Understanding drug-induced torsades de pointes: a genetic stance.
Drugs may produce a variety of arrhythmias, but drug-induced QT prolongation and the risk of the polymorphic ventricular tachycardia torsades de pointes (drug-induced long QT syndrome) has garnered the most attention. The wide array of drugs with potential for QT prolongation, the correspondingly large number of patients exposed to such drugs, the difficulty in predicting an individual's risk, and the potentially fatal outcome, make drug-induced long QT syndrome an important public health problem for clinicians, researchers, drug development programs, and regulatory agencies. This review focuses on the genetic risk factors and mechanisms underlying QT prolongation and proarrhythmia. The post-genomic era hints at an improved understanding (and prediction) of how the gene-environment interaction produces this particular adverse drug response.
Kannankeril
Prince J
PJ
Vanderbilt Children's Hospital, Division of Cardiology, 2200 Children's Way, Suite 5230, Nashville, TN 37232-9119, USA. prince.kannankeril@vanderbilt.edu
D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D006801:Humans; D008133:Long QT Syndrome / Q000139:chemically induced / Q000235:genetics / Q000503:physiopathology; D010597:Pharmacogenetics; D012307:Risk Factors; D016171:Torsades de Pointes / Q000139:chemically induced* / Q000235:genetics* / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents