The virtual heart model successfully differentiates the arrhythmogenic profiles of cisapride and amiodarone by simulating their distinct multi-channel blocking effects on cardiac electrophysiology.
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May aid differentiation of proarrhythmic risk beyond QT prolongation; leaves open clinical validation of virtual heart screening.
To predict the safety of a drug at an early stage in its development is a major challenge as there is a lack of in vitro heart models that correlate data from preclinical toxicity screening assays with clinical results. A biophysically detailed computer model of the heart, the virtual heart, provides a powerful tool for simulating drug-ion channel interactions and cardiac functions during normal and disease conditions and, therefore, provides a powerful platform for drug cardiotoxicity screening. In this article, we first review recent progress in the development of theory on drug-ion channel interactions and mathematical modelling. Then we propose a family of biomarkers that can quantitatively characterize the actions of a drug on the electrical activity of the heart at multi-physical scales including cellular and tissue levels. We also conducted some simulations to demonstrate the application of the virtual heart to assess the pro-arrhythmic effects of cisapride and amiodarone. Using the model we investigated the mechanisms responsible for the differences between the two drugs on pro-arrhythmogenesis, even though both prolong the QT interval of ECGs. Several challenges for further development of a virtual heart as a platform for screening drug cardiotoxicity are discussed.
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Yuan et al. (2014) conducted a review in Drug cardiotoxicity. Cisapride and amiodarone vs. Control (simulated baseline) was evaluated on Action potential duration and pro-arrhythmic substrates.
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