Figure 1 (A) QRS fragmentation in lead V1 (black arrow). (B) Late gadolinium enhancement (LGE) in the anteroseptal region (white arrow). (C) QRS fragmentation in leads DIII, aVF and aVL (black arrows). (D) LGE in the infernolateral region (white arrow). (E) Magnification of fragmented QRS pattern in DIII (circle with arrow). The latter is not always routinely performed in clinical practice, particularly in the acute setting. The definition of readily available diagnostic and prognostic tools is still warranted. The electrocardiogram (ECG) is usually deemed not completely diagnostic as a number of changes affecting the depolarization phase have been described.3 We hypothesize that pathological changes observed in patients with myocarditis might affect the local depolarization expressed as QRS fragmentation (fQRS) in one or more leads. Indeed, fQRS has been consistently reported in a wide range of heart diseases characterized by the development of myocardial fibrosis. This study aims to validate the observation of fQRS in patients with myocarditis as an ECG marker of fibrosis. All patients admitted between 2008 and 2018 at a single centre, with symptom onset within 30 days, were included. The diagnosis was supported by a consistent clinical presentation, increased markers of myocardial necrosis, and the presence of oedema/late gadolinium enhancement (LGE) on CMR. Endocardial biopsy was performed only in a minority of selected cases. Presence of fQRS was defined as at least two R’ high-frequency spikes in the QRS.4 Forty patients were included in the analysis (37 male; mean age 38±11 years). At presentation, 30 patients (75%) showed ST-T changes, while 12 (30%) exhibited fQRS. Median echocardiographic acute lowest ejection fraction was 56% [interquartile range (IQR) 10–65), in almost complete agreement with CMR estimation. Overall, 35 patients (90%) displayed LGE. ECG leads showing fragmentation grossly correlated with
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