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Fragmented QRS (fQRS) results from localised disruption of conduction due to myocardial fibrosis and scar and is evident on 12-lead ECG. Inhomogeneous myocardial electrical activation consequently manifests as spikes within the QRS complex. fQRS has been shown to be associated with increased mortality, ventricular arrhythmias and major adverse coronary events across a spectrum of pathologies ranging from coronary artery disease, cardiomyopathies (dilated cardiomyopathy, hypertrophic cardiomyopathy and left ventricular non-compaction) to acute pulmonary embolism.1 fQRS has also been defined as a marker of arrhythmogenic right ventricular (RV) dysplasia, long QT and Brugada syndrome.
fQRS morphologies are not only confined to acquired and hereditary cardiac conditions, but are also present on the surface ECGs of patients with congenital heart disease—including tetralogy of Fallot (TOF) and Ebstein's anomaly. fQRS has been reported to occur predominantly in the right and mid-praecordial leads in patients with repaired TOF (rTOF), with fragmented intracardiac electrograms previously demonstrated through invasive endocardial mapping.2 Until now, two cross-sectional studies of adult patients with rTOF have elucidated associations between fQRS and the extent of RV dilatation, dysfunction and myocardial fibrosis burden.3 ,4 RV fibrosis as quantified by late gadolinium enhancement (LGE) cardiovascular MR showed a strong correlation between the extent of fQRS (measured by the number of ECG leads in which fQRS was detectable) and the RV LGE score. …
Contributors All authors prepared and revised the manuscript critically for important intellectual content and have given final approval of the manuscript for publication.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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