An early repolarization electrocardiogram（ER-ECG）pattern is caused by various pathophysiological conditions. However, little evidence on the relationship between ER-ECG pattern and acute myocarditis has been reported. The purpose of this study was to investigate the prevalence and significance of the ER-ECG pattern in acute myocarditis. Thirty patients（23 males, 39.2±19.1 years）diagnosed with acute myocarditis by clinical presentations between March 2011 and April 2018 were retrospectively evaluated. Nine cases showed localized ER-ECG pattern which was defined as terminal QRS notching or slurring with amplitude of＞0.1mV in at least 2 leads（ER Group）, while the remaining 21 cases had broad ST elevation or pathologic Q waves（non-ER group）. Cardiac troponin T level was much higher in the non-ER group than in the ER-group（3.2±4.3 vs 0.9±1.2ng/ml, p=0.036）. ECG changes returned to baseline along with the normalization of cardiac biomarkers. Nine of the 21 non-ER group patients, but none of the 9 ER-group patients, developed fulminant course and lethal ventricular tachyarrhythmias. T2-weighted cardiac MRI showed high intensity signal over the entire transmural left ventricle（LV）in the non-ER group, whereas it showed at only LV epicardial lesion in the ER group. In conclusion, inflammation/swelling localized to the LV epicardium due to acute myocarditis leading to a ventricular transmural voltage gradient might provide a mechanistic insight for the ER-ECG pattern. The ER-ECG pattern in patients with acute myocarditis was not associated with the development of lethal ventricular tachyarrhythmias.

An 83-year-old man presented 5 types of QRS complexes during 30 years of observation. At his first visit at age 53, his electrocardiogram（ECG）showed sinus rhythm and QRS complex was complete right bundle branch block pattern（CRBBBp）with QRS axis＋15˚［C15］. At the age of 74, QRS complex remained CRBBBp, but the QRS axis shifted rightward to＋60˚［C60］. At the age of 76, atrial fibrillation was recorded for the first time, but QRS complex still showed［C60］. At the age of 78,［C15］was intermittently exhibited when preceding RR interval was above 1.01sec. At the age of 79, IRBBBp-QRS complex was intermittently exhibited when preceding RR interval was above 0.98sec, but the QRS axis remained unchanged at＋60˚［I60］regardless of the preceding RR interval. At the age of 80, 3 types of QRS complexes of［C60］, ［C15］, and IRBBBp with QRS axis＋15˚［I15］were observed. At the age of 83, in addition to［I60］, normal narrow QRS with axis＋70˚［N70］was exhibited when preceding RR interval was in the range of 0.44-0.48sec. Thus, QRS complexes remained right bundle branch block pattern, but QRS duration and QRS axis changed at different critical preceding RR intervals. These phenomena cannot be explained by the right bundle branch block only. However, they might be explained by the hypothesis of a triple pathway derived from the longitudinal dissociation within the His bundle.