Drug therapy may induce Q-T prolongation by alteration of potassiumion currents in cardiac cells, resulting in abnormal repolarization. Q-T prolongation, whether congenital or acquired, has been associated with the development of the malignant dysrhythmia Torsade de Pointes (TdP), which may result in sudden death. Recent regulatory actions and drug withdrawals due to Q-T prolongation or TdP have focused attention on this issue. Although our understanding of the pathophysiology continues to evolve, both patient and medication factors contribute to the individual risk of drug-induced Q-T prolongation or TdP. The clinician should be aware of these issues when prescribing new drugs and should weigh the risks and benefits carefully when prescribing drugs known to prolong the Q-T interval.
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