Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA.
ALTEX. 2024 Jan 9;41(1):37-49. doi: 10.14573/altex.2306231. Epub 2023 Oct 19.
QT prolongation and the potentially fatal arrhythmia Torsades de Pointes are common causes for withdrawing or restricting drugs; however, little is known about similar liabilities of environmental chemicals. Current in vitro-in silico models for testing proarrhythmic liabilities, using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM), provide an opportunity to address this data gap. These methods are still low- to medium-throughput and not suitable for testing the tens of thousands of chemicals in commerce. We hypothesized that combining high-throughput population- based in vitro testing in hiPSC-CMs with a fully in silico data analysis workflow can offer sensitive and specific predictions of proarrhythmic potential. We calibrated the model with a published hiPSC-CM dataset of drugs known to be positive or negative for proarrhythmia and tested its performance using internal cross-validation and external validation. Additionally, we used computational down-sampling to examine three study designs for hiPSC-CM data: one replicate of one donor, five replicates of one donor, and one replicate of a population of five donors. We found that the population of five donors had the best performance for predicting proarrhythmic potential. The resulting model was then applied to predict the proarrhythmic potential of environmental chemicals, additionally characterizing risk through margin of exposure (MOE) calculations. Out of over 900 environmental chemicals tested, over 150 were predicted to have proarrhythmic potential, but only seven chemicals had a MOE < 1. We conclude that a high-throughput in vitro-in silico approach using population-based hiPSC-CM testing provides a reasonable strategy to screen environmental chemicals for proarrhythmic potential.
QT 延长和潜在致命的心律失常尖端扭转型室性心动过速是撤回或限制药物的常见原因;然而,对于环境化学物质的类似责任知之甚少。目前,使用人诱导多能干细胞衍生的心肌细胞(hiPSC-CM)进行测试致心律失常性的体外-计算机模拟模型为解决这一数据空白提供了机会。这些方法仍然是低到中通量的,不适合测试商业上数以万计的化学物质。我们假设,将高通量基于人群的 hiPSC-CM 体外测试与完全基于计算机的数据分析工作流程相结合,可以对致心律失常的潜力进行敏感和特异性预测。我们用已知对致心律失常呈阳性或阴性的药物的已发表 hiPSC-CM 数据集对模型进行了校准,并使用内部交叉验证和外部验证测试了其性能。此外,我们还使用计算下采样来检查 hiPSC-CM 数据的三种研究设计:一个供体的一个重复、一个供体的五个重复和一个供体群体的一个重复。我们发现,五个供体群体在预测致心律失常潜力方面表现最好。然后将得到的模型应用于预测环境化学物质的致心律失常潜力,并通过暴露边际(MOE)计算来表征风险。在测试的 900 多种环境化学物质中,有 150 多种被预测具有致心律失常的潜力,但只有 7 种化学物质的 MOE<1。我们得出结论,使用基于人群的 hiPSC-CM 测试的高通量体外-计算机模拟方法是筛选环境化学物质致心律失常潜力的合理策略。