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Sudden cardiac death due to arrhythmia following myocardial infarction (MI) is the most common cause of mortality from heart disease. In recent years, myocyte intracellular calcium dysregulation has been increasingly recognized as an important mechanism of cellular triggers and tissue substrates that are responsible for arrhythmias. However, the molecular mechanisms underlying such calcium dysregulation in MI have remained elusive. Oxidative stress is increased in MI and is known to cause calcium dysregulation and promote a broad range of arrhythmia triggers and substrates. Interestingly, however, chronic-MI patients do not see a reduction in cardiac events with general anti-oxidant therapy, suggesting that our understanding of oxidative stress-mediated arrhythmias is incomplete. Recent studies suggest that the location and source of reactive oxygen and nitrogen species is a key determinant of their action …