Discussion
In this case, the recorded ventricular tachyarrhythmia on the ICD log at our hospital was monomorphic VT, not VF. On the other hand, the recorded log from the other hospital after SCA was fast VT including a partially polymorphic waveform. Thus, the cardiologists in that hospital judged that the cause of his SCA was VT or VF and diagnosed him with IVF. This difference could be explained as follows. VF has been reported to be sometimes promoted by VT accompanied with hemodynamic instability and can develop into VF or SCA.1 Most VTs originating from the RVOT are considered as benign arrhythmias; however, some VTs can be malignant and develop into VF or polymorphic VT; the characteristics of these malignant VTs are more likely to occur in patients with a history of syncope and short CL.2 This patient had several events of syncope of unknown cause and monomorphic VT with a very short CL (185 ms). Therefore, we estimated that his repetitive SCAs were primarily due to a malignant type of VT originating from the RVOT. 
When a patient with SCA is taken to a hospital, there could be an initial lack of clinical history and information; therefore, the initial diagnosis of IVF might be incomplete. In fact, it has been reported that more than one-fifth of patients initially diagnosed with IVF are re-diagnosed with another specific disease; hence, continuous follow-up and reassessment of patients with IVF has become very important.3 This patient presented to our hospital with IVF and was uneventfully followed-up in the ICD clinic for several years. When multiple ICD shock events due to monomorphic VT were detected, we suspected that his diagnosis was possibly not IVF. In the subsequent ablation session, 3D mapping revealed the existence of an LVA on the RVOT, which showed that he had a structural arrhythmic substrate. Moreover, the induced ventricular arrhythmia, which was reproducibly a monomorphic VT, showed a regular fixed sequence of ventricular potentials that arose from the LVA. Ablation of the LVA resulted in the successful elimination of the target PVC and VT. Based on these results, the patient was finally diagnosed with a scar-related VT, not IVF.
Although cardiac biopsy and genetic examination were not performed, we ruled out other specific heart diseases before ablation therapy. For example, his echocardiogram, cardiac MRI, and pilsicainide infusion test did not show any positive features of Brugada syndrome. Further, the present case did not match the current diagnostic criteria of arrhythmogenic right ventricular cardiomyopathy.4 For analyzing other underlying diseases, cardiac biopsy and DNA testing could have been performed; however, as cardiac biopsy for unexplained ventricular arrhythmia is not strongly recommended,5 we did not perform it. Moreover, a DNA test was not performed because he was less likely to have genetic arrhythmia based on his 12-lead ECG at rest and family history.
Our patient who was initially diagnosed with IVF was eventually re-diagnosed with a scar-related VT via 3D mapping. In most cases, 3D mapping has been rarely performed as one of the initial diagnostic tests for IVF.6 Therefore, we suggest that a 3D mapping system might be useful in finding a missed substrate and in clarifying another specific arrhythmic disease like in the present case.
Conclusion