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.