Cardiac diseases, along with cancers, are the biggest causes of deaths in Europe. Almost half of cardiac deaths are linked with racing cardiac rates as a result of ventricular arrhythmias. Advances in pharmacology and intervention introduced in the 1980's helped to considerably improve survival rates among infarct patients. However, over the longer term these patients can develop a cardiac deficiency, as well as fatal ventricular arrhythmias. Such sudden cardiac deaths are not confined only to patients who have suffered an infarct but also include young and apparently healthy patients; there are several hereditary syndromes that can trigger fatal arrhythmias, often before any anomaly has even been diagnosed.
The contractions of a healthy heart are highly optimized movements that depend on an electrically activated mechanism. This mechanism is operated by some twenty different types of molecular "machines" in the external membrane of each cardiac cell. Although very effective in a healthy heart, it can trigger serious problems in the event of illness. For example, the activation can turn in circle in a cicatrized muscle or abnormal pulses can be triggered at a high rate by diseased cells.
The team used scientific computing to understand these mechanisms, using mathematical models that were developed based on the results of experiments on cardiac cells. Already very complex in a single cell, these models require high performance computing to simulate the interaction of the 2 billion cells in a heart. This work took place at IHU Liryc, a research institute dedicated to cardiac arrhythmias, with one of the largest clinical teams in the world specializing in the treatment of these diseases. The modellers worked closely with cardiologists as well as with biologists, physiologists, etc., to cover all the various aspects of cardiac arrhythmias. Thanks to this collaboration they were able to produce work that has a real impact in terms of the diagnosis and treatment of patients.