open access

Vol 14, No 6 (2007)
Review articles
Published online: 2007-10-10
Submitted: 2013-01-14
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Drug induced QT prolongation

Wojciech Zaręba
Cardiol J 2007;14(6):523-533.

open access

Vol 14, No 6 (2007)
Review articles
Published online: 2007-10-10
Submitted: 2013-01-14

Abstract

The drug-induced QT prolongation predisposes to development of torsades de pointes (TdP) ventricular tachycardia and sudden death. The association between specific drug and development of TdP is difficult to document, therefore, QT prolongation is considered as a surrogate marker of the proarrhythmia risk. Most of the drugs prolong QT interval usually by blocking the potassium IKr current or altering trafficking of proteins forming the channel. Improved understanding of ion channel structure and kinetics and its role in repolarization has tremendous impact on understanding of the mechanisms of drug-induced QT prolongation and TdP. Proarrhythmia caused by a QT-prolonging drug occurs infrequently, and usually multiple factors need to operate to precipitate such an event including a combination of two or more drugs affecting the same pathway, hypokalemia, and possibly genetic predisposition. ECG provides unique opportunity to ensure safety of administered therapy. QT measurement is the most routine approach to a drug safety monitoring, however, there are many challenges related to methodology of measurements, accuracy of measurements, or optimal heart rate correction. Since drugs affecting repolarization not only prolong QT but also they alter T wave morphology, novel computerized methods quantifying these changes are being developed to assist physicians and drug manufacturers in monitoring safety of the drugs. The response of a patient to a drug is very individual and therefore an individualized system of drug administration and monitoring needs to be developed, which takes into account baseline QTc duration and its changes after a drug was introduced. (Cardiol J 2007; 14: 523-533)

Abstract

The drug-induced QT prolongation predisposes to development of torsades de pointes (TdP) ventricular tachycardia and sudden death. The association between specific drug and development of TdP is difficult to document, therefore, QT prolongation is considered as a surrogate marker of the proarrhythmia risk. Most of the drugs prolong QT interval usually by blocking the potassium IKr current or altering trafficking of proteins forming the channel. Improved understanding of ion channel structure and kinetics and its role in repolarization has tremendous impact on understanding of the mechanisms of drug-induced QT prolongation and TdP. Proarrhythmia caused by a QT-prolonging drug occurs infrequently, and usually multiple factors need to operate to precipitate such an event including a combination of two or more drugs affecting the same pathway, hypokalemia, and possibly genetic predisposition. ECG provides unique opportunity to ensure safety of administered therapy. QT measurement is the most routine approach to a drug safety monitoring, however, there are many challenges related to methodology of measurements, accuracy of measurements, or optimal heart rate correction. Since drugs affecting repolarization not only prolong QT but also they alter T wave morphology, novel computerized methods quantifying these changes are being developed to assist physicians and drug manufacturers in monitoring safety of the drugs. The response of a patient to a drug is very individual and therefore an individualized system of drug administration and monitoring needs to be developed, which takes into account baseline QTc duration and its changes after a drug was introduced. (Cardiol J 2007; 14: 523-533)
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Keywords

drug-induced QT prolongation; QT interval; torsade de pointes; long QT syndrome

About this article
Title

Drug induced QT prolongation

Journal

Cardiology Journal

Issue

Vol 14, No 6 (2007)

Pages

523-533

Published online

2007-10-10

Bibliographic record

Cardiol J 2007;14(6):523-533.

Keywords

drug-induced QT prolongation
QT interval
torsade de pointes
long QT syndrome

Authors

Wojciech Zaręba

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