Abstract
Long QT syndromes can be either acquired or congenital. Drugs are one of the many etiologies that may induce acquired long QT syndrome. In fact, many drugs frequently used in the clinical setting are a known risk factor for a prolonged QT interval, thus increasing the chances of developing torsade de pointes. The molecular mechanisms involved in the prolongation of the QT interval are common to most medications. However, there is considerable inter-individual variability in drug response, thus making the application of personalized medicine a relevant aspect in long QT syndrome, in order to evaluate the risk of every individual from a pharmacogenetic standpoint.
Highlights
The association between QT interval prolongation and drug therapy dates back to the 1970–1980s with reports indicating a strange correlation between the use of antibiotics, antipsychotics, and other types of drugs with QT interval prolongation and torsade de pointes (TdP) [1]
Perhaps the most up-to-date list appears on the CredibleMeds.org website, where the Arizona Center for Education and Research on Therapeutics (AZCERT) [24], based on an ongoing systematic analysis of available evidence, places drugs in different categories [67]. These categories are drugs with a known risk of TdP, those with a possible risk of TdP, those with a conditional risk of TdP, and drugs to avoid in congenital form of long QT syndrome (cLQTS) [67]
A method that can effectively prevent a drug from causing QT interval prolongation, early after-depolarizations (EADs), and——TdP is lacking so far
Summary
The association between QT interval prolongation and drug therapy dates back to the 1970–1980s with reports indicating a strange correlation between the use of antibiotics, antipsychotics, and other types of drugs with QT interval prolongation and torsade de pointes (TdP) [1]. Regulatory agencies have adopted International Conference for Harmonization (ICH) guidelines S7B and E14 to establish the pro-arrhythmic characteristics of drugs before they are marketed, these guidelines focus on the reduction of repolarizing cardiac ionic currents and the prolongation of the QT interval induced by drugs. These efforts demonstrate the importance that providing pro-arrhythmic cardiac safety considerations in the development and use of therapeutic measures has in the field of pharmacology [25]. There is a compelling need to identify genetic markers of diLQTS and drug-induced TdP susceptibility, in order to guide genotyping and genetic data analysis, as well as to deliver a personalized medicine approach that allows for reductions in the incidence of these adverse drug reactions
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