- 期刊
Drug-Induced Long QT Syndrome
並列摘要
Drug-induced LQTS is the most common cause of drug-withdrawal in the recent decade. Human ether-a-go-go related gene (HERO) channel block results in prolongation of action potential duration and is the culprit for the majority of these acquired forms of LQTS. Some structural characteristics have been demonstrated in HERO channel and have been proposed as the mechanism for the susceptibility of the HERO channel, but it is difficult to predict the potential for a new drug to block HERO channel solely based on the molecular structure of the drug. QT prolongation precipitates torsades de pointes (TDP), a special form of polymorphic ventricular tachycardia, leading to ventricular fibrillation in some patients. A key feature of drug-induced LQTS is its unpredictable nature. QTc prolongation alone does not predict TDP, other mechanisms such as QTc dispersion might be involved. The theory of ”repolarization reserve” has been raised recently as a potential mechanism for allowing individuals to respond differently to QTc prolongation. On the other hand, higher serum concentration of HERO-blocking agents usually induces a longer QTc interval and increases the likelihood of TDP. Thus, pharmacokinetic interactions should always be taken into account when prescribing these agents. Genetic mutations or polymorphisms account for about 5 to 10 percent of cases of drug-induced TDR Finally, preclinical assessment of the risk of drug-induced LQTS relies on a systemic approach on cellular, tissue, and whole animal levels. Every clinician is strongly encouraged to update their information to improve patient care.
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