Sudden cardiac death in early repolarization syndrome despite detailed evaluation for syncope: a case report

Figures

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  Figure 1. Twelve-lead electrocardiogram at the time of admission. Electrocardiogram revealed 0.2 mV J-waves in leads V4 through V6, without Brugada pattern or QT prolongation. Electrocardiograms were recorded at a paper speed of 25 mm/s and a calibration of 10 mm/mV with baseline drift filtering.

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  Figure 2. Changes in J-wave detected by 12-lead Holter electrocardiogram. (A) Holter electrocardiogram (baseline recording period) showed no significant J-waves. (B) At 4:15 a.m., electrocardiogram demonstrated prominent J-wave augmentation in leads V4–V6, with newly apparent subtle J-waves in inferior leads. (C) AT 5:45 a.m., electrocardiogram revealed progressive J-wave augmentation in both lateral and inferior leads, suggesting circadian rhythm-associated dynamic changes. (D) J-wave was enhanced after the atrial premature beat.

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  Figure 3. Pilsicainide loading test. Pilsicainide was administered intravenously at a rate of 1 mg/kg/h. The infusion was continued for 13 min. The 12-lead electrocardiogram following a pilsicainide challenge demonstrated a 0.18 mV J-point elevation in V1 at the second intercostal space, reduced J-wave amplitude in the inferior leads compared to baseline, and no significant change in the third or fourth intercostal spaces.

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  Figure 4. The insertable cardiac monitor recorded during the fatal event demonstrated a sequence of premature ventricular contractions with a 300-ms coupling interval, initiation of sustained ventricular fibrillation, and subsequent progression to sudden cardiac arrest.