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Review
. 2012:2012:212178.
doi: 10.1100/2012/212178. Epub 2012 Apr 19.

Mechanisms, risk factors, and management of acquired long QT syndrome: a comprehensive review

Affiliations
Review

Mechanisms, risk factors, and management of acquired long QT syndrome: a comprehensive review

Eleftherios M Kallergis et al. ScientificWorldJournal. 2012.

Abstract

Long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram and is associated with precipitation of torsade de pointes (TdP), a polymorphic ventricular tachycardia that may cause sudden death. Acquired long QT syndrome describes pathologic excessive prolongation of the QT interval, upon exposure to an environmental stressor, with reversion back to normal following removal of the stressor. The most common environmental stressor in acquired long QT syndrome is drug therapy. Acquired long QT syndrome is an important issue for clinicians and a significant public health problem concerning the large number of drugs with this adverse effect with a potentially fatal outcome, the large number of patients exposed to these drugs, and our inability to predict the risk for a given individual. In this paper, we focus on mechanisms underlying QT prolongation, risk factors for torsades de pointes and describe the short- and long-term treatment of acquired long QT syndrome.

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Figures

Figure 1
Figure 1
Torsades de pointes.
Figure 2
Figure 2
Myocardial action potential. Phase 0 rapid depolarization is mediated by sodium entry into cells. Phase 1 and 3 repolarization results from potassium efflux from cells. Balanced slow calcium entry and potassium exit cause the plateau in phase 2. Potassium reenters and sodium exits cells during phase 4 recovery.
Figure 3
Figure 3
Multiple early afterdepolarizations (EADs) from progressively more negative transmembrane potential.
Figure 4
Figure 4
Short-long-short sequence preceding TdP.

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