did those in the control group, which
might reflect septal wall remodeling due to chronic stimulation by the
prosthetic aortic valves. Therefore, we believe that if the periaortic
scars occur in the septum after SAVR, they could lead to injury to the
conduction system and, possibly, result in a bundle block re-entry VT,
which was previously reported long after SAVR (7).
Another possible explanation for the periaortic scars may include hidden
cardiomyopathies before SAVR. While all patients underwent screening
tests before SAVR, hidden cardiomyopathies cannot be sufficiently ruled
out completely. In fact, Castano et al. reported that 16% of patients
with severe AS had hidden transthyretin cardiac amyloidosis (14). The
presence of more clinical data on echocardiography, cardiac MRI, SAECG,
and Holter earlier in the time course, including before AVR, would have
been useful in proving when periaortic scar developed.
Another concern is how many of the other 105 patients without periaortic
VTs also have abnormal substrate in the periaortic region. SAECG
positive (7/30 [23%]) and sporadic NSVTs were observed in 5/41
(23%) patients without periaortic VTs; sustained OTVT or incessant
NS-OTVT. They could be potential candidates for periaortic VTs, and risk
stratification methods should be considered.
Regarding the prognosis of VTs after AVR, Liang JJ et al. demonstrated
the safety and good outcomes of catheter ablation (6). In contrast,
Nishimura et al. reported that sixty-five percent of reentrant circuits
of periaortic VT with and without AVR had endocardial activation gaps
within the tachycardia cycle length (three-dimensional circuitry), which
were associated with higher rates of recurrence than two-dimensional
complete circuits at 1 year (73% vs 37%).In our study, we could not
analyze the precise circuits of the periaortic VTs after AVR. However,
because LGE, which could be the arrhythmic substrate of periaortic VTs,
was present in the mid-layer of LV, the circuit could include
three-dimensional circuitry and total elimination of the arrhythmic
substrate with endocardial ablation alone appeared difficult. Soejima et
al. also reported the importance of endo and epicardial mapping for
ventricular tachycardia in patients with mechanical valves (15). We
should analyze precise VT circuits after AVR and long-term prognosis for
periaortic VTs after AVR.
Based on our results, we suggest that arrhythmic risk stratification for
patients after SAVR should be considered. From our findings, wider IVSd,
lower LVEF, larger LVDs, NSVTs on Holter monitoring, positive SAECG, and
cardiac MRI should be considered prognostic factors in periaortic VTs
after SAVR.