Format

Send to:

Choose Destination
See comment in PubMed Commons below
Annu Rev Pharmacol Toxicol. 2003;43:441-61. Epub 2002 Jan 10.

K+ channel structure-activity relationships and mechanisms of drug-induced QT prolongation.

Author information

  • 1Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. cc2114@columbia.edu

Abstract

Pharmacological intervention, often for the purpose of treating syndromes unrelated to cardiac disease, can increase the vulnerability of some patients to life-threatening rhythm disturbances. This may be due to an underlying propensity stemming from genetic defects or polymorphisms, or structural abnormalities that provide a substrate allowing for the initiation of arrhythmic triggers. A number of pharmacological agents that have proven useful in the treatment of allergic reactions, gastrointestinal disorders, and psychotic disorders, among others, have been shown to reduce repolarizing K(+) currents and prolong the QT interval on the electrocardiogram. Understanding the structural determinants of K(+) channel blockade may provide new insights into the mechanism and rate-dependent effects of drugs on cellular physiology. Drug-induced disruption of cellular repolarization underlies electrocardiographic abnormalities that are diagnostic indicators of arrhythmia susceptibility.

PMID:
12540747
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Atypon
    Loading ...
    Write to the Help Desk