Abstract
The term early repolarization (ER) is defined electrocardiographically by either (1) a sharp well-defined positive deflection or notch immediately following a positive QRS complex at the onset of the ST-segment, or (2) slurring at the terminal part of the QRS complex (also termed J-waves or J-point elevation, Figure 1). Specifically, the ER pattern is present when J-point elevation of ≥0.1 mV is seen in 2 adjacent leads with either a slurred or notched morphology.1,2 Although ER was historically considered benign, this perception changed as numerous studies1–5 established an association with increased risk of death and idiopathic ventricular fibrillation (VF). The incidental discovery of early repolarization now poses numerous questions, including defining and quantitating the risk of sudden death. With the emerging reports of a genetic contribution, defining the genetic basis, inheritance, and the role of screening relatives broadens the implications of early repolarization beyond the index case. Insights into the molecular mechanism of early repolarization and therapeutic strategies continue to highlight its evolving significance. Figure 1. Prominent early repolarization manifest as inferior J-point slurring and lateral J-point notching each >2 mm in 2 contiguous leads. This review seeks to provide a concise summary of the current evidence surrounding these issues, contextualize its clinical significance, and present an approach to the clinical evaluation and management of these patients. This review will emphasize that the majority of individuals with ER are at no or minimal risk for arrhythmic events. In others the ER substrate may potentially increase arrhythmic risk associated with underlying cardiac pathology. Very rarely, clinicians will encounter individuals in whom ER is a manifestation of a primary arrhythmogenic disorder. The first study to seriously question the convention that ER is a benign phenomenon compared 206 patients with idiopathic VF with 412 healthy subjects,1 and demonstrated …
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