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• W2010461965 endingPage "72" @default.
• W2010461965 startingPage "57" @default.
• W2010461965 abstract "Background: Voltage-gated ion channels are the main providers of drug-induced delayed repolarization and, therefore, first line targets in cardiac safety assessments. Objectives/methods: We review mechanisms of drug-induced ventricular arrhythmias that may be associated with sudden cardiac death. We focus on Ca2+-dependent mechanisms with drug safety concerns. Results: Early afterdepolarizations occur during abnormally prolonged action potential repolarization. QT interval measurement is commonly used to assess the proarrhythmic risk of a drug. However, delayed afterdepolarizations are triggered by intracellular Ca2+ overload and/or abnormal spontaneous openings of ryanodine receptors in diastole. A drug promoting alterations of Ca2+ handling may be pro-arrhythmogenic without QT interval change at rest. Conclusion: Ca2+-dependent arrhythmia should be investigation matter in drug safety evaluation." @default.
• W2010461965 created "2016-06-24" @default.
• W2010461965 creator A5009366353 @default.
• W2010461965 creator A5019805247 @default.
• W2010461965 date "2009-01-01" @default.
• W2010461965 modified "2023-10-18" @default.
• W2010461965 title "Prolongation in QT interval is not predictive of Ca²⁺-dependent arrhythmias: implications for drug safety" @default.
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