The opioid oxycodone use‐dependently inhibits the cardiac sodium channel NaV1.5

Background and Purpose Oxycodone is a potent semi‐synthetic opioid that is commonly used for the treatment of severe acute and chronic pain. However, treatment with oxycodone can lead to cardiac electrical changes, such as long QT syndrome, potentially inducing sudden cardiac arrest. Here, we investigate whether the cardiac side effects of oxycodone can be explained by modulation of the cardiac Nav1.5 sodium channel.