In recent years, the field of computational cardiac modeling and simulation has matured in both scope and methodology such that it can contribute significantly to the present understanding of heart physiology and disease.
Research focus
The CaMo (Computational Cardiac Modeling) department at Simula is an integrated team of researchers working collaboratively with both experimentalists and clinicians to address current challenges in cardiology. The multifarious backgrounds of CaMo member scientists, a particular strength of the Group, enables focus on both development of state-of-the-art heart simulation tools and the targeted application of these tools to gain mechanistic insight into diverse biophysical cardiac phenomena: our work ranges from investigation of subcellular calcium ion channel phenomena to organ-level analysis of the ischemic heart.
Research projects
Current projects include development of a robust and accurate simulator for the electrical and mechanical behavior of the heart and associated applications, as well as investigation of the role of pathological cardiac tissue structure in arrhythmogenesis and arrhythmia maintenance.
- Cardiac Mechano-Electric Activity. Electrical and mechanical phenomena in the mammalian heart are tightly coupled: electrical activation precedes and triggers mechanical activation, and mechanical deformation of the tissue influences the electrical properties (mechano-electric feedback or MEF). The simplest and most common approach to simulate this process is to ignore MEF, pre-compute an electrical activation sequence, and subsequently solve the mechanical problem. However, realistic simulation of the mechanical performance of the heart is not possible without solving the fully-coupled problem. Mathematically, the problem is formulated as a system of partial and ordinary differential equations, and the challenge lies in development of methods and software to solve the problem efficiently. Possible applications of the simulator include the heart's performance (cardiac output) under normal and pathological conditions, analysis of predisposing factors for arrhythmias and prospective drug treatments, as well as further insight into defibrillation mechanisms.
- Cardiac Fibrosis and Arrhythmias. Arrhythmias, pathological disturbances in the normal rhythmic contraction of the heart, may either seriously reduce pumping capacity of the heart, or lead to complete failure to circulate blood, causing death within minutes. As arrhythmias are mostly caused by abnormalities in excitation of the cardiac muscle, we have focused on the modeling of normal and abnormal electrophysiology of cardiac cells, tissue and the whole heart. To increase the clinical applicability of our research, we use detailed quantitative models of human cardiac cells and tissue. Our research focuses on a factor that has received considerable attention for its potential role in arrhythmogenesis in recent years: cardiac fibrosis. This refers to the deposition of larger-than-normal amounts of extracellular matrix (ECM) proteins surrounding heart tissue, and is also characterized by a larger-than-normal number of ECM-producing cells (fibroblasts). Although this occurs in normal hearts during aging, it also occurs in response to infarction or chronic heart disease. The presence of fibrosis and arrhythmias are strongly correlated. However, this connection is still poorly understood. Our goal is to further understanding as to why and how cardiac fibrosis influences arrhythmogenesis and the maintenance of arrhythmias.
- Computational Biology. This project focuses on two different areas in computational or systems biology, namely the dynamics and mechanisms of cardiac arrhythmias, and the dynamics of evolutionary processes. This project is described in more detail on a separate project page.
