Early repolarization (ER) has been defined by end-QRS notching or slurring, elevation of the ST-segment, and also an upward-sloping ST-segment followed by a tall, symmetrical T wave; it has traditionally been considered to be benign [1]. In recent years, ER has gained attention since the report of Haïssaguerre et al [2] on the association of an early repolarization pattern (ERP) and the risk of ventricular fibrillation (VF). They defined early repolarization as an elevation of the J-point, as either QRS slurring or notching, in at least 2 leads. Later, Tikkanen et al. proposed that the ST-segment slope is significant in ER [3]. They also discussed the characteristics of “malignant” vs “benign” patterns of ER [3]. Thus, the definition of ER has been changing and subsequently confusing; hence, an expert consensus report has recommended that for ER the peak of an end-QRS notch and/or the onset of an end-QRS slur is designated as a J-point and that J-point should exceed 0.1 mV in ≥2 contiguous inferior and/or lateral leads [4,5]. The consensus report also recommends that ST-segment elevation in the absence of a slur or notch should not be reported as ER [4]. Concurrently, the term J-wave syndromes, as characterized by J-point and ST-segment elevation in distinct ECG leads, has been proposed by Antzelevitch and Yan based on the concept that Brugada syndrome and ER syndromes represent a continuous spectrum [6]. In this concept, Brugada syndrome patients show J-point and ST-segment elevation in the right precordial leads [5,6].

On the other hand, in 2009, Jastrzebski and Kukla reported the new concept of ischemic J waves in patients with ischemia-induced VF and J waves during transient coronary spasms and acute myocardial infarctions [7]. Similar observations had been reported in several papers [8,9]. Also, the relationship between an ERP and VF in patients with vasospastic angina (VSA) has been systematically investigated [10]. More recently, Oh et al. reported that patients with VSA presenting with an ERP have a higher incidence of cardiac events including, cardiac death, aborted sudden cardiac death, and fatal arrhythmias compared to those with no ER [11]. In contrast, it has recently been reported that hyponatremia can induce a Brugada-type ECG, one subtype of J wave syndromes, probably due to the reduced sodium current [12]. From the experimental point of view, ACh and Na channel block by ajmaline can induce J wave syndrome and facilitate the induction of ventricular arrhythmias [13]. In addition, a simulation study has shown that reduced sodium current in the lateral ventricular wall induces inferolateral J-waves [14].

We encountered a patient with ER syndrome with VSA in whom concomitant hyponatremia might have synergically induced VF. We hereby discuss the clinical implications of the association among hyponatremia, ischemia, and VF episodes in ER syndrome based on the present case.