Published in:
01-08-2014 | Commentary
What Causes Some Patients with Drug-Induced QT Interval Prolongation to Develop Torsades de Pointes but Not Others? The Elusive Missing Link
Author:
James E. Tisdale
Published in:
Drugs & Aging
|
Issue 8/2014
Login to get access
Excerpt
Cardiac arrest due to torsades de pointes (TdP) is an uncommon but potentially catastrophic event associated with QT interval-prolonging drugs [
1]. Numerous medications that may cause TdP are available for use in clinical practice, and include drugs for management of cardiovascular diseases, primarily arrhythmias, but also noncardiovascular agents from multiple classes, including anti-infectives, antipsychotics, antidepressants, methadone, and many more [
2]. The risk of TdP increases as the heart rate-corrected QT (QT
c) interval increases [
3‐
6], particularly when it exceeds 500 ms [
5,
6]. Numerous independent risk factors for QT
c interval prolongation and TdP have been identified, and include female sex, hypokalemia, hypomagnesemia, acute myocardial infarction, sepsis, supratherapeutic concentrations of QT
c interval-prolonging drugs, rapid intravenous infusion of QT
c interval-prolonging drugs, concomitant administration of two or more QT
c interval-prolonging drugs, concomitant administration of a loop diuretic, bradycardia, heart failure with reduced ejection fraction (HFrEF), pretreatment QT
c interval prolongation, and ion channel polymorphisms [
7,
8]. …