Drug induced QT prolongation: lessons from congenital and acquired long QT syndromes.
Recent developments regarding the underlying genetic and intracardiac ion channel causes of congenital long QT syndrome have shed new light in the area of repolarization disorders and their resultant cardiac arrhythmias. Drug induced or acquired QT prolongation often represents a latent form of congenital long QT syndrome, though the genetic basis of this has not been elucidated in the majority of cases. Understanding this has lead to a new concept of repolarization reserve, a measure of inherent susceptibility to repolarization-mediated arrhythmias. The majority of pharmacologic agents that cause significant QT prolongation have potassium channel blocking characteristics, predominantly affecting the rapidly activating current I(Kr). The list of agents known to affect I(Kr)continues to grow, best monitored through several websites that collate reports of drug-induced QT prolongation and arrhythmias. Discontinuation of the offending agent and supportive care are often all that is necessary when clinical arrhythmias arise.
Walker
Bruce D
BD
Division of Cardiology, University of Western Ontario, London Ontario Canada.
Krahn
Andrew D
AD
Klein
George J
GJ
Skanes
Allan C
AC
Yee
Raymond
R
D000889:Anti-Arrhythmia Agents / Q000009:adverse effects* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008133:Long QT Syndrome / Q000139:chemically induced* / Q000151:congenital* / Q000235:genetics; D008875:Middle Aged; D015221:Potassium Channels / Q000235:genetics / Q000502:physiology; D016171:Torsades de Pointes / Q000139:chemically induced
D000889:Anti-Arrhythmia Agents; D015221:Potassium Channels