Decades of intensive experimental and clinical research have revealed a great deal about how the human heart works. Though incomplete, this knowledge has been used to construct computer models that represent the activity of this organ as a whole, and of its individual chambers, the atria and ventricles, down to its tissues and cells. Such models have been used to better understand life-threatening irregular heartbeats; they are also beginning to be used to guide decisions about the treatment of patients and the development of new drugs by the pharmaceutical industry.
Yet existing computer models of the electrical activity of the human heart are sometimes inconsistent with experimental data. This issue led Dr Jakub Tomek, now a Postdoctoral Researcher in Department of Physiology, Anatomy & Genetics, to try and find an answer to this problem during his tenure in the Department of Computer Science as part of Professor Blanca Rodriguez’s Computational Cardiovascular Science Team. At the start of the project, the team observed that the most popular computer model at the time predicted a large increase in cellular contractility in response to sodium blockade, which is not compatible with clinical and experimental data. “This observation made us start working on a new model, but in the end, the journey towards success was much longer and more complicated than we initially expected.” (Dr Tomek).