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Salt Lake City, UT, USA USA
Nov. 10, 2012 to Nov. 16, 2012
ISBN: 978-1-4673-0805-2
pp: 1-11
We have developed a highly efficient and scalable cardiac electrophysiology simulation capability that supports groundbreaking resolution and detail to elucidate the mechanisms of sudden cardiac death from arrhythmia. We can simulate thousands of heartbeats at a resolution of 0.1 mm, comparable to the size of cardiac cells, thereby enabling scientific inquiry not previously possible. Based on scaling results from the partially deployed Sequoia IBM Blue Gene/Q machine at Lawrence Livermore National Laboratory and planned optimizations, we estimate that by SC12 we will simulate 8 -- 10 heartbeats per minute -- a time-to-solution 400 -- 500 times faster than the state-of-the-art. Performance between 8 and 11 PFlop/s on the full 1,572,864 cores is anticipated, representing 40 -- 55 percent of peak. The power of the model is demonstrated by illuminating the subtle arrhythmogenic mechanisms of anti-arrhythmic drugs that paradoxically increase arrhythmias in some patient populations.
Heart, Mathematical model, Logic gates, Instruction sets, Biological system modeling, Equations, Message systems
Arthur A. Mirin, David F. Richards, James N. Glosli, Erik W. Draeger, Bor Chan, Jean-luc Fattebert, William D. Krauss, Tomas Oppelstrup, John Jeremy Rice, John A. Gunnels, Viatcheslav Gurev, Changhoan Kim, John Magerlein, Matthias Reumann, Hui-Fang Wen, "Toward real-time modeling of human heart ventricles at cellular resolution: Simulation of drug-induced arrhythmias", SC, 2012, SC Conference, SC Conference 2012, pp. 1-11, doi:10.1109/SC.2012.108
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