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Department of Emergency Medicine, Indiana University School of Medicine, Indianapolis, IN 46206, USA. lkao@clarian.org
Drug therapy may induce Q-T prolongation by alteration of potassium ion 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. Re-cent 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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