br Conflict of interest br Introduction A

Conflict of interest
Introduction A large number of recent reports suggest that early repolarization (ER) and J waves are associated with the occurrence of ventricular fibrillation (VF) [1–4]. In particular, the presence of J waves in global leads, including the inferolateral leads, is thought to increase the probability of VF [3]. Moreover, the prominence of J waves occasionally precedes the patient\'s degeneration into VF [2]. Here, we present a case of Brugada syndrome with dramatic alteration of J waves and the appearance of “pseudo-epsilon” wiggle waves in the lateral leads, which has not yet been reported. The significance of J wave variability and the presence of pseudo-epsilon wiggle waves in VF are discussed in this KN-93 Phosphate report.
Case report
Discussion The main finding of this case report was possible conduction delay in a patient with frequent VFs associated with multiple J waves. In a multicenter study, Haïssaguerre et al. reported that an increased prevalence of ER was observed among patients with a history of VF [1]. Moreover, Antzelevitch et al. described ER/J-wave syndrome and proposed 3 subtypes of the disorder [3]. According to their definitions, type 3 of the J-wave syndrome shows a global ER pattern in the inferior, lateral, and right precordial leads and includes a specific type of Brugada syndrome. In fact, with regard to our case, the morphology of the J waves in leads V1 and V2 (coved-type ST-segment elevation) and its response to pilsicainide were compatible with Brugada syndrome. Therefore, we viewed our patient as having overlapping Brugada syndrome and J-wave syndrome (i.e., type 3 J-wave syndrome) because of the widespread appearance of J waves, although the definition of J-wave syndrome remains controversial [5,6]. In the present case, the ER/J-wave inscribed various forms on ECG recordings. Morphologies of ER/J-waves detected in this case consisted of 3 types: positive deflection, slurring, and nonspecific ST-segment elevation. Quinidine, a sodium-channel blocker that also inhibits the transient outward current (Ito), eliminated these ERs and restored a normal ECG. Thus, the prominence of J waves was likely to be associated with an increase in Ito, which might lead to phase 2 re-entry [3]. Notably, just after the second VF attack, beat-to-beat alteration of the J wave was clearly recorded in lead V2. The appearance of a similar fluctuation in the J wave followed by an electrical storm has been previously reported by Haïssaguerre et al. [1] and Letsas et al. [7] In our case, as Fig. 3A shows, J waves were temporally aligned with pseudo-epsilon wiggle waves. Moreover, J waves (i.e., second R waves) were augmented following short coupling intervals (beats 1 and 4). These findings suggest that the J wave, which forms an early phase in ST-segment elevation, is likely to belong in the depolarization period. Therefore, the variability of J-wave amplitude might be interpreted as depolarization heterogeneity, triggering an increased vulnerability to VF. The mechanism underlying Brugada syndrome and J-wave syndrome still remains controversial [8,9]. The prevailing view is the repolarization disorder theory, although the depolarization disorder theory is also acceptable. Recently, Letsas et al. indicated that delayed waves, such as epsilon waves, were detected in the right precordial leads in patients with Brugada syndrome, demonstrating the possibility of right ventricular conduction delay in Brugada syndrome [10]. However, there have been no reports describing these delayed waves in other leads among patients with Brugada syndrome or/and J-wave syndrome. In our case, minimal jagged deflections resembling epsilon waves were clearly visible at the terminal portion of the QRS-complexes in leads V5 and V6. To the best of our knowledge, the present case is the first report that demonstrated the appearance of pseudo-epsilon wiggle waves in the lateral leads in a patient with an overlapping phenotype of Brugada syndrome and J-wave syndrome. These waves were interpreted as non-J waves in that the morphology was neither notching nor slurring; however, it can be challenging to distinguish epsilon waves from J waves. During the periods when VF attacks occurred, the pseudo-epsilon wiggle waves were accompanied by prominent J waves, and the wiggle waves were so small that we could not always detect them. Under administration of quinidine at a dose of 300–600mg/d, the wiggle waves were never visible. Given that these small deflections were primarily recorded just after VF episodes, both the pseudo-epsilon wiggle waves and the J waves may be related to the occurrence of VF. On the basis of a single-case report, we cannot suggest the potential clinical implication of these pseudo-epsilon wiggle waves. However, we would like to propose that these wiggle waves and J waves share a common etiology and that these pseudo-epsilon waves be regarded as a type of J wave. If so, J waves may be related to delayed conduction, which is associated with enhanced VF vulnerability. Moreover, Fig. 3 may give us a clue as to the mechanism of ST-segment elevation in Brugada-type ECG. In Fig. 3B, the near coved-type ST-segment elevation in lead V2 clearly outlasted the pseudo-epsilon waves in leads V5 and V6. Therefore, the latter phase of ST-segment elevation was thought to reflect repolarization, and it is likely that the near coved-type ST-segment elevation in lead V2 consists of both depolarization and repolarization components. Interestingly, Abe et al. recently described the nocturnal enhancement of depolarization abnormalities in idiopathic VF with J waves by detecting late potentials [11]. It is likely that both depolarization and repolarization abnormalities exist in J-wave syndrome [11] and Brugada syndrome [12,13]. Further investigations are recommended.