The U-wave was first identified on the surface electrocardiogram (ECG) and described by Einthoven in 1906, but its electrophysiological origin remains unknown. The main theories about the origin, summarised by Lepeschkin already in 1957, are still under debate [1]. A possible association between the morphological characteristics of the U-wave and numerous clinical conditions has been described [[2], [3], [4], [5], [6]], and its potential clinical importance has recently attracted new interest [5]. The standard 12‑lead ECG recording is an inexpensive, noninvasive and widely available method used to diagnose heart disorders, cardiac conduction defects and abnormal repolarisation, and to identify patients with increased risk for serious cardiac arrhythmias. All waveforms on the ECG can be categorised into the phases of cardiac depolarisation or repolarisation. The P-wave represents atrial depolarisation and the QRS complex represents ventricular depolarisation, while repolarisation is represented by the J-wave, T-wave and the QT-interval. The U-wave follows the T-wave (Fig. 1a), and debate continues as to whether the normal U-wave is due to late electrical repolarisation or mechanical stretch of the ventricle. Research during the past decades has increased the understanding of cellular and ionic mechanisms of ventricular repolarisation as well as its clinical importance [7].

The aim of the study was to summarise and present any new information regarding the U-wave and, based on the currently applied U-wave definition, to describe its appearance and characteristics in different cardiac conditions. Furthermore, we present and review the theories proposed for the mechanism behind the U-wave along with potential pathophysiologic and prognostic implications related to its presence, polarity and morphology and to describe remaining knowledge gaps. This review paper is based on a thorough literature search.