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    • The risk stratification of patients with ERS is

    2019-04-29

    The risk stratification of patients with ERS is even more confusing and further studies are required. As mentioned in the demographics, the traditional definition of ER emphasizes the presence of ST segment elevation, and the subjects with ER with this traditional concept do not have adverse outcomes [17,18]. In contrast, patients with ER according to the new definition (the presence of the terminal QRS notch or slur, irrespective of the ST segment changes) [19–22], have prognostic implications. More specifically, individuals with J waves that were followed by ascending ST segment changes do not show an increased risk of arrhythmic death; however, those with J waves that were accompanied by horizontal/descending ST segment changes had an increased risk of arrhythmic death compared with those without the ER pattern [22]. Nevertheless, the hazard ratio of the arrhythmic death risk in the latter subgroup rises only slightly (hazard ratio, 1.43). Considering the low risk of arrhythmic death observed in the population study, even the high-risk marker of ER pattern (J wave and horizontal/descending ST) seems to reflect a modifying factor for specific arrhythmic risk in patients with acquired structural lpa receptor diseases, rather than an indicator of a primary arrhythmic syndrome, as discussed by the authors [22]. Although other risk markers such as high amplitude J waves in the inferior leads have been suggested, a better scheme for risk stratification is necessary. The presence of a type I BS ECG pattern indicates the necessity for ICD implantation in patients with syncope of unknown causes. Currently, electrocardiographic ER parameters are hardly useful for risk stratification in primary prevention purposes, and none of these parameters are used as indicators of ICD implantation [57]. Global appearance of J waves and ST segment elevation has been known to indicate a highly arrhythmogenic substrate [13]. However, patients with electrical storm manifest this phenotype only during a short time window of peri-event periods that last several minutes or hours. The “ambulatory” phase ECG in these patients with electrical storms shows an ER pattern that is practically indistinguishable from that of a benign ER pattern [58].
    Treatment and prevention of VF in patients with BS or ERS Pharmacologic management of BS and ERS is identical owing to the shared pathophysiologic mechanism. The suppression of electrical storm in patients with BS or ERS can be achieved by administering intravenous isoproterenol [45,59,60]. In patients with ERS, the occurrence of VF episodes is always accompanied by a prominent accentuation of the J wave and commonly preceded by bigeminy PVC in a short–long–short sequence [45]. These electrocardiographic indicators are extremely useful for guiding therapy and estimating the response to treatment in patients admitted for the management of the electrical storm. In patients with a pacemaker or ICD, atrial pacing at >90beats/min abolished the ECG changes and prevented the recurrence of VF [45]. For long-term management, quinidine and cilostazol have been shown to be effective in both BS and ERS [45,59–62]. Catheter ablation of trigger PVCs targeting the earliest ventricular endocardial activation or targeting the Purkinje potential may be successfully performed in patients with BS and ERS [12,63]. In selected patients with BS, substrate ablation in the epicardial region of delayed potentials has also been proposed [64].
    Conclusions
    Conflict of interest
    Acknowledgments
    Introduction Early repolarization or J-wave is characterized by an elevation at the junction between the end of the QRS complex and the beginning of the ST-segment (J-point) in a 12-lead electrocardiogram (ECG). Early repolarization is a common electrocardiographic finding that occurs in 1% to 10% of healthy persons, and it has been generally considered benign for decades [1]. However, early repolarization can be observed under various biological abnormalities, such as low body temperature, hypercalcemia, and ischemia [2–5]. Furthermore, there is increasing evidence showing that early repolarization is associated with an increased risk of ventricular fibrillation and sudden cardiac death [6–8]. In a number of case reports, early repolarization has been associated with the pathogenesis of idiopathic ventricular fibrillation [9,10]. In 2008, Haissaguerre et al. [6] reported in a case-control study that the early repolarization pattern is more frequent in patients with idiopathic ventricular fibrillation (31%) than in matched controls (5%). After this report was published in the New England Journal of Medicine, idiopathic ventricular fibrillation associated with early repolarization, the so-called early repolarization or J-wave syndrome, started receiving increasing attention. Brugada syndrome is characterized by ST-segment elevation in the right precordial leads (V1 to V3) of a 12-lead ECG and episodes of ventricular fibrillation [11]. Brugada syndrome is another form of idiopathic ventricular fibrillation associated with J-point elevation, and this led Antzelevitch and Yan [12] to hypothesize about “J-wave syndromes.” This review presents the available evidence about the similarities and differences between Brugada syndrome and early repolarization syndrome.