1.

Record Nr.

UNISA996214620003316

Autore

Camm A. John

Titolo

Acquired long QT syndrome [[electronic resource] /] / A. John Camm, Yee Guan Yap, Marek Malik

Pubbl/distr/stampa

Malden, Mass., : Futura, c2004

ISBN

1-280-19666-1

9786610196661

0-470-79942-0

0-470-99477-0

1-4051-4616-8

Descrizione fisica

1 online resource (208 p.)

Altri autori (Persone)

YapYee Guan

MalikMarek

Disciplina

616.128

Soggetti

Long QT syndrome

Lingua di pubblicazione

Inglese

Formato

Materiale a stampa

Livello bibliografico

Monografia

Note generali

Description based upon print version of record.

Nota di bibliografia

Includes bibliographical references and index.

Nota di contenuto

Acquired Long QT Syndrome; Contents; Preface; 1 Introduction; 2 Mechanisms of acquired QT prolongation and torsades de pointes; 3 Measurement of QT interval and repolarization assessment; 4 Introduction to drug-induced long QT syndrome; 5 Risk of QT prolongation and torsades de pointes with antiarrhythmic drugs; 6 Risk of QT prolongation and torsades de pointes with antihistamines; 7 Risk of QT prolongation and torsades de pointes with psychotropic drugs; 8 Risk of QT prolongation and torsades de pointes with antimicrobial and antimalarial drugs

9 Risk of QT prolongation and torsades de pointes with prokinetics and miscellaneous other drugs10 Acquired long QT syndrome secondary to cardiac conditions; 11 Acquired long QT syndrome secondary to noncardiac conditions; 12 Perspective on drug-induced repolarization changes; Index

Sommario/riassunto

In recent years there has been considerable interest in the diagnosis and understanding of ventricular repolarisation, particularly the QT interval prolongation and abnormal T and T/U wave morphology associated with torsades de pointes. Advances in ion channel cloning



have greatly improved our understanding of the role of ionic channels in mediating cardiac repolarisation. Unfortunately, it is increasingly recognised that a number of drugs, both those associated with altering repolarisation, and others for non-cardiac conditions can increase the propensity for polymorphic ventricular tachycard