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Repolarization abnormalities typically evolve as a consequence of impaired function of outward K<jats:sup>+<\/jats:sup>currents in cardiac myocytes, which may be caused by genetic defects or result from various acquired pathophysiological conditions, including electrical remodelling in cardiac disease, ion channel modulation by clinically used pharmacological agents, and systemic electrolyte disorders seen in heart failure, such as hypokalaemia. Cardiac electrical instability attributed to abnormal repolarization relies on the complex interplay between a provocative arrhythmic trigger and vulnerable arrhythmic substrate, with a central role played by the excessive prolongation of ventricular action potential duration, impaired intracellular Ca<jats:sup>2+<\/jats:sup>handling, and slowed impulse conduction. This review outlines the electrical activity of ventricular myocytes in normal conditions and cardiac disease, describes classical electrophysiological mechanisms of cardiac arrhythmia, and provides an update on repolarization\u2010related surrogates currently used to assess arrhythmic propensity, including spatial dispersion of repolarization, activation\u2013repolarization coupling, electrical restitution,<jats:styled-content style=\"fixed-case\">TRI<\/jats:styled-content>aD (triangulation, reverse use dependence, instability, and dispersion), and the electromechanical window. This is followed by a discussion of the mechanisms that account for the dependence of arrhythmic vulnerability on the location of the ventricular pacing site. Finally, the review clarifies the electrophysiological basis for cardiac arrhythmia produced by hypokalaemia, and gives insight into the clinical importance and pathophysiology of drug\u2010induced arrhythmia, with particular focus on class Ia (quinidine, procainamide) and Ic (flecainide) Na<jats:sup>+<\/jats:sup>channel blockers, and class<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>antiarrhythmic agents that block the delayed rectifier K<jats:sup>+<\/jats:sup>channel (dofetilide).<\/jats:p>","DOI":"10.1111\/apha.12902","type":"journal-article","created":{"date-parts":[[2017,7,14]],"date-time":"2017-07-14T04:25:18Z","timestamp":1500006318000},"page":"1-71","source":"Crossref","is-referenced-by-count":40,"title":["Role of abnormal repolarization in the mechanism of cardiac arrhythmia"],"prefix":"10.1111","volume":"220","author":[{"given":"O. 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